Study of risk factors for ascending aortic dilatation in different age groups using cardiac ultrasound indices

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Imaging techniques have been crucial in monitoring these patients, with cardiac ultrasound being increasingly used due to its noninvasive nature and high temporal resolution. However, most studies have focused on valve morphology and less on the role of age in hemodynamic changes. This study aims to analyze the risk factors for ascending aortic dilatation using cardiac ultrasound indices in BAV patients across different age groups. Methods: We included 300 patients diagnosed with BAV at the First Central Hospital of Baoding, with cardiac ultrasound data compared between those with and without aortic dilatation. Multifactorial analysis was performed to identify independent predictors of ascending aortic dilatation, focusing on age, hemodynamic load, and clinical comorbidities. Results: Age was significantly associated with peak transvalvular pressure difference and ascending aortic internal diameter. The analysis showed that in young patients, aortic dilatation was mainly linked to valve-derived hemodynamic abnormalities, whereas in middle-aged patients, risk factors included hemodynamic load and diabetes. In older patients, the primary factors were smoking-induced oxidative stress and degenerative lesions. Age was found to significantly affect the predictive efficacy of peak transvalvular pressure difference. Conclusion: This study highlights age-specific differences in the mechanisms of ascending aortic dilatation. In young patients, valve dysfunction predominates; in middle-aged individuals, metabolic diseases such as diabetes become important risk factors; and in the elderly, long-term smoking and degenerative changes dominate. The findings suggest the importance of individualized risk assessment based on age for better management of ascending aortic dilatation in clinical practice. Bileaflet Aortic Valve Ascending Aortic Dilatation Cardiac Ultrasound Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 Introduction Patients with bileaflet aortic valves (BAV) often present with structural lesions of the ascending aorta, significantly increasing the risk of aortic aneurysm and its acute complications such as entrapment or rupture. As the most common congenital malformation of the heart, the BAV patient population faces a significant risk of ascending aortic aneurysm [ 1 ][ 2 ][ 8 ] . Currently, the clinical management of BAV-associated aortopathy is challenging, with the main difficulty being the difficulty in accurately predicting the risk of progression of aortic dilatation. Although emerging imaging markers are being developed, the use of biomechanical indicators as an assessment may be of significant value. Studies have shown that segmental aortic remodeling occurs early in patients with BAV, as evidenced by loss of elastic lamellar structure and increased extracellular matrix collagen content. However, accurate assessment of this aortic deformation is difficult. Ultrasound imaging itself has the potential for higher temporal resolution. Given that echocardiography is the method of choice for routine follow-up of patients with BAV (for assessment of left ventricular function, the aortic valve, and the ascending aorta), convenient access to these sensitive markers during follow-up would be of great clinical value because it is rapid, cost-effective, and radiation-free. PATIENTS AND METHODS 1. Subjects This study was approved by the Ethics Committee of Hebei Medical University. Coronary computed tomography angiography (CCTA) imaging was performed according to clinical indications; therefore, patients were not exposed to additional radiation doses. The clinical treatment of the patients was not affected by the study. Systematic review of 300 patients diagnosed with BAV and underwent cardiac ultrasonography in the First Central Hospital of Baoding from 2019 to 2024. 1.1 Inclusion criteria ① Clear diagnosis of BAV on admission or discharge, with diagnostic methods including thoracic echocardiography and cardiac computed tomography (CT); ② At least one preoperative cardiac two-dimensional ultrasound or Doppler ultrasound result. 1.2 Exclusion criteria ① Previously underwent any aortic related surgery, left ventricular system valve surgery; ② Previously infected with infective endocarditis; ③ Combined with aortic constriction; ④ Combined with other congenital anomalies; ⑤ Poor quality of the image can not be categorized for the type of fusion of valves; ⑥ Tumor patients. 2. Definition of aortic dilatation The main classification of aortic dilatation is that AA is considered dilated when its maximum diameter exceeds 40 mm in any of the three measurement planes of CT, regardless of gender. 3. valve morphology All study subjects were classified according to the typing criteria proposed by Michelena et al. in 2014, which categorized patients into 3 types based on the fusion of the aortic valve on transthoracic echocardiographic parasternal long-axis and short-axis views: type I, right coronary valve-left coronary valve fusion (type R-L); type II, right coronary valve-no coronary valve fusion (type R-N); and type III, left coronary valve- uncinate fusion (type L-R) (Fig. 1 ). This typology does not take into account the presence or absence of fused crests. Due to the small number of types II and III, they were collectively categorized as no coronary fusion. type R-L, although it accounted for the majority of the cases, did not show significant differentiation between valve morphology and ascending aortic dilatation (P > 0.05) [ 5 ] . 4.Acquisition of cardiac echocardiograms A Philips EPIQ7C diagnostic cardiovascular ultrasound machine was used in this study, and the probe model was selected: S5-1 (standard probe for adults, frequency range 1–5 MHz) or the appropriate frequency probe according to the patient's body size. The patients were placed in the left lateral position, with the left upper limb elevated to the side of the head or placed naturally, the anterior thoracic region of the patients (from the clavicle to the epigastrium) was fully exposed, and the synchronized electrocardiogram (ECG) lead was connected to ensure the accurate marking of the temporal phase of the cardiac cycle. The probe frequency and depth are adjusted to the patient's size and acoustic window conditions in standard 2D and Doppler views to ensure imaging stability. The examination was performed by a board-certified cardiac ultrasound specialist with extensive experience in cardiac ultrasound to ensure that the images were acquired to standard and that the measurements were accurate and reliable. Aortic valve staging and cardiac ultrasound measurements were performed by two specialists. 4.1 Cardiac ultrasound index settings Cardiac ultrasound indexes acquired were all tied to synchronized echocardiography (ECG) and measured at their specific time phases (e.g., aortic valve flow velocity was acquired at peak mid-systolic flow velocity; peak transvalvular pressure difference was peak pressure at mid-systole). Observations Patients with BAV who developed dilatation of the ascending aorta were categorized as the experimental group, and those who did not develop dilatation were defined as the control group. Cardiac measurements of the BAV group were compared with those of the control group. Statistical analysis Data were analyzed using SPSS 27.0 statistical software. All continuous variables were first tested for normality (Shapiro-Wilk test), and if the data did not conform to normal distribution, they were expressed as medians and quartiles, and the Mann-Whitney U test was used to compare the differences between the two groups; for normally distributed data, means and standard deviations were used, and independent samples t-tests were performed. Categorical variables were analyzed using the chi-square test (Chi-square test). To control for the risk of false positives in multiple comparisons, all statistical tests were Bonferroni corrected.Screening for potential risk factors was performed using binary logistic regression analysis, and significant variables were selected by stepwise regression, and the odds ratio (OR) and its 95% confidence interval were calculated. Results Summary Statistics Out of a total sample size of 300 cases (220 males, 80 females), the number of cases of patients with dilated ascending aorta was 106 and the number of non-dilated cases was 194. The range of left ventricular shortening measurements was 33.85 (16.40–45.00) in the dilated group and 34.28 (12.00–45.00) in the nondilated group; except for left ventricular shortening which was smaller in the case group than in the control group, the rest of the demographics and cardiac ultrasonography data were overall higher in the dilated group than in the nondilated group, and the data are summarized in Table 1 . Table 1 Summary statistics of patient demographics and cardiac ultrasound including IVSd; IVSs; LVIDd; LVIDs; LVPWd; LVPWs; EDV; ESV; FS; EF. Summary expansionist group(n = 106) non-expansion group(n = 194) age 54.42 ± 11.49 48.06 ± 15.06 hypertensive(mmHg) * 150(116–197) 135(105–190) IVSd(cm) * 1.00(0.68–1.63) 0.92(0.70–1.43) IVSs(cm) * 1.39(0.84–2.45) 1.33(0.84–2.17) LVIDd(cm) * 5.02(3.82–7.65) 4.75(3.70–9.67) LVIDs(cm) * 3.32(1.26–5.44) 3.09(2.33–7.78) LVPWd(cm) * 0.99(0.56–1.94) 0.96(0.67–1.42) LVPWs(cm) * 1.37(0.56–1.94) 1.32(0.95–2.70) FS * 33.85(16.40–45.00) 34.28(12.00–45.00) EDV(ml) * 120.12(72.42-315.13) 104.46(59.89-363.38) ESV(ml) * 46.67(21.04-148.92) 42.25(20.67–213.20) SV(ml) * 73.75(40.63–201.90) 62.87(32.00-210.15) EF(%) * 0.61(0.40–0.79) 0.60(0.40–0.76) Aortic valve flow rate * 2.54(1.70–3.86) 2.30(1.38–3.35) Peak Transvalve Differential Pressure * 33.75(29.52–44.42) 29.69(26.06–40.99) Ascending aortic diameter * 4.23(4.05–4.29) 3.31(2.95–3.98) *: Data are non-normally distributed and are expressed as median (quartiles). IVSd: interventricular septal thickness end-diastolic; IVSs: interventricular septal thickness end-systolic; LVIDd: left ventricular end-diastolic internal diameter; LVIDs: left ventricular end-systolic internal diameters; LVPWd: left ventricular posterior wall thickness end-diastolic; LVPWs: left ventricular posterior wall thickness end-systolic; EDV: left ventricular volume in diastole; ESV: left ventricular volume in systole; FS: left ventricular shortening rate; EF: ejection fraction. It was found that patients with bileaflet aortic valves who developed ascending aortic dilatation were more likely to be male, at 75%. The age and cardiac ultrasound parameters of the group were significantly higher than those who did not develop ascending aortic dilatation, whereas the left ventricular shortening rate (FS) was lower than that of the control group. This occurs considering that LV shortening rate is linearly and negatively correlated with vessel wall shear stress in both longitudinal and circumferential directions, with higher vessel wall stress resulting in lower LV shortening rate [8]. Since the cardiac ultrasound data were non-normally distributed, the Mann-Whieney U test was applied to test the difference between the case group and the control group using the Mann-Whieney U test (see Table 2 ), whereas the chi-square test was applied for the categorical variables of age, hypertension, gender, valvular morphology and valvular complications (see Table 3 ). The results showed that valvular complications (stenosis and closure insufficiency), age, hypertension, hyperlipidemia, diabetes mellitus, smoking, IVSd, LVIDd, LVIDs, LVPWd, EDV, SV, ESV, aortic flow velocities, peak transvalvular pressure difference, and ascending aortic internal diameter in the case group differed significantly from that of the group that did not experience dilatation. Table 2 Differences between cardiac ultrasound indices in dilated and non-dilated groups Variability between cardiac ultrasound indicators Cardiac ultrasound indicators Mann-Whieney U P IVSd(mm) 7846.00 <0.01 IVSs(mm) 9030.50 0.081 LVIDd(mm) 8041.500 0.002 LVIDs(mm) 8447.00 0.011 LVPWd(mm) 8443.50 0.01 LVPWs(mm) 9342.00 0.19 FS 9493.50 0.272 EDV(ml) 7583.00 <0.001 ESV(ml) 9272.50 0.16 SV(ml) 7080.00 <0.001 EF(%) 8758.00 0.034 Aortic valve flow rate 6691.00 <0.01 Peak Transvalve Differential Pressure 2904.00 <0.01 Ascending aortic diameter .00 <0.01 Table 3 Demographic intergroup differences between the expanded and unexpanded groups Differences between demographic groups Demographic indicators χ² P gender 0.383 0.536 age 13.756 0.01 hypertensive 51.928 <0.01 Valve morphology 0.012 0.914 Valve Complications 16.569 <0.01 hyperlipidemia 25.394 <0.01 diabetes 64.705 <0.01 cigarette smoking 25.394 <0.01 Age Among 106 patients with BAV ascending aortic dilatation, patients ≤ 45 years old were categorised as young, 46–59 years old as middle-aged and ≥ 60 years old as old. Age-complications, valve morphology, gender, hypertension, hyperlipidemia, diabetes mellitus, and smoking were analysed using the chi-square test; age-cardiac ultrasound indices, aortic valve flow velocity, pressure, and ascending aortic internal diameter did not follow a normal distribution and were analysed using a nonparametric test (Kruskal-Wallis test) (see Table 4 ). Table 4 Difference between age groups and demographic indicators Differences in age groupings and demographic indicators χ² P gender 1.290 0.525 hypertensive 3.624 0.727 Hyperlipidemia 2.418 0.298 diabetes 0.029 0.985 cigarette smoking 1.039 0.595 Valve Complications 3.546 0.170 Valve morphology 2.996 0.224 Table 5 Difference between age grouping and cardiac ultrasound indices Blood pressure H P Aortic valve flow rate 2.517 0.284 Peak Transvalve Differential Pressure 64.696 <0.001 Ascending aortic diameter 52.150 <0.001 IVSd 0.713 0.700 IVSs 0.489 0.783 LVIDd 0.697 0.706 LVIDs 0.661 0.718 LVPWd 0.392 0.822 LVPWs 0.158 0.924 FS 0.055 0.973 EDV 0.668 0.716 ESV 1.296 0.523 SV 0.174 0.917 EF 1.178 0.555 The results showed that age was not differentiated from other differentials, age was significant with peak transvalvular pressure difference (H = 64.696, P < 0.001) and with ascending aortic internal diameter (H = 52.150, P < 0.001). In a post hoc test with the Bonferroni correction method, peak transvalvular pressure difference: young-middle-aged group, middle-aged group, and old-aged group had a P value of < 0.01; and ascending aortic internal diameter: young-middle-aged group, and middle-aged group, and old-aged group had a P value of < 0.01. Based on the graph of peak transvalvular pressure difference-ascending aortic internal diameter, the larger the peak transvalvular pressure difference, the more pronounced was the dilatation of the ascending aorta. According to the age-peak transvalvular pressure difference graph, peak transvalvular pressure difference and ascending aortic internal diameter showed a decreasing trend from youth to middle age and an increasing trend from middle age to old age. This result is consistent with the conclusion of Thompson MA et al [ 4 ] , which suggests to some extent that middle age is a critical stage of aortic valve pressure change, and should be used as a ‘window period’ for the prevention of ascending aortic dilatation. When the enrolled population was analysed, the median (quartiles) was used to express the blood pressure because it did not conform to normal distribution.The blood pressure grading was based on the Chinese Guidelines for the Prevention and Control of High Blood Pressure (Revised 2024).Grade 1 hypertension (mild): systolic blood pressure 140–159 mmHg; grade 2 hypertension (moderate): systolic blood pressure 160–179 mmHg; and grade 3 hypertension (severe): Systolic blood pressure ≥ 180 mmHg and/or diastolic blood pressure ≥ 110 mmHg. The median blood pressure in the dilated group was 150 (116–197) mmHg, and in the undilated group it was 135 (105–190) mmHg. It can be found that the blood pressure of those who developed dilatation of the ascending aorta was significantly higher than that of those who did not have dilatation. The chi-square test of blood pressure grouping with gender, age, valve morphology, and valve complications showed that blood pressure possessed variability with valve complications, diabetes mellitus, and hyperlipidemia (see Table 6 ). With the help of Mann-Whieney U test for stenosis and incomplete group, the rank mean value of hypertension in stenosis group was 58.56 and that in incomplete group was 44.81 with a P value of 0.026, which suggests that blood pressure in stenosis group is higher than that in incomplete group, which is considered to be related to the fact that after stenosis of aortic valves, the heart needs more pressure to pump out the blood. Table 6 Difference between hypertension and demographic indicators Hypertension and Sex, Age, Valve Morphology, and Differential Valve Complications χ² P gender 6.023 0.110 diabetes 26.850 <0.01 hyperlipidemia 39.767 <0.01 cigarette smoking 4.222 0.238 Valve morphology 2.727 0.436 Valve Complications 11.974 0.007 When the blood pressure groupings and cardiac ultrasound indices were tested using the Kruskal-Wallis test, the test results showed that blood pressure was significant with IVSs, LVID, LVPW, EDV, ESV, SV and ascending aortic internal diameter, with a P value of < 0.05 (see Table 7 ). Post hoc tests were performed with the help of Bonferroni correction method, in which the between-group P was < 0.05 for LVIDd, LVIDs, EDV and SV, in the LVPWs factor: normotensive versus hypertensive grade 2 (P = 0.028); in the ESV factor: normotensive versus hypertensive grades 2 and 3 had a differentiation (P < 0.01), and hypertensive grade 1 versus hypertensive grades 2 and 3 had a difference (P0.05). The results suggest that hypertension leads to thickening of the LV wall and enlargement of the ventricular cavity, and that the significance of this remodelling correlates with the grade of hypertension; whereas ESV differed significantly in all groups and increased significantly with the grade of hypertension, which is a strong signal of progressive decline in LV systolic function. Table 7 Correlation between hypertension and cardiac ultrasound indices Complications Correlation of hypertension with cardiac ultrasound indices H P IVSd 6.073 0.108 IVSs 8.390 0.039 LVIDd 68.971 <0.001 LVIDs 43.991 <0.001 LVPWd 13.129 0.004 LVPWs 16.488 <0.001 FS 3.953 0.267 EDV 76.130 <0.001 ESV 35.301 <0.001 SV 90.608 <0.001 EF 1.983 0.576 Aortic valve flow rate 1.618 0.655 Peak Transvalve Differential Pressure 1.601 0.659 Internal diameter of the ascending aorta 7.809 0.048 Patients with bileaflet aortic valves are most likely to have complications of aortic stenosis and valve closure insufficiency, the subsequent result of which is dilatation of the ascending aorta. The development of valvular complications is correlated with haemodynamic abnormalities, inherent structural abnormalities of the aortic wall, genetic molecules and secondary pathologies [ 9 ] . All enrolled patients had valvular complications, and if stenosis and insufficiency of closure coexisted, the group was classified as the one with the more severe lesion (e.g., severe stenosis combined with moderate valvular insufficiency was included in the stenosis group). By performing a chi-square test between the case and control groups, the chi-square value was 16.569, p < 0.001, suggesting that bilobed aortic valvular lesions may be one of the factors in the occurrence of ascending aortic dilatation. With the help of chi-square test for demographic indicators, it was seen that valvular complications and hyperlipidemia were differentiated, and valvular complications - aortic valve flow velocity, pressure, and ascending aortic internal diameter did not follow a normal distribution, so they were analysed using a non-parametric test (Kruskal-Wallis test) and Spearman correlation test. In the analysis of variance and correlation with complications as a control factor, the cardiac ultrasound parameters were not significant, and the cases were divided into stenosis and incomplete closure groups for discussion, considering the presence of confounding factors of stenosis and incomplete closure. Interestingly, when the case groups were further divided into stenosis and incomplete closure groups, no significant variability in mitral valve morphology was observed (see Table 8 ), and the correlation between cardiac ultrasound parameters and the aorta was significantly improved. Table 8 Correlation of cardiac ultrasound indices with demographic and haemodynamic indices in the stenosis group Differential Valve Complications and Demographic Indicators χ² P gender 0.07 0.791 age 3.546 0.17 diabetes 1.108 0.292 hyperlipidemia 7.932 0.005 cigarette smoking 0.027 0.870 Valve morphology 0.041 0.84 Among 106 patients with dilated ascending aorta of BAV, there were a total of 67 cases of stenosis, of which 74% were males, age 54 ± 12.06 years, hypertension 153 (121–197) mmHg, IVSd 1 (0.68–1.63) mm, IVSs 1.40 (0.84–2.45) mm, LVIDd 5.03 (3.82–7.65 ) mm, LVIDs 3.36 (1.26–4.91) mm, LVPWd 0.99 (0.68–1.33) mm, LVPWs 1.36 (1.03–1.85) mm, FS 34.10 (16.40–45.00), EDV 121.53 (76.82-315.13) ml, ESV 45.31 ( 21.04-113.23) ml, SV 77.06 (45.70-201.90) ml,EF 0.64 (0.51–0.79), aortic valve flow velocity 2.54 (1.95–3.17), peak transvalvular pressure difference 33.95 (30.20-44.42), and ascending aortic internal diameter 4.20 (4.06–4.89). When the cardiac ultrasound indices of the stenosis group were analysed for correlation with age, hypertension, aortic valve flow velocity, pressure and ascending aortic internal diameter, the following were seen (Table 9 ): 1) aortic valve flow velocity - LVIDd (r = -0.401, P < 0.01), aortic valve flow velocity - LVIDd (r = -0.594, P < 0.01), aortic valve flow velocity - FS (r = 0.823, P < 0.01), aortic valve flow velocity-EDV (r=-0.343, P = 0.04), aortic valve flow velocity-ESV (r=-0.639, P < 0.01), and aortic valve flow velocity-EF (r = 0.923, P < 0.001); and (ii) peak transvalvular pressure difference-age (r = 0.636,P < 0.01), peak transvalvular pressure difference - ascending aortic internal diameter (r = 0.578, P < 0.01); and (iii) ascending aortic internal diameter - age (r = 0.590, P < 0.001). Table 9 Correlation of cardiac ultrasound indices with demographic and haemodynamic indices in the stenosis group Correlation of cardiac ultrasound indices with demographic and haemodynamic indices in the stenosis group r P Peak transvalvular pressure difference - age 0.636 <0.001 Peak Transvalvular Differential Pressure - Ascending Aortic Internal Diameter 0.578 <0.01 Aortic valve flow rate-LVIDd −0.401 <0.01 Aortic valve flow velocities-LVIDs −0.594 <0.01 Aortic valve flow rate-FS 0.823 <0.01 Aortic valve flow velocity - EDV −0.343 0.04 Aortic Valve Flow Rate - ESV −0.639 <0.01 Aortic valve flow rate-EF 0.923 <0.001 Ascending aortic diameter - age 0.59 <0.001 Incomplete closure In 39 patients, 77% were male, age 56 ± 10.40 years, hypertension 142 (116–192) mmHg, IVSd 1 (0.69–1.60) mm, IVSs 1.37 (1.05–1.94) mm, LVIDd 5.00 (3.95–7.10) mm, LVIDs 3.30 (2.16–5.14) mm, LVPWd 1 (0.66–1.32) mm, LVPWs 1.38 (0.56–1.94) mm, FS 33.33 (21.20–42.00), EDV 117.23 (72.42-266.51) ml, ESV 48.92 (25.14-148.92) ml, SV 67.27 (40.63-136.07) ml, EF 0.58 (0.40–0.70), aortic valve flow rate 2.54 (1.70–3.86), peak transvalvular pressure difference 32.94 (29.52–42.65), and ascending aortic internal diameter 4.29 (4.05–4.83). The correlation of haemodynamic indices in cardiac ultrasound with age, hypertension, aortic valve flow velocity, pressure and ascending aortic internal diameter could be similarly examined by Spearman's correlation (see Table 10 ). The results showed that: (i) aortic valve flow velocity -LVIDd (r=-0.337, P < 0.001), aortic valve flow velocity -LVIDs (r=-0.421, P < 0.001), aortic valve flow velocity -FS (r = 0.494, P < 0.001), aortic valve flow velocity -EDV (r=-0.316, P < 0.001), aortic valve flow velocity -ESV (r=-0.463, P < 0.001), aortic valve flow velocity-EF (r = 0.486, P < 0.001); (ii) peak transvalvular pressure difference-age (r = 0.646, P < 0.001), peak transvalvular pressure difference-ascending aortic internal diameter (r = 0.564, P < 0.001); and (iii) ascending aortic internal diameter-age (r = 0.626, P < 0.001). Table 10 Correlation of cardiac ultrasound indices with demographic and haemodynamic indices in the Incomplete closure group Correlation of cardiac ultrasound indices with demographic and haemodynamic indices in the incomplete closure group r P Aortic valve flow rate-LVIDd −0.337 <0.001 Aortic valve flow rate-LVIDs -0.421 <0.001 Aortic valve flow rate-FS 0.494 <0.001 Aortic Valve Flow Rate - EDV -0.316 <0.001 Aortic Valve Flow Rate - ESV -0.463 <0.001 Aortic valve flow rate-EF 0.486 <0.001 Peak Transvalvular Differential Pressure - Age 0.646 <0.001 Peak Transvalvular Differential Pressure - Ascending Aortic Internal Diameter 0.564 <0.001 Ascending aortic diameter - age 0.626 <0.001 Discusssion The pathogenesis of ascending aortic dilatation (aneurysm) is dynamic: it leads to changes in the intima-media composition of the vessel wall with increased aortic wall stress, and the vessel dilates with the time of the lesion, which is denatured through the interaction of extracellular aortic matrix abnormalities and smooth muscle cell dysfunction. Hemodynamic abnormalities lead to irregular turbulence in the vasculature (especially eccentric flow), and abnormal flow impingement causes endothelial loss and increased wall stress, which further promotes altered intima-media composition and structural remodeling [ 10 ][ 11 ][ 20 ] . Cardiac ultrasound is one of the primary diagnostic tests for cardiac-related diseases, which not only assesses the state of cardiac function of the patient, but also provides guidance for assessing and predicting the risk of progression of dilatation of the ascending aorta and surgery through cardiac ultrasound-related indexes. The causes of ascending aortic dilatation vary in different age groups, and for this reason the causes were explored by binary logistic regression analysis. The factors were first explored independently in relation to ascending aortic dilatation to find risk factors with P < 0.05, and then independent risk factors were screened multifactorially. P < 0.05 for valve complications, hypertension, EF, aortic valve flow velocity, peak transvalvular pressure difference, diabetes mellitus, and hyperlipidemia in the young group; P < 0.05 for valve complications, hypertension, aortic valve flow velocity, peak transvalvular pressure difference, diabetes mellitus, hyperlipidemia, and cigarette smoking in the middle-aged group; P < 0.05 for hypertension, aortic valve flow velocity, peak transvalvular pressure difference, diabetes mellitus, and cigarette smoking in the elderly group. A further multifactorial binary logistic regression analysis, using stepwise backward method and iterative removal of non-significant variables (likelihood ratio test), revealed that: risk factors for the occurrence of ascending aortic dilatation in the young group were valvular complications (P = 0.011, OR = 8.197), aortic valve flow velocity (P = 0.009, OR = 26.355), peak transvalvular pressure differential (P = 0.009, OR = 1.395); risk factors for the development of ascending aortic dilatation in the middle-aged group were peak transvalvular pressure difference (P < 0.01, OR = 2.186), and diabetes mellitus (P < 0.01, OR = 7.170); and in the elderly group were peak transvalvular pressure difference (P < 0.01, OR = 2.853), and cigarette smoking (P < 0.01, OR = 13.534). OR = 13.534) (see Table 11 ). As can be seen from the results, the occurrence of ascending aortic dilatation in the young group was mainly related to valve function and hemodynamics; in the middle-aged group, the risk factors began to appear as metabolic diseases superimposed on hemodynamic factors; and in the elderly group, factors of long-term vascular loss and degenerative lesions predominated. Table 11 Risk factors for occurrence of ascending aortic dilatation in different age groups Age grouping factors OR(95%CI) P Youth group Valve Complications 5.161(1.071–24.864) 0.041 Aortic valve flow rate 45.062(4.485–62.772) 0.001 Peak Transvalve Differential Pressure 1.416(1.117–1.795) 0.004 Middle-aged group Peak Transvalve Differential Pressure 2.186(1.626–2.938) <0.01 diabetes 7.170(2.532–20.300) <0.01 senior group Peak Transvalve Differential Pressure 2.853(1.537–5.295) <0.01 cigarette smoking 13.534(1.438–30.332) 0.023 Age structure and ascending aortic dilatation The central finding of age as an effect modifier is that the spectrum of risk factors for ascending aortic dilatation varies significantly with age. This suggests that age is not a simple confounding variable, but rather a powerful “effect modifier” that alters the strength and/or nature of the relationship between other factors and ascending aortic dilatation. There are fundamental differences in aortic wall characteristics, underlying disease spectrum, and duration of exposure between age groups. For the younger age groups, ascending aortic dilatation strongly points to congenital disease (BAV) or early-onset acquired valvular disease (e.g., rheumatic heart disease), and valvular complications, high flow velocities, and high-peak transvalvular pressure differentials are a direct consequence of these pathologies, which produce abnormal wall shear stresses and pressure loads. In contrast, the traditional cardiovascular risk factors of diabetes mellitus, hyperlipidemia, and smoking require a longer period of cumulative storminess to become apparent and have not yet reached the threshold of pathogenesis in youth. In young patients with ascending aortic dilatation, valve disease must be prioritized for screening and close monitoring. In the middle-aged group, diabetes becomes a key metabolic factor, which damages the extracellular matrix (collagen, elastin) of the vascular wall and reduces its elasticity and strength by loss of vascular matrix, with the help of hyperglycemia, accumulation of end products of late glycosylation, oxidative stress, inflammation, and other pathways, which make the aortic wall more susceptible to dilatation in response to the stresses of blood flow, and diabetes is a strong promoter of both atherosclerosis and vascular sclerosis that alters the biomechanical properties of the vessel wall. Therefore, in middle-aged patients with ascending aortic dilatation, tight glycemic control and management of diabetes mellitus and its complications, in addition to concern for valve function, are critical and require a more comprehensive cardiovascular risk assessment. For the older age group, long-term cumulative damage to the vessel wall and valve degeneration predominated, and peak transvalvular pressure difference remained a significant factor (OR = 2.853), which may largely reflect the high prevalence of severe degenerative calcific aortic stenosis in the older age group, with persistent mechanical stresses acting on the already aged vessel wall. At the same time, smoking has emerged as the most prominent emerging risk factor in the elderly group, with prolonged smoking leading to a sustained systemic and vascular wall inflammatory response, increased oxidative stress, direct damage to endothelial and smooth muscle cells, and promotion of matrix metalloproteinase expression, which accelerates the degradation of collagen and elastin and destroys the structural support of the aortic wall. For patients with dilated ascending aorta in the elderly, the importance of lifelong smoking cessation is emphasized, along with management of severe aortic valve lesions (assessed for indications for intervention) and assessment of overall vascular health.With the increase of age, lysyl oxidase (LOX) activity decreases, vascular elastin cross-linking is insufficient, and calcium ions are gradually deposited, the elastic plate layer calcification and fracture, combined with telomere shortening + P53/P161NK4a activity increases, and vascular repair ability decreases, these chain reaction to the failure of the vascular wall of the Cauchy's stress gradually decreases, and the hardness of the vascular wall gradually rises, on behalf of the vascular tissue elasticity worse and worse. The elasticity begins to decline (with increased collagen deposition), leading to a decrease in the minimum impact force threshold for the ascending aorta to withstand blood flow, which predisposes it to dilatation [ 5 ][ 11 ][ 12 ][ 13 ] . Whereas peak transvalvular pressure difference is always a significant risk factor regardless of the patient's age, suggesting that close monitoring of the diameter of the ascending aorta is necessary in patients with BAV at any age. Valve Complications and Ascending Aortic Dilatation - Complicated Stenosis of the Leaflet Aortic Valve The left ventricle is required to pump intraluminal blood into the aorta at higher pressures, and high velocity turbulence (especially eccentric jets) is created by the narrowed valve orifice. This unstable flow impacts the localized area of the ascending aorta for a long period of time, resulting in local endothelial loss and mechanical stress, “similar to a high-pressure water pistol repeatedly flushing the inner wall of a water pipe,” which further induces remodeling of the middle layer of the vessel wall [ 14 ] . At the same time post-stenotic turbulence also activates the inflammatory response of the vessel wall through wall shear stress: the inflammatory process consists of macrophage and lymphocyte migration associated with a small increase in mast cells and neutrophils, with the meso- and epicardium of the aorta being the most affected structures, which in turn further destroys the vascular structure leading to dilatation of the ascending aorta [ 13 ] . -Diaphragmatic Aortic Valve Complicated Closure Insufficiency The systolic high-flow ejection of blood from the heart exposes the aorta to greater volume shocks in a short period of time, with compensatory thickening of the systolic thickness of the interventricular septum, while diastolic regurgitation leads to an abrupt drop in the aortic root pressure, resulting in the formation of a high pulse pressure difference (systolic high pressure-diastolic low pressure). This cyclic stress causes the wall of the ascending aorta to dilate and retract repeatedly, forming the “Windkessel effect”, and the highly oscillatory WSS activates the endothelial NF-κB pathway, resulting in an increase in the release of inflammatory factors (IL-6, TNF-α) and accelerating the elastic fiber rupture and intima-media regression in the aortic wall, which results in the overall dilatation of the aorta in relation to the loss of localized areas of the stenotic wall. The overall dilatation of the ascending aorta is more pronounced compared to the loss of localized areas of the vessel wall after stenosis [ 15 ][ 16 ][ 17 ][ 18 ] . In the young population, ascending aortic dilatation in BAV with valvular insufficiency is 5.161 times higher than that in patients with concomitant stenosis. Prolonged high volume loading and high differential pulse pressure result in sustained tension of the ascending aortic wall, which mechanically stretches the smooth muscle cells, and over-activation of TGF-β1 leads to an increase in secretion of matrix metalloproteinases (MMP-2/9), which accelerate degradation of elastin, cleave elastin fibers, and destroy extracellular matrix (see Figure). extracellular matrix (see Fig. 2 ). At the same time, abnormal activation of the transforming growth factor (TGF-β) signaling pathway, which is a regulatory cytokine expressed by vascular smooth muscle cells in the arterial wall, regulates the activity of MMP, which further promotes fibrosis, and the elasticity of the vascular wall decreases, and the dilation is more pronounced [ 10 ] [ 12 ] [ 13 ][ 20 ][ 21 ] . The results also showed that LVPW and ESV were higher in the incomplete closure group than in the stenosis group due to diastolic regurgitation of blood into the left ventricle, which resulted in a significant increase in left ventricular volume load. The LV compensatorily increases the volume per beat (forward blood flow + regurgitant flow) through the Frank-Starling mechanism, and the systolic ejection rate is accelerated, which elevates the valvular flow rate. Chronic volume loading results in LV isolated hypertrophy and enlarged ventricular chambers. In the early compensatory phase, ESV remains normal; when ascending aortic dilatation occurs, the myocardium has become fibrotic, systolic function decreases, and ESV rises. In addition, diastolic regurgitation causes the left ventricle to empty in a shorter period of time, further affecting the end-systolic residual volume. Aortic wall “congenital defects” and genetic factors Patients with bileaflet aortic valve (BAV) often have congenital structural defects of the ascending aorta. Whereas the normal intima consists of a spring-like mechanical support system of regularly arranged elastic fibers and smooth muscle cells, patients with BAV are characterized by a structural disorder of the intima: broken elastic fibers, abnormal collagen arrangement, and absence of smooth muscle cells, resulting in a wall that resembles the mechanical properties of an inelastic, aging rubber band. It has been suggested that this pathological change is associated with mutations in genes that regulate aortic development during embryonic life (e.g., NOCTH-1) [ 11 ] [ 12 ] [ 13 ] , which serve the dual function of valve morphology and vessel wall maturation, leading to aberrant SMC differentiation and ultimately to the resultant mesangial cystic necrosis. Analyzed at the level of molecular mechanisms, BAV-associated aortopathy has a dual regulatory pathway. At the genetic level, mutations directly affect the function of vascular structural proteins: mutations in myosin heavy chain 11 (MYH11), a core component of the smooth muscle contractile unit, not only impede the multimerization of myosin to form thick myofilaments, but also reduce the expression of contractile proteins and induce cellular de-differentiation, resulting in impaired response to mechanical stresses and susceptibility to vessel wall injury. Mutations in the myosin light chain kinase (MYLK) gene, on the other hand, impair the regulation of light chain phosphorylation, weakening myosin II ATPase activity and ultimately triggering degenerative changes in the midmembrane [ 11 ] [ 12 ] [ 13 ] . Clinical comorbidities in relation to ascending aortic dilatation Mechanisms of diabetic vascular injury(See Fig. 6 ): ① Activation of AGEs-RAGE axis: high blood glucose leads to the accumulation of AGEs, and their products bind to the RAGE receptor, resulting in excessive bursts of ROS, leading to the sustained activation of the NF-κB inflammatory pathway, and the subsequent result of this pathway is the destruction of elastin fibers and intima-media components of the aortic wall by inflammatory factors [ 19 ] . ② Destruction of matrix structure: 1) abnormal collagen cross-linking: AGEs covalently bind to collagen, which increases the fragility of aortic fibers [ 19 ] ; 2) elastin degradation: elevated MMP-2/9 activity combined with decreased TIMP-1 activity leads to rupture of the elastic network of the vascular wall; and 3) SMC failure: high glucose-induced apoptosis of SMCs, which leads to the thinning of vascular mesangium. ③Peak transvalvular pressure difference continuously exerts mechanical load, diabetes weakens matrix tensile strength, and the risk of aortic dilatation doubles under the same pressure difference; meanwhile, high glucose promotes the synthesis of abnormal collagen by SMCs, and the stiffness of ascending aortic wall increases, and wall shear stress is more likely to be concentrated locally. Smoking vascular injury mechanisms(See Fig. 7 ): ① nicotine in cigarettes activates α7-nACHR pathway, causing SMC proliferation or migration abnormalities, resulting in structural disorders in the middle layer of the vasculature [ 23 ] ; ② cigarettes on the one hand, through the consumption of NO by free radicals, resulting in endothelium-dependent diastolic disorders of the vasculature, on the other hand, through the activation of NADPH oxidase, the outbreak of superoxide anion (O₂-) → lipid peroxidation [ 24 ] ; (iii) smoke exhaled during smoking induces MMP-12 (macrophage elastase) activation, leading to fragmentation of vascular elastic fibers. Study Strengths and Limitations The In this study, we found that age and hemodynamic load (especially peak transvalvular pressure difference) were independent predictors of ascending aortic dilatation in patients with BAV. Consistent with existing studies, we found that the risk of ascending aortic dilatation increased significantly with age, especially in middle-aged and elderly patients, and the role of traditional cardiovascular risk factors, such as diabetes mellitus and smoking, was more pronounced. This suggests that the impact of age and metabolic diseases such as diabetes cannot be ignored in the management of patients with BAV. Our first stratified analysis incorporating the age factor showed that the risk of ascending aortic dilatation in young patients was mainly associated with abnormal valve function, whereas middle-aged and elderly patients were characterized by the superimposition of metabolic diseases such as diabetes mellitus with hemodynamic load. The finding that the role of peak transvalvular pressure difference as a hemodynamic index in predicting ascending aortic dilatation increases with age suggests that individualized follow-up strategies should be developed according to differences in the age groups of patients. However, this study also has some limitations. First, this study was a single-center retrospective study with a relatively small sample size and a lack of long-term follow-up data. Future studies could further validate our results with a multicenter, large-sample prospective design. CONCLUSION The present study revealed significant differences in the pathogenic mechanisms of ascending aortic dilatation by age-stratified analysis in different age groups. Ascending aortic dilatation in young patients was mainly associated with valve-derived hemodynamic abnormalities; in middle-aged patients, risk factors included hemodynamic load and diabetes mellitus; and in older patients, it was dominated by long-term smoking-induced oxidative stress and degenerative lesions. The predictive efficacy of peak transvalvular pressure difference as an important hemodynamic index increases significantly with age. Declarations Declaration of competing interest The authors declare that there is no conflict of interest. Funding This research was supported by Baoding First Center Hospital Author Contribution Yujia Shen was responsible for data analysis and article writing; Jiabao Guo was responsible for data collection; and Zhenyu Xing was responsible for article review. References Nimrat Grewal AC, Gittenberger-de Groot RE, Poelmann, Robert JM, Klautz, Johannes HN, Lindeman M-J, Goumans M, Palmen SA, Mohamed H-H, Sievers AJJC, Bogers MC. DeRuiter,Ascending aorta dilation in association with bicuspid aortic valve: A maturation defect of the aortic wall,The. J Thorac Cardiovasc Surg Volume. 2014;148:1583–90. Rodríguez-Palomares JF, et al. Mechanisms of Aortic Dilation in Patients With Bicuspid Aortic Valve. J Am Coll Cardiol. 2023;81(14):1333–49. Maros Ferencik, Linda A. Pape,Changes in size of ascending aorta and aortic valve function with time in patients with congenitally bicuspid aortic valves. Am J Cardiol Volume 92, Issue 1,2003,Pages 43–6. Jose F, Rodríguez-Palomares L, Dux-Santoy A, Guala. Laura Galian-Gay, Arturo Evangelista,Mechanisms of Aortic Dilation in Patients With Bicuspid Aortic Valve: JACC State-of-the-Art Review,Journal of the American College of Cardiology,82, Issue 5,2023,Pages 448–64. Thompson MA, Kramer B, Tarraf SA, Vianna E, Gillespie C, Germano E, Gentle B, Cikach F, Lowry AM, Pande A, Blackstone E, Hargrave J, Colbrunn R, Bellini C, Roselli EE. Age is superior to aortopathy phenotype as a predictor of aortic mechanics in patients with bicuspid valve. J Thorac Cardiovasc Surg. 2025;169(2):531–e5414. Goldfinger JZ, Halperin JL, Marin ML, Stewart AS, Eagle KA. Fuster V,Thoracic aortic aneurysm and dissection. J Am Coll Cardiol. 2014;64:1725–39. Hatzaras I, Tranquilli M, Coady M, Barrett PM, Bible J, Elefteriades JA. Weight,lifting and aortic dissection: more evidence for a connection. Cardiology. 2007;107:103–6. Ho SY. Structure and anatomy of the aortic root. Eur J Echocardiogr. 2009;10:i3–10. Murai D, Yamada S, Hayashi T, Okada K, Nishino H, Nakabachi M, Yokoyama S, Abe A, Ichikawa A, Ono K, Kaga S, Iwano H, Mikami T, Tsutsui H. Relationships of left ventricular strain and strain rate to wall stress and their afterload dependency. Heart Vessels. 2017;32(5):574–83. Spanos K, Nana P, von Kodolitsch Y, Behrendt CA, Kouvelos G, Panuccio G, Athanasiou T, Matsagkas M, Giannoukas A, Detter C, Kölbel T. Management of Ascending Aorta and Aortic Arch: Similarities and Differences Among Cardiovascular Guidelines. J Endovasc Ther. 2022;29(5):667–77. Verma R, Cohen G, Colbert J, Fedak PWM. Bicuspid aortic valve associated aortopathy: 2022 guideline update. Curr Opin Cardiol. 2023;38(2):61–7. Della Corte A, Lo Presti F. La bicuspidia aortica e le sue complicanze: dalle molecole al bisturi [Bicuspid aortic valve and its complications: from molecules to surgery]. G Ital Cardiol (Rome). 2022;23(7):542–52. Mozzini C, Girelli D, Cominacini L, Soresi M. An Exploratory Look at Bicuspid Aortic Valve (Bav) Aortopathy: Focus on Molecular and Cellular Mechanisms. Curr Probl Cardiol. 2021;46(3):100425. Bararu Bojan I, Pleșoianu CE, Badulescu OV, Vladeanu MC, Badescu MC, Iliescu D, Bojan A, Ciocoiu M. Molecular and Cellular Mechanisms Involved in Aortic Wall Aneurysm Development. Volume 13. Diagnostics; 2023. p. 253. Soulat G, Scott MB, Allen BD, Avery R, Bonow RO, Malaisrie SC, McCarthy P, Fedak PWM, Barker AJ, Markl M. Association of Regional Wall Shear Stress and Progressive Ascending Aorta Dilation in Bicuspid Aortic Valve. JACC Cardiovasc Imaging. 2022;15(1):33–42. Barker AJ, Markl M, Burk J, et al. Bicuspid Aortic Valve Is Associated With Altered Wall Shear Stress in the Ascending Aorta. Circ Cardiovasc Imaging. 2012;5:457–66. van Ooij P, Garcia J, Potters WV, et al. Age-related changes in aortic 3D blood flow velocities and wall shear stress: Implications for the identification of altered hemodynamics in patients with aortic valve disease: Age-Related Changes in 3D Velocity and WSS. J Magn Reson Imaging. 2016;43:1239–49. van Ooij P, Potters WV, Collins J, et al. Characterization of abnormal wall shear stress using 4D flow MRI in human bicuspid aortopathy. Ann Biomed Eng. 2015;43:1385–97. Bollache E, Guzzardi DG, Sattari S, et al. Aortic valve-mediated wall shear stress is heterogeneous and predicts regional aortic elastic fiber thinning in bicuspid aortic valve-associated aortopathy. J Thorac Cardiovasc Surg. 2018;156:2112–20. e2. Ahmad HM, et al. Emerging imaging and circulating biomarkers in relation to aortopathy in bicuspid aortic valve disease. Front Physiol. 2025;16:11930195. Făgărășan A, et al. Circulating Matrix Metalloproteinases for Prediction of Aortic Dilation in Children with Bicuspid Aortic Valve. Int J Mol Sci. 2024;25(19):10538. Zhou M, Zhang Y, Shi L, Li L, Zhang D, Gong Z, Wu Q. Activation and modulation of the AGEs-RAGE axis: Implications for inflammatory pathologies and therapeutic interventions - A review. Pharmacol Res. 2024;206:107282. 10.1016/j.phrs.2024.107282 . Epub 2024 Jun 22. PMID: 38914383. Yang J, Li Y, Wang H, Li X, Chen H, Hou H, Hu Q. Nicotine Attenuates Pathogenesis of Parkinson's Disease via α7-nAChR-Mediated Lipid Metabolic Reprogramming and Anti-inflammatory Signaling. Mol Neurobiol. 2025 Jun 9. 10.1007/s12035-025-05124-9 . Epub ahead of print. PMID: 40490660. Carlström M, Weitzberg E, Lundberg JO. Nitric Oxide Signaling and Regulation in the Cardiovascular System: Recent Advances. Pharmacol Rev. 2024;76(6):1038–1062. 10.1124/pharmrev.124.001060 . PMID: 38866562. Additional Declarations No competing interests reported. Supplementary Files Statement.docx Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7378654","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":502110002,"identity":"39ea56e0-6772-45b2-83ab-3b87d94122f8","order_by":0,"name":"Yujia Shen","email":"","orcid":"","institution":"First Central Hospital of Baoding","correspondingAuthor":false,"prefix":"","firstName":"Yujia","middleName":"","lastName":"Shen","suffix":""},{"id":502110003,"identity":"ebd38306-b871-4219-a289-8f90dacd536c","order_by":1,"name":"Jiabao Guo","email":"","orcid":"","institution":"First Central Hospital of 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05:53:21","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-7378654/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-7378654/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":89984998,"identity":"d56df0dd-a1f4-4df5-a21c-dd7970dcf1f7","added_by":"auto","created_at":"2025-08-27 06:38:56","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":667103,"visible":true,"origin":"","legend":"\u003cp\u003eSchematic diagram of BAV ultrasound staging\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-7378654/v1/8b1cc7b2e98ca9a87ad0947e.png"},{"id":89983010,"identity":"f6afdb7b-70ec-4fb8-a413-532921f27c1b","added_by":"auto","created_at":"2025-08-27 06:30:56","extension":"jpeg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":64582,"visible":true,"origin":"","legend":"\u003cp\u003eAge and peak transvalvular pressure difference\u003c/p\u003e","description":"","filename":"floatimage2.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7378654/v1/1d25a8e42c562400d4ae9262.jpeg"},{"id":89983011,"identity":"d5bf86ee-9f44-4edb-bdda-8715d15c37dc","added_by":"auto","created_at":"2025-08-27 06:30:57","extension":"jpeg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":60910,"visible":true,"origin":"","legend":"\u003cp\u003eAge and ascending aortic diameter\u003c/p\u003e","description":"","filename":"floatimage3.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7378654/v1/2db75340354f073ee83c95f9.jpeg"},{"id":89983020,"identity":"56ad194c-ef36-487c-8dfe-0b07f5752b57","added_by":"auto","created_at":"2025-08-27 06:30:57","extension":"jpeg","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":39989,"visible":true,"origin":"","legend":"\u003cp\u003ePeak Transvalvular Differential Pressure and Ascending Aortic Diameter\u003c/p\u003e","description":"","filename":"floatimage4.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7378654/v1/c7429ab7995511b8dcd36d15.jpeg"},{"id":89983019,"identity":"5367a081-d696-45ea-b04f-19056190bd35","added_by":"auto","created_at":"2025-08-27 06:30:57","extension":"jpeg","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":76174,"visible":true,"origin":"","legend":"\u003cp\u003eActivation of the MMP-2-induced dilatation activation pathway in the ascending aorta\u003c/p\u003e","description":"","filename":"floatimage5.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7378654/v1/e22ded4a11de2d745b4ecd46.jpeg"},{"id":89985001,"identity":"f4550195-bb6e-4c49-8df2-65e9a5adeab3","added_by":"auto","created_at":"2025-08-27 06:38:57","extension":"jpeg","order_by":6,"title":"Figure 6","display":"","copyAsset":false,"role":"figure","size":1037365,"visible":true,"origin":"","legend":"\u003cp\u003eMechanisms of diabetic vascular injury\u003c/p\u003e","description":"","filename":"floatimage7.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7378654/v1/439f88749a605f1cfc8d0938.jpeg"},{"id":89983025,"identity":"5c5ce216-14f7-4ba7-853c-349c0ed2b633","added_by":"auto","created_at":"2025-08-27 06:30:57","extension":"jpeg","order_by":7,"title":"Figure 7","display":"","copyAsset":false,"role":"figure","size":401357,"visible":true,"origin":"","legend":"\u003cp\u003eSmoking vascular injury mechanisms\u003c/p\u003e","description":"","filename":"floatimage8.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7378654/v1/faf728c493781db6ba48723e.jpeg"},{"id":96365847,"identity":"0d7307a0-4ade-46ba-a635-be632f33795d","added_by":"auto","created_at":"2025-11-20 10:10:52","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":3590277,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7378654/v1/16f50978-4571-4a62-8373-692526932ef4.pdf"},{"id":89984999,"identity":"87a3a02f-521d-46ee-a9de-4d862b6ba354","added_by":"auto","created_at":"2025-08-27 06:38:56","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":11168,"visible":true,"origin":"","legend":"","description":"","filename":"Statement.docx","url":"https://assets-eu.researchsquare.com/files/rs-7378654/v1/9911e77977828c926eb3c60b.docx"}],"financialInterests":"No competing interests reported.","formattedTitle":"Study of risk factors for ascending aortic dilatation in different age groups using cardiac ultrasound indices","fulltext":[{"header":"Introduction","content":"\u003cp\u003ePatients with bileaflet aortic valves (BAV) often present with structural lesions of the ascending aorta, significantly increasing the risk of aortic aneurysm and its acute complications such as entrapment or rupture. As the most common congenital malformation of the heart, the BAV patient population faces a significant risk of ascending aortic aneurysm\u003csup\u003e[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e][\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e][\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]\u003c/sup\u003e. Currently, the clinical management of BAV-associated aortopathy is challenging, with the main difficulty being the difficulty in accurately predicting the risk of progression of aortic dilatation. Although emerging imaging markers are being developed, the use of biomechanical indicators as an assessment may be of significant value.\u003c/p\u003e\u003cp\u003eStudies have shown that segmental aortic remodeling occurs early in patients with BAV, as evidenced by loss of elastic lamellar structure and increased extracellular matrix collagen content. However, accurate assessment of this aortic deformation is difficult. Ultrasound imaging itself has the potential for higher temporal resolution. Given that echocardiography is the method of choice for routine follow-up of patients with BAV (for assessment of left ventricular function, the aortic valve, and the ascending aorta), convenient access to these sensitive markers during follow-up would be of great clinical value because it is rapid, cost-effective, and radiation-free.\u003c/p\u003e"},{"header":"PATIENTS AND METHODS","content":"\n\u003ch3\u003e1. Subjects\u003c/h3\u003e\n\u003cp\u003e This study was approved by the Ethics Committee of Hebei Medical University. Coronary computed tomography angiography (CCTA) imaging was performed according to clinical indications; therefore, patients were not exposed to additional radiation doses. The clinical treatment of the patients was not affected by the study. Systematic review of 300 patients diagnosed with BAV and underwent cardiac ultrasonography in the First Central Hospital of Baoding from 2019 to 2024.\u003c/p\u003e\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003ch2\u003e1.1 Inclusion criteria\u003c/h2\u003e\u003cp\u003e① Clear diagnosis of BAV on admission or discharge, with diagnostic methods including thoracic echocardiography and cardiac computed tomography (CT); ② At least one preoperative cardiac two-dimensional ultrasound or Doppler ultrasound result.\u003c/p\u003e\u003c/div\u003e\u003cdiv id=\"Sec4\" class=\"Section2\"\u003e\u003ch2\u003e1.2 Exclusion criteria\u003c/h2\u003e\u003cp\u003e① Previously underwent any aortic related surgery, left ventricular system valve surgery; ② Previously infected with infective endocarditis; ③ Combined with aortic constriction; ④ Combined with other congenital anomalies; ⑤ Poor quality of the image can not be categorized for the type of fusion of valves; ⑥ Tumor patients.\u003c/p\u003e\u003c/div\u003e\n\u003ch3\u003e2. Definition of aortic dilatation\u003c/h3\u003e\n\u003cp\u003eThe main classification of aortic dilatation is that AA is considered dilated when its maximum diameter exceeds 40 mm in any of the three measurement planes of CT, regardless of gender.\u003c/p\u003e\n\u003ch3\u003e3. valve morphology\u003c/h3\u003e\n\u003cp\u003eAll study subjects were classified according to the typing criteria proposed by Michelena et al. in 2014, which categorized patients into 3 types based on the fusion of the aortic valve on transthoracic echocardiographic parasternal long-axis and short-axis views: type I, right coronary valve-left coronary valve fusion (type R-L); type II, right coronary valve-no coronary valve fusion (type R-N); and type III, left coronary valve- uncinate fusion (type L-R) (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e1\u003c/span\u003e). This typology does not take into account the presence or absence of fused crests. Due to the small number of types II and III, they were collectively categorized as no coronary fusion. type R-L, although it accounted for the majority of the cases, did not show significant differentiation between valve morphology and ascending aortic dilatation (P\u0026thinsp;\u0026gt;\u0026thinsp;0.05) \u003csup\u003e[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\n\u003ch3\u003e4.Acquisition of cardiac echocardiograms\u003c/h3\u003e\n\u003cp\u003eA Philips EPIQ7C diagnostic cardiovascular ultrasound machine was used in this study, and the probe model was selected: S5-1 (standard probe for adults, frequency range 1\u0026ndash;5 MHz) or the appropriate frequency probe according to the patient's body size. The patients were placed in the left lateral position, with the left upper limb elevated to the side of the head or placed naturally, the anterior thoracic region of the patients (from the clavicle to the epigastrium) was fully exposed, and the synchronized electrocardiogram (ECG) lead was connected to ensure the accurate marking of the temporal phase of the cardiac cycle. The probe frequency and depth are adjusted to the patient's size and acoustic window conditions in standard 2D and Doppler views to ensure imaging stability. The examination was performed by a board-certified cardiac ultrasound specialist with extensive experience in cardiac ultrasound to ensure that the images were acquired to standard and that the measurements were accurate and reliable. Aortic valve staging and cardiac ultrasound measurements were performed by two specialists.\u003c/p\u003e\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e\u003ch2\u003e4.1 Cardiac ultrasound index settings\u003c/h2\u003e\u003cp\u003eCardiac ultrasound indexes acquired were all tied to synchronized echocardiography (ECG) and measured at their specific time phases (e.g., aortic valve flow velocity was acquired at peak mid-systolic flow velocity; peak transvalvular pressure difference was peak pressure at mid-systole).\u003c/p\u003e\u003cp\u003eObservations\u003c/p\u003e\u003cp\u003ePatients with BAV who developed dilatation of the ascending aorta were categorized as the experimental group, and those who did not develop dilatation were defined as the control group. Cardiac measurements of the BAV group were compared with those of the control group.\u003c/p\u003e\u003c/div\u003e\u003cdiv id=\"Sec9\" class=\"Section2\"\u003e\u003ch2\u003eStatistical analysis\u003c/h2\u003e\u003cp\u003eData were analyzed using SPSS 27.0 statistical software. All continuous variables were first tested for normality (Shapiro-Wilk test), and if the data did not conform to normal distribution, they were expressed as medians and quartiles, and the Mann-Whitney U test was used to compare the differences between the two groups; for normally distributed data, means and standard deviations were used, and independent samples t-tests were performed. Categorical variables were analyzed using the chi-square test (Chi-square test). To control for the risk of false positives in multiple comparisons, all statistical tests were Bonferroni corrected.Screening for potential risk factors was performed using binary logistic regression analysis, and significant variables were selected by stepwise regression, and the odds ratio (OR) and its 95% confidence interval were calculated.\u003c/p\u003e\u003c/div\u003e"},{"header":"Results","content":"\u003cp\u003eSummary Statistics\u003c/p\u003e\u003cp\u003eOut of a total sample size of 300 cases (220 males, 80 females), the number of cases of patients with dilated ascending aorta was 106 and the number of non-dilated cases was 194. The range of left ventricular shortening measurements was 33.85 (16.40\u0026ndash;45.00) in the dilated group and 34.28 (12.00\u0026ndash;45.00) in the nondilated group; except for left ventricular shortening which was smaller in the case group than in the control group, the rest of the demographics and cardiac ultrasonography data were overall higher in the dilated group than in the nondilated group, and the data are summarized in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e.\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eSummary statistics of patient demographics and cardiac ultrasound including IVSd; IVSs; LVIDd; LVIDs; LVPWd; LVPWs; EDV; ESV; FS; EF.\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\" morerows=\"1\" rowspan=\"2\"\u003e\u0026nbsp;\u003c/th\u003e\u003cth align=\"left\" colspan=\"2\" nameend=\"c3\" namest=\"c2\"\u003e\u003cp\u003eSummary\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003eexpansionist group(n\u0026thinsp;=\u0026thinsp;106)\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\"\u003e\u003cp\u003enon-expansion group(n\u0026thinsp;=\u0026thinsp;194)\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eage\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e54.42\u0026thinsp;\u0026plusmn;\u0026thinsp;11.49\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e48.06\u0026thinsp;\u0026plusmn;\u0026thinsp;15.06\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ehypertensive(mmHg)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e150(116\u0026ndash;197)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e135(105\u0026ndash;190)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eIVSd(cm)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.00(0.68\u0026ndash;1.63)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.92(0.70\u0026ndash;1.43)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eIVSs(cm)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.39(0.84\u0026ndash;2.45)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e1.33(0.84\u0026ndash;2.17)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVIDd(cm)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e5.02(3.82\u0026ndash;7.65)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e4.75(3.70\u0026ndash;9.67)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVIDs(cm)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e3.32(1.26\u0026ndash;5.44)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e3.09(2.33\u0026ndash;7.78)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVPWd(cm)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.99(0.56\u0026ndash;1.94)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.96(0.67\u0026ndash;1.42)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVPWs(cm)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.37(0.56\u0026ndash;1.94)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e1.32(0.95\u0026ndash;2.70)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eFS\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e33.85(16.40\u0026ndash;45.00)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e34.28(12.00\u0026ndash;45.00)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eEDV(ml)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e120.12(72.42-315.13)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e104.46(59.89-363.38)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eESV(ml)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e46.67(21.04-148.92)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e42.25(20.67\u0026ndash;213.20)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSV(ml)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e73.75(40.63\u0026ndash;201.90)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e62.87(32.00-210.15)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eEF(%)\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.61(0.40\u0026ndash;0.79)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.60(0.40\u0026ndash;0.76)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e2.54(1.70\u0026ndash;3.86)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e2.30(1.38\u0026ndash;3.35)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePeak Transvalve Differential Pressure\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e33.75(29.52\u0026ndash;44.42)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e29.69(26.06\u0026ndash;40.99)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAscending aortic diameter\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e4.23(4.05\u0026ndash;4.29)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e3.31(2.95\u0026ndash;3.98)\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003ctfoot\u003e\u003ctr\u003e\u003ctd colspan=\"3\"\u003e*: Data are non-normally distributed and are expressed as median (quartiles).\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd colspan=\"3\"\u003eIVSd: interventricular septal thickness end-diastolic; IVSs: interventricular septal thickness end-systolic; LVIDd: left ventricular end-diastolic internal diameter; LVIDs: left ventricular end-systolic internal diameters; LVPWd: left ventricular posterior wall thickness end-diastolic; LVPWs: left ventricular posterior wall thickness end-systolic; EDV: left ventricular volume in diastole; ESV: left ventricular volume in systole; FS: left ventricular shortening rate; EF: ejection fraction.\u003c/td\u003e\u003c/tr\u003e\u003c/tfoot\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eIt was found that patients with bileaflet aortic valves who developed ascending aortic dilatation were more likely to be male, at 75%. The age and cardiac ultrasound parameters of the group were significantly higher than those who did not develop ascending aortic dilatation, whereas the left ventricular shortening rate (FS) was lower than that of the control group. This occurs considering that LV shortening rate is linearly and negatively correlated with vessel wall shear stress in both longitudinal and circumferential directions, with higher vessel wall stress resulting in lower LV shortening rate [8]. Since the cardiac ultrasound data were non-normally distributed, the Mann-Whieney U test was applied to test the difference between the case group and the control group using the Mann-Whieney U test (see Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e), whereas the chi-square test was applied for the categorical variables of age, hypertension, gender, valvular morphology and valvular complications (see Table\u0026nbsp;\u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). The results showed that valvular complications (stenosis and closure insufficiency), age, hypertension, hyperlipidemia, diabetes mellitus, smoking, IVSd, LVIDd, LVIDs, LVPWd, EDV, SV, ESV, aortic flow velocities, peak transvalvular pressure difference, and ascending aortic internal diameter in the case group differed significantly from that of the group that did not experience dilatation.\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eDifferences between cardiac ultrasound indices in dilated and non-dilated groups\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colspan=\"3\" nameend=\"c3\" namest=\"c1\"\u003e\u003cp\u003eVariability between cardiac ultrasound indicators\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eCardiac ultrasound indicators\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eMann-Whieney U\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eIVSd(mm)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e7846.00\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eIVSs(mm)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e9030.50\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.081\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVIDd(mm)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e8041.500\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.002\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVIDs(mm)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e8447.00\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.011\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVPWd(mm)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e8443.50\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVPWs(mm)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e9342.00\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.19\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eFS\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e9493.50\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.272\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eEDV(ml)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e7583.00\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eESV(ml)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e9272.50\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.16\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSV(ml)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e7080.00\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eEF(%)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e8758.00\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.034\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e6691.00\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePeak Transvalve Differential Pressure\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e2904.00\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAscending aortic diameter\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e.00\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab3\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eDemographic intergroup differences between the expanded and unexpanded groups\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colspan=\"3\" nameend=\"c3\" namest=\"c1\"\u003e\u003cp\u003eDifferences between demographic groups\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eDemographic indicators\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eχ\u0026sup2;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003egender\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.383\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.536\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eage\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e13.756\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ehypertensive\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e51.928\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eValve morphology\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.012\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.914\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eValve Complications\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e16.569\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ehyperlipidemia\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e25.394\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ediabetes\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e64.705\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ecigarette smoking\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e25.394\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eAge\u003c/p\u003e\u003cp\u003eAmong 106 patients with BAV ascending aortic dilatation, patients\u0026thinsp;\u0026le;\u0026thinsp;45 years old were categorised as young, 46\u0026ndash;59 years old as middle-aged and \u0026ge;\u0026thinsp;60 years old as old. Age-complications, valve morphology, gender, hypertension, hyperlipidemia, diabetes mellitus, and smoking were analysed using the chi-square test; age-cardiac ultrasound indices, aortic valve flow velocity, pressure, and ascending aortic internal diameter did not follow a normal distribution and were analysed using a nonparametric test (Kruskal-Wallis test) (see Table\u0026nbsp;\u003cspan refid=\"Tab4\" class=\"InternalRef\"\u003e4\u003c/span\u003e).\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab4\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 4\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eDifference between age groups and demographic indicators\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colspan=\"3\" nameend=\"c3\" namest=\"c1\"\u003e\u003cp\u003eDifferences in age groupings and demographic indicators\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eχ\u0026sup2;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003egender\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.290\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.525\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ehypertensive\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e3.624\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.727\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eHyperlipidemia\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e2.418\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.298\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ediabetes\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.029\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.985\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ecigarette smoking\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.039\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.595\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eValve Complications\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e3.546\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.170\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eValve morphology\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e2.996\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.224\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab5\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 5\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eDifference between age grouping and cardiac ultrasound indices Blood pressure\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003eH\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e2.517\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.284\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePeak Transvalve Differential Pressure\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e64.696\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAscending aortic diameter\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e52.150\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eIVSd\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e0.713\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.700\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eIVSs\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e0.489\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.783\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVIDd\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e0.697\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.706\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVIDs\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e0.661\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.718\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVPWd\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e0.392\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.822\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVPWs\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e0.158\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.924\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eFS\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e0.055\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.973\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eEDV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e0.668\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.716\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eESV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e1.296\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.523\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e0.174\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.917\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eEF\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e\u003cp\u003e1.178\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e0.555\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eThe results showed that age was not differentiated from other differentials, age was significant with peak transvalvular pressure difference (H\u0026thinsp;=\u0026thinsp;64.696, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001) and with ascending aortic internal diameter (H\u0026thinsp;=\u0026thinsp;52.150, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001). In a post hoc test with the Bonferroni correction method, peak transvalvular pressure difference: young-middle-aged group, middle-aged group, and old-aged group had a P value of \u0026lt;\u0026thinsp;0.01; and ascending aortic internal diameter: young-middle-aged group, and middle-aged group, and old-aged group had a P value of \u0026lt;\u0026thinsp;0.01. Based on the graph of peak transvalvular pressure difference-ascending aortic internal diameter, the larger the peak transvalvular pressure difference, the more pronounced was the dilatation of the ascending aorta. According to the age-peak transvalvular pressure difference graph, peak transvalvular pressure difference and ascending aortic internal diameter showed a decreasing trend from youth to middle age and an increasing trend from middle age to old age. This result is consistent with the conclusion of Thompson MA et al \u003csup\u003e[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]\u003c/sup\u003e, which suggests to some extent that middle age is a critical stage of aortic valve pressure change, and should be used as a \u0026lsquo;window period\u0026rsquo; for the prevention of ascending aortic dilatation.\u003c/p\u003e\u003cp\u003e When the enrolled population was analysed, the median (quartiles) was used to express the blood pressure because it did not conform to normal distribution.The blood pressure grading was based on the Chinese Guidelines for the Prevention and Control of High Blood Pressure (Revised 2024).Grade 1 hypertension (mild): systolic blood pressure 140\u0026ndash;159 mmHg; grade 2 hypertension (moderate): systolic blood pressure 160\u0026ndash;179 mmHg; and grade 3 hypertension (severe): Systolic blood pressure\u0026thinsp;\u0026ge;\u0026thinsp;180 mmHg and/or diastolic blood pressure\u0026thinsp;\u0026ge;\u0026thinsp;110 mmHg. The median blood pressure in the dilated group was 150 (116\u0026ndash;197) mmHg, and in the undilated group it was 135 (105\u0026ndash;190) mmHg. It can be found that the blood pressure of those who developed dilatation of the ascending aorta was significantly higher than that of those who did not have dilatation.\u003c/p\u003e\u003cp\u003eThe chi-square test of blood pressure grouping with gender, age, valve morphology, and valve complications showed that blood pressure possessed variability with valve complications, diabetes mellitus, and hyperlipidemia (see Table\u0026nbsp;\u003cspan refid=\"Tab6\" class=\"InternalRef\"\u003e6\u003c/span\u003e). With the help of Mann-Whieney U test for stenosis and incomplete group, the rank mean value of hypertension in stenosis group was 58.56 and that in incomplete group was 44.81 with a P value of 0.026, which suggests that blood pressure in stenosis group is higher than that in incomplete group, which is considered to be related to the fact that after stenosis of aortic valves, the heart needs more pressure to pump out the blood.\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab6\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 6\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eDifference between hypertension and demographic indicators\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colspan=\"3\" nameend=\"c3\" namest=\"c1\"\u003e\u003cp\u003eHypertension and Sex, Age, Valve Morphology, and Differential Valve Complications\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eχ\u0026sup2;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003egender\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e6.023\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.110\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ediabetes\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e26.850\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ehyperlipidemia\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e39.767\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ecigarette smoking\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e4.222\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.238\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eValve morphology\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e2.727\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.436\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eValve Complications\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e11.974\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.007\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eWhen the blood pressure groupings and cardiac ultrasound indices were tested using the Kruskal-Wallis test, the test results showed that blood pressure was significant with IVSs, LVID, LVPW, EDV, ESV, SV and ascending aortic internal diameter, with a P value of \u0026lt;\u0026thinsp;0.05 (see Table\u0026nbsp;\u003cspan refid=\"Tab7\" class=\"InternalRef\"\u003e7\u003c/span\u003e). Post hoc tests were performed with the help of Bonferroni correction method, in which the between-group P was \u0026lt;\u0026thinsp;0.05 for LVIDd, LVIDs, EDV and SV, in the LVPWs factor: normotensive versus hypertensive grade 2 (P\u0026thinsp;=\u0026thinsp;0.028); in the ESV factor: normotensive versus hypertensive grades 2 and 3 had a differentiation (P\u0026thinsp;\u0026lt;\u0026thinsp;0.01), and hypertensive grade 1 versus hypertensive grades 2 and 3 had a difference (P\u0026lt;0.01), hypertension grade 2 and hypertension grade 3 had a difference (P\u0026thinsp;=\u0026thinsp;0.011); in the factor of ascending aortic internal diameter, no significant difference was seen between the groups (P\u0026gt;0.05). The results suggest that hypertension leads to thickening of the LV wall and enlargement of the ventricular cavity, and that the significance of this remodelling correlates with the grade of hypertension; whereas ESV differed significantly in all groups and increased significantly with the grade of hypertension, which is a strong signal of progressive decline in LV systolic function.\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab7\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 7\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eCorrelation between hypertension and cardiac ultrasound indices Complications\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colspan=\"3\" nameend=\"c3\" namest=\"c1\"\u003e\u003cp\u003eCorrelation of hypertension with cardiac ultrasound indices\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eH\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eIVSd\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e6.073\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.108\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eIVSs\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e8.390\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.039\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVIDd\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e68.971\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVIDs\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e43.991\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVPWd\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e13.129\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.004\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eLVPWs\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e16.488\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eFS\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e3.953\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.267\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eEDV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e76.130\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eESV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e35.301\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eSV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e90.608\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eEF\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.983\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.576\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.618\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.655\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePeak Transvalve Differential Pressure\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.601\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.659\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eInternal diameter of the ascending aorta\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e7.809\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.048\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003ePatients with bileaflet aortic valves are most likely to have complications of aortic stenosis and valve closure insufficiency, the subsequent result of which is dilatation of the ascending aorta. The development of valvular complications is correlated with haemodynamic abnormalities, inherent structural abnormalities of the aortic wall, genetic molecules and secondary pathologies \u003csup\u003e[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]\u003c/sup\u003e. All enrolled patients had valvular complications, and if stenosis and insufficiency of closure coexisted, the group was classified as the one with the more severe lesion (e.g., severe stenosis combined with moderate valvular insufficiency was included in the stenosis group). By performing a chi-square test between the case and control groups, the chi-square value was 16.569, p\u0026thinsp;\u0026lt;\u0026thinsp;0.001, suggesting that bilobed aortic valvular lesions may be one of the factors in the occurrence of ascending aortic dilatation.\u003c/p\u003e\u003cp\u003eWith the help of chi-square test for demographic indicators, it was seen that valvular complications and hyperlipidemia were differentiated, and valvular complications - aortic valve flow velocity, pressure, and ascending aortic internal diameter did not follow a normal distribution, so they were analysed using a non-parametric test (Kruskal-Wallis test) and Spearman correlation test. In the analysis of variance and correlation with complications as a control factor, the cardiac ultrasound parameters were not significant, and the cases were divided into stenosis and incomplete closure groups for discussion, considering the presence of confounding factors of stenosis and incomplete closure. Interestingly, when the case groups were further divided into stenosis and incomplete closure groups, no significant variability in mitral valve morphology was observed (see Table\u0026nbsp;\u003cspan refid=\"Tab8\" class=\"InternalRef\"\u003e8\u003c/span\u003e), and the correlation between cardiac ultrasound parameters and the aorta was significantly improved.\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab8\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 8\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eCorrelation of cardiac ultrasound indices with demographic and haemodynamic indices in the stenosis group\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colspan=\"3\" nameend=\"c3\" namest=\"c1\"\u003e\u003cp\u003eDifferential Valve Complications and Demographic Indicators\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eχ\u0026sup2;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003egender\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.07\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.791\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eage\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e3.546\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.17\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ediabetes\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.108\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.292\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ehyperlipidemia\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e7.932\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.005\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ecigarette smoking\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.027\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.870\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eValve morphology\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.041\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.84\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eAmong 106 patients with dilated ascending aorta of BAV, there were a total of 67 cases of stenosis, of which 74% were males, age 54\u0026thinsp;\u0026plusmn;\u0026thinsp;12.06 years, hypertension 153 (121\u0026ndash;197) mmHg, IVSd 1 (0.68\u0026ndash;1.63) mm, IVSs 1.40 (0.84\u0026ndash;2.45) mm, LVIDd 5.03 (3.82\u0026ndash;7.65 ) mm, LVIDs 3.36 (1.26\u0026ndash;4.91) mm, LVPWd 0.99 (0.68\u0026ndash;1.33) mm, LVPWs 1.36 (1.03\u0026ndash;1.85) mm, FS 34.10 (16.40\u0026ndash;45.00), EDV 121.53 (76.82-315.13) ml, ESV 45.31 ( 21.04-113.23) ml, SV 77.06 (45.70-201.90) ml,EF 0.64 (0.51\u0026ndash;0.79), aortic valve flow velocity 2.54 (1.95\u0026ndash;3.17), peak transvalvular pressure difference 33.95 (30.20-44.42), and ascending aortic internal diameter 4.20 (4.06\u0026ndash;4.89). When the cardiac ultrasound indices of the stenosis group were analysed for correlation with age, hypertension, aortic valve flow velocity, pressure and ascending aortic internal diameter, the following were seen (Table\u0026nbsp;\u003cspan refid=\"Tab9\" class=\"InternalRef\"\u003e9\u003c/span\u003e): 1) aortic valve flow velocity - LVIDd (r = -0.401, P\u0026thinsp;\u0026lt;\u0026thinsp;0.01), aortic valve flow velocity - LVIDd (r = -0.594, P\u0026thinsp;\u0026lt;\u0026thinsp;0.01), aortic valve flow velocity - FS (r\u0026thinsp;=\u0026thinsp;0.823, P\u0026thinsp;\u0026lt;\u0026thinsp;0.01), aortic valve flow velocity-EDV (r=-0.343, P\u0026thinsp;=\u0026thinsp;0.04), aortic valve flow velocity-ESV (r=-0.639, P\u0026thinsp;\u0026lt;\u0026thinsp;0.01), and aortic valve flow velocity-EF (r\u0026thinsp;=\u0026thinsp;0.923, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001); and (ii) peak transvalvular pressure difference-age (r\u0026thinsp;=\u0026thinsp;0.636,P\u0026thinsp;\u0026lt;\u0026thinsp;0.01), peak transvalvular pressure difference - ascending aortic internal diameter (r\u0026thinsp;=\u0026thinsp;0.578, P\u0026thinsp;\u0026lt;\u0026thinsp;0.01); and (iii) ascending aortic internal diameter - age (r\u0026thinsp;=\u0026thinsp;0.590, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001).\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab9\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 9\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eCorrelation of cardiac ultrasound indices with demographic and haemodynamic indices in the stenosis group\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colspan=\"3\" nameend=\"c3\" namest=\"c1\"\u003e\u003cp\u003eCorrelation of cardiac ultrasound indices with demographic and haemodynamic indices in the stenosis group\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003er\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePeak transvalvular pressure difference - age\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.636\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePeak Transvalvular Differential Pressure - Ascending Aortic Internal Diameter\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.578\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate-LVIDd\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\u0026minus;0.401\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow velocities-LVIDs\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\u0026minus;0.594\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate-FS\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.823\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow velocity - EDV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\u0026minus;0.343\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.04\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic Valve Flow Rate - ESV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\u0026minus;0.639\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate-EF\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.923\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAscending aortic diameter - age\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.59\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eIncomplete closure\u003c/p\u003e\u003cp\u003eIn 39 patients, 77% were male, age 56\u0026thinsp;\u0026plusmn;\u0026thinsp;10.40 years, hypertension 142 (116\u0026ndash;192) mmHg, IVSd 1 (0.69\u0026ndash;1.60) mm, IVSs 1.37 (1.05\u0026ndash;1.94) mm, LVIDd 5.00 (3.95\u0026ndash;7.10) mm, LVIDs 3.30 (2.16\u0026ndash;5.14) mm, LVPWd 1 (0.66\u0026ndash;1.32) mm, LVPWs 1.38 (0.56\u0026ndash;1.94) mm, FS 33.33 (21.20\u0026ndash;42.00), EDV 117.23 (72.42-266.51) ml, ESV 48.92 (25.14-148.92) ml, SV 67.27 (40.63-136.07) ml, EF 0.58 (0.40\u0026ndash;0.70), aortic valve flow rate 2.54 (1.70\u0026ndash;3.86), peak transvalvular pressure difference 32.94 (29.52\u0026ndash;42.65), and ascending aortic internal diameter 4.29 (4.05\u0026ndash;4.83). The correlation of haemodynamic indices in cardiac ultrasound with age, hypertension, aortic valve flow velocity, pressure and ascending aortic internal diameter could be similarly examined by Spearman's correlation (see Table\u0026nbsp;\u003cspan refid=\"Tab10\" class=\"InternalRef\"\u003e10\u003c/span\u003e). The results showed that: (i) aortic valve flow velocity -LVIDd (r=-0.337, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001), aortic valve flow velocity -LVIDs (r=-0.421, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001), aortic valve flow velocity -FS (r\u0026thinsp;=\u0026thinsp;0.494, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001), aortic valve flow velocity -EDV (r=-0.316, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001), aortic valve flow velocity -ESV (r=-0.463, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001), aortic valve flow velocity-EF (r\u0026thinsp;=\u0026thinsp;0.486, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001); (ii) peak transvalvular pressure difference-age (r\u0026thinsp;=\u0026thinsp;0.646, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001), peak transvalvular pressure difference-ascending aortic internal diameter (r\u0026thinsp;=\u0026thinsp;0.564, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001); and (iii) ascending aortic internal diameter-age (r\u0026thinsp;=\u0026thinsp;0.626, P\u0026thinsp;\u0026lt;\u0026thinsp;0.001).\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab10\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 10\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eCorrelation of cardiac ultrasound indices with demographic and haemodynamic indices in the Incomplete closure group\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"3\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colspan=\"3\" nameend=\"c3\" namest=\"c1\"\u003e\u003cp\u003eCorrelation of cardiac ultrasound indices with demographic and haemodynamic indices in the incomplete closure group\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u0026nbsp;\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003er\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate-LVIDd\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\u0026minus;0.337\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate-LVIDs\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e-0.421\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate-FS\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.494\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic Valve Flow Rate - EDV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e-0.316\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic Valve Flow Rate - ESV\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e-0.463\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAortic valve flow rate-EF\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.486\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePeak Transvalvular Differential Pressure - Age\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.646\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003ePeak Transvalvular Differential Pressure - Ascending Aortic Internal Diameter\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.564\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAscending aortic diameter - age\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.626\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026lt;0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e"},{"header":"Discusssion","content":"\u003cp\u003eThe pathogenesis of ascending aortic dilatation (aneurysm) is dynamic: it leads to changes in the intima-media composition of the vessel wall with increased aortic wall stress, and the vessel dilates with the time of the lesion, which is denatured through the interaction of extracellular aortic matrix abnormalities and smooth muscle cell dysfunction. Hemodynamic abnormalities lead to irregular turbulence in the vasculature (especially eccentric flow), and abnormal flow impingement causes endothelial loss and increased wall stress, which further promotes altered intima-media composition and structural remodeling \u003csup\u003e[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e][\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e][\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eCardiac ultrasound is one of the primary diagnostic tests for cardiac-related diseases, which not only assesses the state of cardiac function of the patient, but also provides guidance for assessing and predicting the risk of progression of dilatation of the ascending aorta and surgery through cardiac ultrasound-related indexes.\u003c/p\u003e\u003cp\u003eThe causes of ascending aortic dilatation vary in different age groups, and for this reason the causes were explored by binary logistic regression analysis. The factors were first explored independently in relation to ascending aortic dilatation to find risk factors with P\u0026thinsp;\u0026lt;\u0026thinsp;0.05, and then independent risk factors were screened multifactorially. P\u0026thinsp;\u0026lt;\u0026thinsp;0.05 for valve complications, hypertension, EF, aortic valve flow velocity, peak transvalvular pressure difference, diabetes mellitus, and hyperlipidemia in the young group; P\u0026thinsp;\u0026lt;\u0026thinsp;0.05 for valve complications, hypertension, aortic valve flow velocity, peak transvalvular pressure difference, diabetes mellitus, hyperlipidemia, and cigarette smoking in the middle-aged group; P\u0026thinsp;\u0026lt;\u0026thinsp;0.05 for hypertension, aortic valve flow velocity, peak transvalvular pressure difference, diabetes mellitus, and cigarette smoking in the elderly group. A further multifactorial binary logistic regression analysis, using stepwise backward method and iterative removal of non-significant variables (likelihood ratio test), revealed that: risk factors for the occurrence of ascending aortic dilatation in the young group were valvular complications (P\u0026thinsp;=\u0026thinsp;0.011, OR\u0026thinsp;=\u0026thinsp;8.197), aortic valve flow velocity (P\u0026thinsp;=\u0026thinsp;0.009, OR\u0026thinsp;=\u0026thinsp;26.355), peak transvalvular pressure differential (P\u0026thinsp;=\u0026thinsp;0.009, OR\u0026thinsp;=\u0026thinsp;1.395); risk factors for the development of ascending aortic dilatation in the middle-aged group were peak transvalvular pressure difference (P\u0026thinsp;\u0026lt;\u0026thinsp;0.01, OR\u0026thinsp;=\u0026thinsp;2.186), and diabetes mellitus (P\u0026thinsp;\u0026lt;\u0026thinsp;0.01, OR\u0026thinsp;=\u0026thinsp;7.170); and in the elderly group were peak transvalvular pressure difference (P\u0026thinsp;\u0026lt;\u0026thinsp;0.01, OR\u0026thinsp;=\u0026thinsp;2.853), and cigarette smoking (P\u0026thinsp;\u0026lt;\u0026thinsp;0.01, OR\u0026thinsp;=\u0026thinsp;13.534). OR\u0026thinsp;=\u0026thinsp;13.534) (see Table\u0026nbsp;\u003cspan refid=\"Tab11\" class=\"InternalRef\"\u003e11\u003c/span\u003e). As can be seen from the results, the occurrence of ascending aortic dilatation in the young group was mainly related to valve function and hemodynamics; in the middle-aged group, the risk factors began to appear as metabolic diseases superimposed on hemodynamic factors; and in the elderly group, factors of long-term vascular loss and degenerative lesions predominated.\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab11\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 11\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eRisk factors for occurrence of ascending aortic dilatation in different age groups\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"4\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\"\u003e\u003cp\u003eAge grouping\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003efactors\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\"\u003e\u003cp\u003eOR(95%CI)\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c4\"\u003e\u003cp\u003eP\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\" morerows=\"2\" rowspan=\"3\"\u003e\u003cp\u003eYouth group\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eValve Complications\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e5.161(1.071\u0026ndash;24.864)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e\u003cp\u003e0.041\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eAortic valve flow rate\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e45.062(4.485\u0026ndash;62.772)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e\u003cp\u003e0.001\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePeak Transvalve Differential Pressure\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e1.416(1.117\u0026ndash;1.795)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e\u003cp\u003e0.004\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\" morerows=\"1\" rowspan=\"2\"\u003e\u003cp\u003eMiddle-aged\u003c/p\u003e\u003cp\u003egroup\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePeak Transvalve Differential Pressure\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e2.186(1.626\u0026ndash;2.938)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ediabetes\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e7.170(2.532\u0026ndash;20.300)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\" morerows=\"1\" rowspan=\"2\"\u003e\u003cp\u003esenior group\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ePeak Transvalve Differential Pressure\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e2.853(1.537\u0026ndash;5.295)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e\u003cp\u003e\u0026lt;0.01\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003ecigarette smoking\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e\u003cp\u003e13.534(1.438\u0026ndash;30.332)\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e\u003cp\u003e0.023\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\u003cp\u003eAge structure and ascending aortic dilatation\u003c/p\u003e\u003cp\u003eThe central finding of age as an effect modifier is that the spectrum of risk factors for ascending aortic dilatation varies significantly with age. This suggests that age is not a simple confounding variable, but rather a powerful \u0026ldquo;effect modifier\u0026rdquo; that alters the strength and/or nature of the relationship between other factors and ascending aortic dilatation. There are fundamental differences in aortic wall characteristics, underlying disease spectrum, and duration of exposure between age groups. For the younger age groups, ascending aortic dilatation strongly points to congenital disease (BAV) or early-onset acquired valvular disease (e.g., rheumatic heart disease), and valvular complications, high flow velocities, and high-peak transvalvular pressure differentials are a direct consequence of these pathologies, which produce abnormal wall shear stresses and pressure loads. In contrast, the traditional cardiovascular risk factors of diabetes mellitus, hyperlipidemia, and smoking require a longer period of cumulative storminess to become apparent and have not yet reached the threshold of pathogenesis in youth. In young patients with ascending aortic dilatation, valve disease must be prioritized for screening and close monitoring. In the middle-aged group, diabetes becomes a key metabolic factor, which damages the extracellular matrix (collagen, elastin) of the vascular wall and reduces its elasticity and strength by loss of vascular matrix, with the help of hyperglycemia, accumulation of end products of late glycosylation, oxidative stress, inflammation, and other pathways, which make the aortic wall more susceptible to dilatation in response to the stresses of blood flow, and diabetes is a strong promoter of both atherosclerosis and vascular sclerosis that alters the biomechanical properties of the vessel wall. Therefore, in middle-aged patients with ascending aortic dilatation, tight glycemic control and management of diabetes mellitus and its complications, in addition to concern for valve function, are critical and require a more comprehensive cardiovascular risk assessment. For the older age group, long-term cumulative damage to the vessel wall and valve degeneration predominated, and peak transvalvular pressure difference remained a significant factor (OR\u0026thinsp;=\u0026thinsp;2.853), which may largely reflect the high prevalence of severe degenerative calcific aortic stenosis in the older age group, with persistent mechanical stresses acting on the already aged vessel wall. At the same time, smoking has emerged as the most prominent emerging risk factor in the elderly group, with prolonged smoking leading to a sustained systemic and vascular wall inflammatory response, increased oxidative stress, direct damage to endothelial and smooth muscle cells, and promotion of matrix metalloproteinase expression, which accelerates the degradation of collagen and elastin and destroys the structural support of the aortic wall. For patients with dilated ascending aorta in the elderly, the importance of lifelong smoking cessation is emphasized, along with management of severe aortic valve lesions (assessed for indications for intervention) and assessment of overall vascular health.With the increase of age, lysyl oxidase (LOX) activity decreases, vascular elastin cross-linking is insufficient, and calcium ions are gradually deposited, the elastic plate layer calcification and fracture, combined with telomere shortening\u0026thinsp;+\u0026thinsp;P53/P161NK4a activity increases, and vascular repair ability decreases, these chain reaction to the failure of the vascular wall of the Cauchy's stress gradually decreases, and the hardness of the vascular wall gradually rises, on behalf of the vascular tissue elasticity worse and worse. The elasticity begins to decline (with increased collagen deposition), leading to a decrease in the minimum impact force threshold for the ascending aorta to withstand blood flow, which predisposes it to dilatation \u003csup\u003e[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e][\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e][\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e][\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]\u003c/sup\u003e. Whereas peak transvalvular pressure difference is always a significant risk factor regardless of the patient's age, suggesting that close monitoring of the diameter of the ascending aorta is necessary in patients with BAV at any age.\u003c/p\u003e\u003cp\u003eValve Complications and Ascending Aortic Dilatation\u003c/p\u003e\u003cp\u003e- Complicated Stenosis of the Leaflet Aortic Valve\u003c/p\u003e\u003cp\u003eThe left ventricle is required to pump intraluminal blood into the aorta at higher pressures, and high velocity turbulence (especially eccentric jets) is created by the narrowed valve orifice. This unstable flow impacts the localized area of the ascending aorta for a long period of time, resulting in local endothelial loss and mechanical stress, \u0026ldquo;similar to a high-pressure water pistol repeatedly flushing the inner wall of a water pipe,\u0026rdquo; which further induces remodeling of the middle layer of the vessel wall \u003csup\u003e[\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]\u003c/sup\u003e. At the same time post-stenotic turbulence also activates the inflammatory response of the vessel wall through wall shear stress: the inflammatory process consists of macrophage and lymphocyte migration associated with a small increase in mast cells and neutrophils, with the meso- and epicardium of the aorta being the most affected structures, which in turn further destroys the vascular structure leading to dilatation of the ascending aorta \u003csup\u003e[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003e-Diaphragmatic Aortic Valve Complicated Closure Insufficiency\u003c/p\u003e\u003cp\u003eThe systolic high-flow ejection of blood from the heart exposes the aorta to greater volume shocks in a short period of time, with compensatory thickening of the systolic thickness of the interventricular septum, while diastolic regurgitation leads to an abrupt drop in the aortic root pressure, resulting in the formation of a high pulse pressure difference (systolic high pressure-diastolic low pressure). This cyclic stress causes the wall of the ascending aorta to dilate and retract repeatedly, forming the \u0026ldquo;Windkessel effect\u0026rdquo;, and the highly oscillatory WSS activates the endothelial NF-κB pathway, resulting in an increase in the release of inflammatory factors (IL-6, TNF-α) and accelerating the elastic fiber rupture and intima-media regression in the aortic wall, which results in the overall dilatation of the aorta in relation to the loss of localized areas of the stenotic wall. The overall dilatation of the ascending aorta is more pronounced compared to the loss of localized areas of the vessel wall after stenosis \u003csup\u003e[\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e][\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e][\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e][\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eIn the young population, ascending aortic dilatation in BAV with valvular insufficiency is 5.161 times higher than that in patients with concomitant stenosis. Prolonged high volume loading and high differential pulse pressure result in sustained tension of the ascending aortic wall, which mechanically stretches the smooth muscle cells, and over-activation of TGF-β1 leads to an increase in secretion of matrix metalloproteinases (MMP-2/9), which accelerate degradation of elastin, cleave elastin fibers, and destroy extracellular matrix (see Figure). extracellular matrix (see Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e2\u003c/span\u003e). At the same time, abnormal activation of the transforming growth factor (TGF-β) signaling pathway, which is a regulatory cytokine expressed by vascular smooth muscle cells in the arterial wall, regulates the activity of MMP, which further promotes fibrosis, and the elasticity of the vascular wall decreases, and the dilation is more pronounced \u003csup\u003e[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e] [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e] [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e][\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e][\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eThe results also showed that LVPW and ESV were higher in the incomplete closure group than in the stenosis group due to diastolic regurgitation of blood into the left ventricle, which resulted in a significant increase in left ventricular volume load. The LV compensatorily increases the volume per beat (forward blood flow\u0026thinsp;+\u0026thinsp;regurgitant flow) through the Frank-Starling mechanism, and the systolic ejection rate is accelerated, which elevates the valvular flow rate. Chronic volume loading results in LV isolated hypertrophy and enlarged ventricular chambers. In the early compensatory phase, ESV remains normal; when ascending aortic dilatation occurs, the myocardium has become fibrotic, systolic function decreases, and ESV rises. In addition, diastolic regurgitation causes the left ventricle to empty in a shorter period of time, further affecting the end-systolic residual volume.\u003c/p\u003e\u003cp\u003eAortic wall \u0026ldquo;congenital defects\u0026rdquo; and genetic factors\u003c/p\u003e\u003cp\u003ePatients with bileaflet aortic valve (BAV) often have congenital structural defects of the ascending aorta. Whereas the normal intima consists of a spring-like mechanical support system of regularly arranged elastic fibers and smooth muscle cells, patients with BAV are characterized by a structural disorder of the intima: broken elastic fibers, abnormal collagen arrangement, and absence of smooth muscle cells, resulting in a wall that resembles the mechanical properties of an inelastic, aging rubber band. It has been suggested that this pathological change is associated with mutations in genes that regulate aortic development during embryonic life (e.g., NOCTH-1) \u003csup\u003e[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e] [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e] [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]\u003c/sup\u003e, which serve the dual function of valve morphology and vessel wall maturation, leading to aberrant SMC differentiation and ultimately to the resultant mesangial cystic necrosis.\u003c/p\u003e\u003cp\u003eAnalyzed at the level of molecular mechanisms, BAV-associated aortopathy has a dual regulatory pathway. At the genetic level, mutations directly affect the function of vascular structural proteins: mutations in myosin heavy chain 11 (MYH11), a core component of the smooth muscle contractile unit, not only impede the multimerization of myosin to form thick myofilaments, but also reduce the expression of contractile proteins and induce cellular de-differentiation, resulting in impaired response to mechanical stresses and susceptibility to vessel wall injury. Mutations in the myosin light chain kinase (MYLK) gene, on the other hand, impair the regulation of light chain phosphorylation, weakening myosin II ATPase activity and ultimately triggering degenerative changes in the midmembrane \u003csup\u003e[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e] [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e] [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eClinical comorbidities in relation to ascending aortic dilatation\u003c/p\u003e\u003cp\u003eMechanisms of diabetic vascular injury(See Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e6\u003c/span\u003e): ① Activation of AGEs-RAGE axis: high blood glucose leads to the accumulation of AGEs, and their products bind to the RAGE receptor, resulting in excessive bursts of ROS, leading to the sustained activation of the NF-κB inflammatory pathway, and the subsequent result of this pathway is the destruction of elastin fibers and intima-media components of the aortic wall by inflammatory factors \u003csup\u003e[\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]\u003c/sup\u003e. ② Destruction of matrix structure: 1) abnormal collagen cross-linking: AGEs covalently bind to collagen, which increases the fragility of aortic fibers \u003csup\u003e[\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]\u003c/sup\u003e; 2) elastin degradation: elevated MMP-2/9 activity combined with decreased TIMP-1 activity leads to rupture of the elastic network of the vascular wall; and 3) SMC failure: high glucose-induced apoptosis of SMCs, which leads to the thinning of vascular mesangium. ③Peak transvalvular pressure difference continuously exerts mechanical load, diabetes weakens matrix tensile strength, and the risk of aortic dilatation doubles under the same pressure difference; meanwhile, high glucose promotes the synthesis of abnormal collagen by SMCs, and the stiffness of ascending aortic wall increases, and wall shear stress is more likely to be concentrated locally.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eSmoking vascular injury mechanisms(See Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e7\u003c/span\u003e): ① nicotine in cigarettes activates α7-nACHR pathway, causing SMC proliferation or migration abnormalities, resulting in structural disorders in the middle layer of the vasculature \u003csup\u003e[\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e]\u003c/sup\u003e; ② cigarettes on the one hand, through the consumption of NO by free radicals, resulting in endothelium-dependent diastolic disorders of the vasculature, on the other hand, through the activation of NADPH oxidase, the outbreak of superoxide anion (O₂-) \u0026rarr; lipid peroxidation \u003csup\u003e[\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e]\u003c/sup\u003e; (iii) smoke exhaled during smoking induces MMP-12 (macrophage elastase) activation, leading to fragmentation of vascular elastic fibers.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eStudy Strengths and Limitations The\u003c/p\u003e\u003cp\u003eIn this study, we found that age and hemodynamic load (especially peak transvalvular pressure difference) were independent predictors of ascending aortic dilatation in patients with BAV. Consistent with existing studies, we found that the risk of ascending aortic dilatation increased significantly with age, especially in middle-aged and elderly patients, and the role of traditional cardiovascular risk factors, such as diabetes mellitus and smoking, was more pronounced. This suggests that the impact of age and metabolic diseases such as diabetes cannot be ignored in the management of patients with BAV.\u003c/p\u003e\u003cp\u003eOur first stratified analysis incorporating the age factor showed that the risk of ascending aortic dilatation in young patients was mainly associated with abnormal valve function, whereas middle-aged and elderly patients were characterized by the superimposition of metabolic diseases such as diabetes mellitus with hemodynamic load. The finding that the role of peak transvalvular pressure difference as a hemodynamic index in predicting ascending aortic dilatation increases with age suggests that individualized follow-up strategies should be developed according to differences in the age groups of patients.\u003c/p\u003e\u003cp\u003eHowever, this study also has some limitations. First, this study was a single-center retrospective study with a relatively small sample size and a lack of long-term follow-up data. Future studies could further validate our results with a multicenter, large-sample prospective design.\u003c/p\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eThe present study revealed significant differences in the pathogenic mechanisms of ascending aortic dilatation by age-stratified analysis in different age groups. Ascending aortic dilatation in young patients was mainly associated with valve-derived hemodynamic abnormalities; in middle-aged patients, risk factors included hemodynamic load and diabetes mellitus; and in older patients, it was dominated by long-term smoking-induced oxidative stress and degenerative lesions. The predictive efficacy of peak transvalvular pressure difference as an important hemodynamic index increases significantly with age.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003ch2\u003eDeclaration of competing interest\u003c/h2\u003e\u003cp\u003eThe authors declare that there is no conflict of interest.\u003c/p\u003e\u003c/p\u003e\u003ch2\u003eFunding\u003c/h2\u003e\u003cp\u003eThis research was supported by Baoding First Center Hospital\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eYujia Shen was responsible for data analysis and article writing; Jiabao Guo was responsible for data collection; and Zhenyu Xing was responsible for article review.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eNimrat Grewal AC, Gittenberger-de Groot RE, Poelmann, Robert JM, Klautz, Johannes HN, Lindeman M-J, Goumans M, Palmen SA, Mohamed H-H, Sievers AJJC, Bogers MC. 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Molecular and Cellular Mechanisms Involved in Aortic Wall Aneurysm Development. Volume 13. Diagnostics; 2023. p. 253.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSoulat G, Scott MB, Allen BD, Avery R, Bonow RO, Malaisrie SC, McCarthy P, Fedak PWM, Barker AJ, Markl M. Association of Regional Wall Shear Stress and Progressive Ascending Aorta Dilation in Bicuspid Aortic Valve. JACC Cardiovasc Imaging. 2022;15(1):33\u0026ndash;42.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBarker AJ, Markl M, Burk J, et al. Bicuspid Aortic Valve Is Associated With Altered Wall Shear Stress in the Ascending Aorta. Circ Cardiovasc Imaging. 2012;5:457\u0026ndash;66.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003evan Ooij P, Garcia J, Potters WV, et al. 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PMID: 38866562.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Bileaflet Aortic Valve, Ascending Aortic Dilatation, Cardiac Ultrasound","lastPublishedDoi":"10.21203/rs.3.rs-7378654/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7378654/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground:\u003c/h2\u003e\u003cp\u003eBileaflet aortic valve (BAV) is a common congenital heart abnormality, associated with ascending aortic dilatation and a higher risk of aneurysm. Imaging techniques have been crucial in monitoring these patients, with cardiac ultrasound being increasingly used due to its noninvasive nature and high temporal resolution. However, most studies have focused on valve morphology and less on the role of age in hemodynamic changes. This study aims to analyze the risk factors for ascending aortic dilatation using cardiac ultrasound indices in BAV patients across different age groups.\u003c/p\u003e\u003ch2\u003eMethods:\u003c/h2\u003e\u003cp\u003eWe included 300 patients diagnosed with BAV at the First Central Hospital of Baoding, with cardiac ultrasound data compared between those with and without aortic dilatation. Multifactorial analysis was performed to identify independent predictors of ascending aortic dilatation, focusing on age, hemodynamic load, and clinical comorbidities.\u003c/p\u003e\u003ch2\u003eResults:\u003c/h2\u003e\u003cp\u003eAge was significantly associated with peak transvalvular pressure difference and ascending aortic internal diameter. The analysis showed that in young patients, aortic dilatation was mainly linked to valve-derived hemodynamic abnormalities, whereas in middle-aged patients, risk factors included hemodynamic load and diabetes. In older patients, the primary factors were smoking-induced oxidative stress and degenerative lesions. Age was found to significantly affect the predictive efficacy of peak transvalvular pressure difference.\u003c/p\u003e\u003ch2\u003eConclusion:\u003c/h2\u003e\u003cp\u003eThis study highlights age-specific differences in the mechanisms of ascending aortic dilatation. In young patients, valve dysfunction predominates; in middle-aged individuals, metabolic diseases such as diabetes become important risk factors; and in the elderly, long-term smoking and degenerative changes dominate. The findings suggest the importance of individualized risk assessment based on age for better management of ascending aortic dilatation in clinical practice.\u003c/p\u003e","manuscriptTitle":"Study of risk factors for ascending aortic dilatation in different age groups using cardiac ultrasound indices","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-08-27 06:30:52","doi":"10.21203/rs.3.rs-7378654/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"e3423536-fd8c-453a-954e-7a93b40eb06f","owner":[],"postedDate":"August 27th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-11-19T21:23:10+00:00","versionOfRecord":[],"versionCreatedAt":"2025-08-27 06:30:52","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-7378654","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7378654","identity":"rs-7378654","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}