Subclinical Association of Aortic Stiffness with Cardiac Structure and Function in African- Americans: the Jackson Heart Study

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Gregory Hundley, and 9 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4189960/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 22 Jun, 2024 Read the published version in The International Journal of Cardiovascular Imaging → Version 1 posted 9 You are reading this latest preprint version Abstract Background Cardiovascular disease (CVD) morbidity and mortality are high among black adults. We aimed to study the granular subclinical relations of aortic stiffness and left ventricular (LV) function and remodeling in blacks, in whom limited data are available. Methods In the Jackson Heart Study, 1,050 U.S. community-dwelling black adults without CVD (mean age 59±10 years, 62% women) underwent 1.5T cardiovascular magnetic resonance. We assessed regional and global aortic stiffness and LV structure and function, including LV mass indexed to body surface area (LVMI), end-diastolic volume (LVEDV), ejection fraction (EF), and global and regional circumferential strain (Ecc). Results Phase contrast images of the cross-sectional aorta at the pulmonary artery bifurcation and abdominal aorta bifurcation were acquired to measure pulse wave velocity of the aortic arch (AA-PWV) and thoracic aorta (T-PWV). Results of multivariable-adjusted analyses are presented as SD unit change in LV variables per SD change in PWV variables. Higher AA-PWV and T-PWV were associated with greater LVMI: for T-PWV, β=0.10, 95% CI=0.03-0.16, p=0.002. Higher AA-PWV and T-PWV were associated with worse (more positive) Ecc at the LV base (for AA-PWV, β=0.13, 95% CI=0.05-0.20, p=0.0007), but not mid-LV or apex. AA-PWV and T-PWV were not associated with LV mass/LVEDV or EF. Conclusions In this cross-sectional study of blacks without CVD in the U.S., aortic stiffness is associated with subclinical adverse LV function in basal segments. Future studies may elucidate the temporal relationships of aortic stiffness on the pattern and progression of LV remodeling, dysfunction, and associated prognosis in blacks. Aortic stiffness pulse wave velocity left ventricle strain cardiovascular magnetic resonance INTRODUCTION Aortic stiffness, a result of fibrosis and degenerative changes that reduce the elasticity of the vascular walls, plays a crucial role in cardiovascular hemodynamics by increasing the afterload encountered by the left ventricle (LV). [ 1 ] [ 2 ] The stiffness of the aorta can be determined non-invasively by pulse wave velocity (PWV), a measure obtainable via various imaging techniques, including cardiovascular magnetic resonance (CMR).[ 3 ] Prior prospective studies in mostly white populations have established PWV as an independent predictor of coronary heart disease, heart failure, and stroke in healthy individuals. [ 4 – 7 ] Aortic stiffness is associated with adverse cardiovascular remodeling including LV hypertrophy as well as systolic dysfunction.[ 1 ] Both LV mass and ventricular strain are markers of cardiovascular structure and function, correlating with heart failure risk and independent predictors of cardiovascular and all-cause mortality.[ 8 , 9 ] Additionally, LV hypertrophy has been shown to carry a relatively greater adverse prognostic significance for survival from coronary artery disease in African Americans (AA) than whites.[ 10 , 11 ] Yet, the vast majority of data on ventricular-vascular relations are derived from studies done on whites, leading to a gap in our understanding of these relationships in AA, who constitute a group particularly vulnerable to CVD. In the Multi-Ethnic Study of Atherosclerosis (MESA), higher regional PWV at the aortic arch was associated with adverse LV remodeling and worse mid-LV cavity systolic Eulerian strain circumferential strain (Ecc).[ 12 ] However, these data represent associations in focal areas of the aorta and LV, and little is understood of the relations and patterns of association of PWV along the length of the aorta and among other regions of the LV. Furthermore, the variability of these associations across different races, important due to differences in LV structure in whites and AA, have not been well studied. The Jackson Heart Study is a community-based study of AA in the U.S. with meticulous phenotyping including CMR assessment of aortic stiffness and both regional and global LV function, offering the opportunity to study these subclinical relations in detail. We hypothesized that increased PWV across the aortic arch (AA-PWV) and ascending and descending thoracic aorta (T-PWV) are associated with adverse LV remodeling and systolic dysfunction detected by strain across the LV in individuals without prevalent CV. We sought to study these associations between measures of vascular stiffness and early metrics of ventricular dysfunction in healthy AA. METHODS Study Population and Clinical Covariates The Jackson Heart Study (JHS) is a longitudinal community cohort study of cardiovascular disease in AA in the Jackson, Mississippi, U.S., tri-county area, with study design previously described.[ 13 , 14 ] Enrolled participants in the study received 3 serial examinations: (Exam 1, 2000–2004; Exam 2, 2005–2008; and Exam 3, 2009–2013). Demographic information, medical history, phlebotomy, and blood pressure were collected at each examination. Participants (n = 1,685) underwent cardiovascular magnetic resonance (CMR) imaging at Exams 2 (n = 264) and Exam 3 (n = 1,421). After exclusions for prevalent CVD (n = 59), clinical covariates (n = 143), LV structure or function measures (n = 9) and missing aortic stiffness variables (n = 424), data for a total of 1,050 individuals were available for analysis. Clinical covariates were taken at Examination 3, with serum samples obtained after an overnight fast. Diabetes was defined as fasting plasma glucose ≥ 126 mg/dl, random blood glucose > 200 mg/dl, the use of hypoglycemic agents, or physician diagnosis. Hypertension was defined as SBP ≥ 140 mm Hg, DBP ≥ 90 mm Hg, or the use of antihypertensive medications. The study protocol was approved by the institutional review board of Jackson State University, Tougaloo College, and the University of Mississippi Medical Center. All participants provided written informed consent. CMR Imaging CMR was performed on a 1.5 T Siemens Espree (Siemens, Erlangen, Germany). Electrocardiographically-gated steady-state free precession images were obtained to quantify LV geometry and systolic function (TrueFISP, repetition time [TR] 45.5 ms, echo time [TE] 1.1 ms, flip angle 78° to 82°, 8-mm slice thickness, matrix 109×192, and field of view 400 mm). By convention, papillary muscles were included in the LV volumes and excluded from LV mass. [ 15 ] CMR structure and function were assessed using Cardiac Image Modeler software (University of Auckland, New Zealand). [ 16 ] CMR tagged images were acquired at the base, mid-cavity, and apex of the LV using a cine radiofrequency grid–tagging sequence (field of view 400 mm, slice thickness 8 mm, 192×256 matrix, TR 60 ms, TE 4 s, and FA of 12° [Siemens sequence: Tl2d1r5]). Tagging analysis on LV short axis images was performed using harmonic phase software (Diagnasoft, Morrisville, NC).[ 17 ] Global peak circumferential strain was calculated as the average peak circumferential systolic Eulerian strain (Ecc) of the base, mid-cavity, and apical segments of the left ventricle. Prospective ECG-gated phase contrast images at the proximal ascending and descending aorta level of the pulmonary artery bifurcation, and at the level of the abdominal aorta 2 cm above its bifurcation were obtained for calculation of pulse wave velocity of the aortic arch (AA-PWV) and full ascending and descending thoracic aorta (T-PWV), respectively. The following image acquisition parameters were used: TR 76.55, TE 3.14, flip angle 15, matrix 108x192, FOV 360, slice thickness 8 mm in the thorax and 4 mm between the diaphragm and aortic bifurcation. The transit time between the regions of the aorta were calculated as the average time difference using the least squares estimate between all data points on the upslope of the ascending and descending aortic flow curves during systole, after peak flow normalization. PWV was calculated as the distance between the phase-contrast acquisitions divided by the transit time, as previously described, using custom designed MATLAB-based software (MIMP).[ 18 ] Intraclass correlation coefficient for interobserver reliability based on 96 scans that were analyzed as new scans after relabeling (to blind analysts) was 0.95, 0.88, 0.85, and 0.96 for LV end-diastolic volume (LVEDV), LV end-systolic volume, LV stroke volume, and LV mass (LVM) indexed to body surface area (LVMI), respectively. The intraclass correlation coefficient for HARP Ecc measures was 0.78 (and for PWV analyses was 0.82) in repeated, blinded analyses of 96 scans.[ 18 ] Statistical Analysis Continuous variables were reported either as mean (standard deviation) or median (interquartile range, IQR) and categorical variables were reported as count (percentage). Skewed cardiac measures for LV mass (positive) and ejection fraction (negative) were log and second power transformed, respectively. PWV was inverse-transformed and multiplied by -1000 to restore the direction of effect. Unsymmetrical winsorization was leveraged to replace the top 2 percentile (n = 20) of aortic pulse wave velocity values to 30 meters/second. The dependent variables were measures of LV function and geometry, including LVMI, LVM/LVEDV ratio, ejection fraction (EF), and global and regional Ecc at the base, midwall, and apex. AA-PWV and T-PWV were independent variables. Multivariable (MV) linear regression analysis was used to assess the association between aortic stiffness measured by PWV and the outcomes of LV remodeling and dysfunction. We estimated two sets of models: 1) adjusting for age and sex, 2) multivariable (MV) model adjusting for age, sex, height, weight, mean arterial pressure, heart rate, total/HDL cholesterol, diabetes mellitus, and use of antihypertensive and lipid lowering medications. Continuous variables were standardized to a mean of 0, SD 1 to facilitate comparisons. Logistic regression was used to examine the association of PWV with abnormal LV structure and function, defined by as LV measures > 90th percentile of the study sample values for LVMI, LV mass/LVEDV, and Ecc measures, and < 10th percentile of the study sample values for EF. Multivariable models included adjustment for the same CVD risk factors as linear regression models. Secondarily, we evaluated for age (by median) and sex interactions in the relations between aortic stiffness and measures of LV structure and function. We report standardized beta coefficients as the standard deviation unit numerical change in the dependent (LV structure and function) variable per standard deviation unit change of the independent (aortic stiffness) variable. A 2-tailed Bonferroni-corrected P value of 0.05/10 tests = 0.005 was used as the threshold for statistical significance. All risk factors were chosen a priori . Statistical analyses were performed using SAS version 9.4 (SAS Institute, Cary, NC). RESULTS Baseline Characteristics of Participants Baseline characteristics of the 1,050 JHS participants in this study are presented in Table 1 . Participants, of whom 63% were women, were middle-aged and had an elevated mean body mass index. Over one-fifth of participants had diabetes, nearly 1/3 used lipid-lowering medications, and the majority used antihypertensive medications. Participants did not have elevated PWV and had normal mean LV systolic function reflected by ejection fraction and Ecc. Comparison of characteristics of individuals included and excluded in the study are reported in the Supplemental Table . Excluded individuals were similar in age, but with greater CVD risk factors including higher prevalence of diabetes and use of anti-hypertensive and lipid lowering medications, slightly higher PWV, and similar to slightly more favorable measures of LV function. Table 1 Characteristics of the study sample (n = 1050) Characteristics Age, yrs 59 (10) Women 658 (63) Body mass index, mg/dL 32 (6) Systolic blood pressure, mm Hg 126 (18) Diastolic blood pressure, mm Hg 76 (10) Heart rate, beats/min 63 (10) Total to HDL cholesterol ratio 3.6 (1.1) Triglyceride, mg/dL 95 (55) Plasma Glucose, mg/dL 102 (30) Diabetes Mellitus 224 (21) Use of hypertensive medications 634 (60) Use of hyperlipidemia medications 321 (31) CMR variables Aortic arch PWV, m/s 7.4 (5.9) Thoracic PWV, m/s 6.5 (2.6) LV mass index, g/m 2 66 (16) LV end-diastolic volume, mL 125 (33) LV Mass to LVEDV ratio 1.1 (0.3) Ejection fraction, % 61 (9) Stroke volume, mL 75 (21) LV Global circumferential strain (Ecc), % -15.8 (2.4) Base -15.7 (2.9) Mid -15.8 (3.2) Apex -16.1 (2.9) Data reported as n (%) for categorical variables and mean (SD) for continuous variables Abbreviations: HDL = High Density Lipoprotein. LV: left ventricular. LVEDV = LV end diastolic volume. CMR = cardiovascular magnetic resonance. Association of LV Structure and Function with Aortic Stiffness The age- and sex- and MV-adjusted associations of aortic stiffness with LV structure are presented in Table 2 . In MV models, AA-PWV and T-PWV were associated with LVMI (β = 0.089, 95% CI 0.026–0.152, p = 0.005 and β = 0.096 95% CI = 0.034–0.158, p = 0.002). There was no association of AA-PWV or T-PWV with LVM/LVEDV (p = 0.09, p = 0.37, respectively). Table 2 Continuous associations of aortic stiffness with LV structure LVMI (g/m 2 ) LVM/LVEDV Ratio R 2 ß (95% CI) P-value R 2 ß (95% CI) P-value Aortic Arch PWV (m/s) Age/sex-adjusted 0.28 0.122 (0.060, 0.185) 0.0001 0.12 0.073 (0.004, 0.142) 0.037 MV-adjusted 0.34 0.089 (0.026, 0.152) 0.005 0.25 0.057 (-0.009, 0.123) 0.091 Thoracic Aorta PWV (m/s) Age/sex-adjusted 0.13 0.128 (0.067, 0.188) < 0.0001 0.12 -0.007 (-0.074, 0.060) 0.84 MV-adjusted 0.34 0.096 (0.034, 0.158) 0.002 0.25 -0.030 (-0.095, 0.035) 0.37 PWV: Pulse wave velocity; LV: left ventricle. LVMI: LV mass indexed to body surface area. LVM/LVEDV: LV Mass to End Diastolic Volume Ratio. MV model adjusted for age, sex; weight, height, mean arterial pressure, heart rate, diabetes, total to HDL ratio, blood pressure medications and antilipidemia medications. The multivariable-adjusted associations of aortic stiffness with LV function are presented in Table 3 . AA-PWV and T-PWV were not associated with global peak LV Ecc (p = 0.012 and 0.13, respectively, for age- and sex-adjusted and MV-adjusted models). However, AA-PWV and T-PWV were associated with worse (more positive) Ecc at the LV base, but not mid or apical segments (AA-PWV: β = 0.126 per SDU, 95% CI = 0.054–0.198, p = 0.0007; T-PWV: β = 0.108 per SDU, 95% CI = 0.037–0.180, p = 0.0029). In analyses relating PWV to dichotomized LV structure or functional measures, there was a borderline association of AA-PWV and T-PWV to elevated (> 90th percentile) LV basal Ecc (HR 2.36, 95% CI 1.27–4.38, p = 0.006 for AA-PWV; T-PWV results were similar (p = 0.006). There was no significant association of PWV with other dichotomous measures of LV structure or function (LVMI, LVM/EDV, EF, or regional Ecc of the mid-ventricle or apex). There were no significant age and sex interactions in the associations between AA-PWV and T-PWV with measures of LV structure or function. Table 3 Continuous associations of aortic stiffness with LV systolic function Ejection Fraction (%) LV global Ecc (%) LV regional Ecc (%) Base Mid Apex R 2 ß (95% CI) R 2 ß (95% CI) R 2 ß (95% CI) R 2 ß (95% CI) R 2 ß (95% CI) Aortic Arch PWV (m/s) Model 1 0.04 -0.098 (-0.170, -0.026) 0.07 0.090 (0.019, 0.161) 0.07 0.129* (0.059, 0.200) 0.04 0.011 (-0.061, 0.083) 0.04 0.084 (0.012, 0.156) Model 2 0.07 -0.086 (-0.160, -0.011) 0.17 0.091 (0.021, 0.162) 0.13 0.126* (0.054, 0.198) 0.10 0.015 (-0.058, 0.089) 0.10 0.087 (0.014, 0.160) Thoracic Aorta PWV (m/s) Model 1 0.031 -0.060 (-0.130, 0.010) 0.07 0.054 (-0.015,0.123) 0.06 0.105* (0.036, 0.175) 0.04 -0.029 (-0.099, 0.041) 0.04 0.066 (-0.004, 0.136) Model 2 0.06 -0.042 (-0.116, 0.031) 0.07 0.054 (-0.015,0.123) 0.13 0.108* (0.037, 0.180) 0.10 -0.030 (-0.102, 0.043) 0.10 0.063 (-0.009, 0.135) * p < 0.005 PWV: Pulse wave velocity; Ecc. = Global circumferential Peak systolic strain; EDV = End-Stage Diastolic Volume Ratio; Model 1: Age- and Sex-Adjusted Model; Model 2: Adjusted for age, sex; weight, height, mean arterial pressure, heart rate, diabetes, total to HDL ratio, blood pressure medications and antilipidemic medications DISCUSSION In this study of 1,050 AA in the community without prevalent CVD, aortic stiffness was associated with subclinical measures of adverse cardiac structural remodeling measured by CMR. The present study elaborates on prior work by exploring the ventricular-vascular associations at distinct segments of the LV and aorta in individuals free of CVD, enhancing our understanding of the relationship between subclinical aortic stiffness and ventricular dysregulation. Greater aortic stiffness measured by either AA-PWV or T-PWV was associated with higher LV mass. Notably, while aortic stiffness was not associated with LVEF or worse global Ecc, PWV had a stronger association with less favorable LV strain at the base, but not mid-LV or apical segments. Our findings are consistent with the growing evidence demonstrating the connection between dysfunction of the aorta and LV structural and functional remodeling that may underlie preclinical CVD, including heart failure in AA. The proximal aorta located immediately distal to the LV, buffers LV afterload, and progressive loss of the elasticity of this segment may create impairment to LV contractility. Greater aortic stiffness and associated higher pressure pulsatility and wave reflection that returns earlier during systole, collectively result in greater workload for the LV.[ 19 ] In this study, we found that the association of LV strain with aortic stiffness was not uniform and varied by segments. Aortic stiffness was associated with unfavorable circumferential strain of the basal segments, perhaps indicating excessive afterload on these areas. The underlying anatomy and physiology of the LV underscores the importance of our findings: the LV base contains a greater proportion of circumferential fibers compared to distal segments,[ 20 ] and the basal segments generate the most stroke volume of all segments in the LV. Such dynamics over time lead to consequences that include LV hypertrophy and declines in systolic and diastolic function, as has been observed in hypertension. Unfavorable ventricular-vascular interactions may perpetuate with the constellation of adverse LV structural and functional remodeling begetting further hemodynamic abnormalities leading to greater aortic stiffness, ultimately leading to adverse CVD events. Because the base of the LV generates the most stroke volume compared to the distal LV segments, functional decline of this region may explain greater susceptibility to development of clinical CVD, including heart failure, in AA. Our study results add to the prior literature on the relationship between aortic stiffness and LV structure and function that has been primarily demonstrated in non-AA samples. Several groups, including the Framingham Heart Study (FHS), MESA, and AGES-Reykjavik have reported similar associations of aortic stiffness assessed with CMR or carotid femoral PWV with LV mass and mass index.[ 12 , 21 , 22 ] Variability in the type and location of the systolic function measure, across cohort studies contribute to differences in, and preclude direct comparison of, the associations of aortic stiffness with LV systolic function. Similar to our study, the FHS reported that carotid femoral PWV was not associated with fractional shortening, a surrogate of LVEF,[ 21 ] but was associated with worse echocardiographic global longitudinal strain,[ 23 ] though circumferential strain was not measured. Using CMR, MESA investigators reported an association of aortic arch PWV with LVEF and LV Ecc as assessed in the mid-ventricle, but did not evaluate the associations of global aortic stiffness or additional segments of LV Ecc.[ 12 ] Additionally, underlying differences in the study samples likely also contribute to differences between our collective study results. In the present study, we excluded individuals with CVD in order to study subclinical ventricular-vascular associations, whereas the sample in MESA included individuals with angina, myocardial infarction, and heart failure. Though the mean values of CMR LV structure and function measures are similar between participants in our study and MESA, notably our study sample was also younger with a greater proportion of women, which may have influenced detection of associations. Additionally, though MESA included non-white participants, only one-quarter of the study participants were AA and study results of aortic stiffness-LV structure and function were not reported by race/ethnicity.[ 12 ] Including over 1000 AA, our study is among the largest to study ventricular–vascular associations of both regional and global aortic and LV function in AA free of CVD. Given the vulnerability of AA to elevated LV mass and associated morbidity,[ 10 , 11 , 24 ] and outcomes including CVD and HF,[ 25 – 27 ] our findings highlight additional pathophysiological associations that may underlie these risks. Future investigation of the effect of modulating arterial stiffness may identify its impact on reversing LV remodeling. Strengths and Limitations Though AA individuals face higher CVD risks than those of other race/ethnicities, they are a relatively understudied group. The strengths of this study include the large community dwelling cohort, study of individuals free of CVD, detailed imaging, and extensive phenotyping of clinical risk factors to study subclinical disease. Our analysis of LV circumferential strain on CMR using tagging is highly reproducible and allows comparison across other cohorts with similar data. We used Bonferroni correction to identify the key associations between aortic stiffness and LV structure and function, to lower the risk of inaccurate associations based upon multiple testing. However, the findings of this study must be interpreted within the context of its limitations. First, the relatively low temporal resolution of PWV transit across the aortic arch may have led to overestimation of PWV, though this is a caveat of all such CMR studies of this aortic region. Though Ecc was the predominant method for strain analysis at the time of CMR, the recent advent of commercially available feature tracking analysis applied post-hoc to cine CMR images allows additional study of myocardial strain in longitudinal and radial orientations and with greater ease, though variability in the latter techniques across vendors remains. Additionally, the study is observational and cannot determine a causal link between aortic stiffness and adverse LV remodeling and function. Further, the studied sample, compared to those excluded, had fewer CVD risk factors. Though this may limit the generalizability of this study to the population at large, it reinforces that observations of abnormal ventricular-vascular relations occur even in the healthier participants with subclinical disease. While the participants in this study represent a region within the U.S., the JHS represents the largest comprehensive study of CVD associations and cardiovascular imaging in Black Americans. CONCLUSION Aortic stiffness is associated with subclinical regional LV systolic dysfunction in a large cohort of AA individuals free of prevalent CVD in the community. Our findings highlight that adverse ventricular-vascular remodeling occur beyond that accounted for CVD risk factors alone, and may provide the substrate on which clinical CVD including heart failure may develop. Future studies will be helpful to elucidate the temporal relationships of aortic stiffness on the pattern and progression of LV dysfunction and clarify the role of modulation of aortic stiffness on the prevention or regression of abnormal LV remodeling and function. Declarations DISCLOSURES Dr. Mitchell is the owner of Cardiovascular Engineering, Inc., a company that develops and manufactures devices to measure vascular stiffness and is a consultant to and receives honoraria from Novartis, Merck, Servier, and Philips. All other authors report no disclosures. Competing Interests Dr. Mitchell is the owner of Cardiovascular Engineering, Inc., a company that develops and manufactures devices to measure vascular stiffness, and is a consultant to and receives honoraria from Novartis, Merck, Servier, and Philips. All other authors report no disclosures. FUNDING The Jackson Heart Study (JHS) is supported and conducted in collaboration with Jackson State University (HHSN268201800013I), Tougaloo College (HHSN268201800014I), the Mississippi State Department of Health (HHSN268201800015I) and the University of Mississippi Medical Center (HHSN268201800010I, HHSN268201800011I and HHSN268201800012I) contracts from the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute for Minority Health and Health Disparities (NIMHD). CWT is partially supported by NIH R03 HL145195. Author Contribution GFM, EF, CWT were the senior authors involved in the study design and critical revision of the manuscript. WGH, JJC, JGT, AO, RSV, JBM, MH, and EF contributed to data collection and analysis. SM was responsible for statistical analysis. MJ, IR, CWT drafted the manuscript. All authors participated in contributing to text and the content of the manuscript, including revisions and edits. 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Circulation 62(1):105–116 PubMed PMID: 7379273 Streeter DD Jr., Spotnitz HM, Patel DP, Ross J Jr., Sonnenblick EH (1969) Fiber orientation in the canine left ventricle during diastole and systole. Circ Res 24(3):339–347 Epub 1969/03/01. 10.1161/01.res.24.3.339 Kaess BM, Rong J, Larson MG, Hamburg NM, Vita JA, Cheng S et al (2016) Relations of Central Hemodynamics and Aortic Stiffness with Left Ventricular Structure and Function: The Framingham Heart Study. J Am Heart Assoc 5(3):e002693 Epub 2016/03/27. 10.1161/jaha.115.002693 1161/JAHA 115.002693. PubMed PMID: 27016574; PubMed Central PMCID: PMCPMC4943246 Bell V, Sigurdsson S, Westenberg JJ, Gotal JD, Torjesen AA, Aspelund T et al (2015) Relations between aortic stiffness and left ventricular structure and function in older participants in the Age, Gene/Environment Susceptibility–Reykjavik Study. Circ Cardiovasc Imaging 8(4):e003039 PubMed PMID: 25795761; PubMed Central PMCID: PMCPMC4380164 Bell V, McCabe EL, Larson MG, Rong J, Merz AA, Osypiuk E et al (2017) Relations Between Aortic Stiffness and Left Ventricular Mechanical Function in the Community. J Am Heart Assoc. ;6(1). Epub 2017/01/11. 10.1161/jaha.116.004903 1161/JAHA 116.004903. PubMed PMID: 28069573; PubMed Central PMCID: PMCPMC5523643 Gardin JM, Wagenknecht LE, Anton-Culver H, Flack J, Gidding S, Kurosaki T et al (1995) Relationship of cardiovascular risk factors to echocardiographic left ventricular mass in healthy young black and white adult men and women. The CARDIA study. Coronary Artery Risk Development in Young Adults. Circulation 92(3):380–387 Epub 1995/08/01. PubMed PMID: 7634452 Martin B, Aday SS, Almarzooq AW (2024) Circulation 149(8):e347–e913. 10.1161/CIR.0000000000001209 . ZI, et al. 2024 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association Bahrami H, Kronmal R, Bluemke DA, Olson J, Shea S, Liu K et al (2008) Differences in the incidence of congestive heart failure by ethnicity: the multi-ethnic study of atherosclerosis. Arch Intern Med 168(19):2138–2145. 10.1001/archinte.168.19.2138 PubMed PMID: 18955644; PubMed Central PMCID: PMCPMC3038918 Bibbins-Domingo K, Pletcher MJ, Lin F, Vittinghoff E, Gardin JM, Arynchyn A et al (2009) Racial differences in incident heart failure among young adults. N Engl J Med 360(12):1179–1190. 10.1056/NEJMoa0807265 PubMed PMID: 19297571; PubMed Central PMCID: PMCPMC2829671 Additional Declarations Competing interest reported. Dr. Mitchell is the owner of Cardiovascular Engineering, Inc., a company that develops and manufactures devices to measure vascular stiffness, and is a consultant to and receives honoraria from Novartis, Merck, Servier, and Philips. All other authors report no disclosures. Supplementary Files SupplementalTable.docx Cite Share Download PDF Status: Published Journal Publication published 22 Jun, 2024 Read the published version in The International Journal of Cardiovascular Imaging → Version 1 posted Editorial decision: Revision requested 04 May, 2024 Reviews received at journal 01 May, 2024 Reviews received at journal 23 Apr, 2024 Reviewers agreed at journal 16 Apr, 2024 Reviewers agreed at journal 02 Apr, 2024 Reviewers invited by journal 02 Apr, 2024 Submission checks completed at journal 30 Mar, 2024 Editor assigned by journal 30 Mar, 2024 First submitted to journal 29 Mar, 2024 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. 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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-4189960","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":286803776,"identity":"3f6a47a9-1274-4b13-95a6-4563a871a37c","order_by":0,"name":"Mawra Jha","email":"","orcid":"","institution":"Beth Israel Deaconess Medical Center, Harvard Medical School","correspondingAuthor":false,"prefix":"","firstName":"Mawra","middleName":"","lastName":"Jha","suffix":""},{"id":286803777,"identity":"b5a003a8-b7f5-4535-81df-05b682e4cb6c","order_by":1,"name":"Solomon Musani","email":"","orcid":"","institution":"University of Mississippi Medical Center","correspondingAuthor":false,"prefix":"","firstName":"Solomon","middleName":"","lastName":"Musani","suffix":""},{"id":286803778,"identity":"a0c0bb7b-9ab9-49fe-9026-88a08e029d87","order_by":2,"name":"Inbar Mccarthy","email":"","orcid":"","institution":"Beth Israel Deaconess Medical Center, Harvard Medical School","correspondingAuthor":false,"prefix":"","firstName":"Inbar","middleName":"","lastName":"Mccarthy","suffix":""},{"id":286803779,"identity":"003d8b66-0134-4ac6-b87d-5ceb2cb85cf3","order_by":3,"name":"W. Gregory Hundley","email":"","orcid":"","institution":"Virginia Commonwealth University Medical Center","correspondingAuthor":false,"prefix":"","firstName":"W.","middleName":"Gregory","lastName":"Hundley","suffix":""},{"id":286803780,"identity":"24b1f735-e341-4909-913d-d2c27b2a6d09","order_by":4,"name":"J. Jeffrey Carr","email":"","orcid":"","institution":"Vanderbilt University Medical Center","correspondingAuthor":false,"prefix":"","firstName":"J.","middleName":"Jeffrey","lastName":"Carr","suffix":""},{"id":286803781,"identity":"999f84fd-bf10-4970-b388-29200c3e14f4","order_by":5,"name":"James G. Terry","email":"","orcid":"","institution":"Virginia Commonwealth University Medical Center","correspondingAuthor":false,"prefix":"","firstName":"James","middleName":"G.","lastName":"Terry","suffix":""},{"id":286803782,"identity":"e6d801fb-5964-4c1d-8f7b-678bd5231780","order_by":6,"name":"Adebamike Oshunbade","email":"","orcid":"","institution":"University of Mississippi Medical Center","correspondingAuthor":false,"prefix":"","firstName":"Adebamike","middleName":"","lastName":"Oshunbade","suffix":""},{"id":286803783,"identity":"c243e117-e091-493d-a1aa-9b34c5ee15d1","order_by":7,"name":"Ramachandran S. Vasan","email":"","orcid":"","institution":"Boston University School of Medicine, Boston University School of Public Health","correspondingAuthor":false,"prefix":"","firstName":"Ramachandran","middleName":"S.","lastName":"Vasan","suffix":""},{"id":286803784,"identity":"c86bedab-4a87-4381-9572-35ddd3783a2c","order_by":8,"name":"Javed Butler","email":"","orcid":"","institution":"University of Mississippi Medical Center","correspondingAuthor":false,"prefix":"","firstName":"Javed","middleName":"","lastName":"Butler","suffix":""},{"id":286803785,"identity":"d45d1a60-2f26-4b10-9cf2-6b0a43c44505","order_by":9,"name":"Michael Hall","email":"","orcid":"","institution":"University of Mississippi Medical Center","correspondingAuthor":false,"prefix":"","firstName":"Michael","middleName":"","lastName":"Hall","suffix":""},{"id":286803786,"identity":"5dc70a9d-334c-4d98-9c5a-3b04f7e21f42","order_by":10,"name":"Gary F. Mitchell","email":"","orcid":"","institution":"Cardiovascular Engineering Inc","correspondingAuthor":false,"prefix":"","firstName":"Gary","middleName":"F.","lastName":"Mitchell","suffix":""},{"id":286803787,"identity":"0032628b-37b6-4bd5-a6c9-78ecf3753cbc","order_by":11,"name":"Ervin Fox","email":"","orcid":"","institution":"University of Mississippi Medical Center","correspondingAuthor":false,"prefix":"","firstName":"Ervin","middleName":"","lastName":"Fox","suffix":""},{"id":286803788,"identity":"e567b498-c304-40cc-a628-1f92c9d5f3fb","order_by":12,"name":"Connie W. Tsao","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA8klEQVRIiWNgGAWjYNACA5sENoYEBgbGBghfgoGBGbdqNhBRkEaylg+HgeqJ1cI/v/3hhw8G5/P42LMTPzDusMs3OH724Q2GCuvEBhxaJI7xGEvOMLhdzMbzdrME45lkyw1n0o0tGM6k49RiwMbDIM1jcDuxTSJ3GwNjG7OBZEMamwRj22E8Wtgf/+YxOAfTUm8g2f8MqOUfPi0MZkBbDsC0HDbglwDZ0oBbi8SxHDPLGQbJEL8kth0HannGbJFwLN0Ylxb+5uOPb3z4Y5cn35678cPHtmoDNv40xhsfaqxlcWlBBQkYjFEwCkbBKBgFZAEAGUpTYt6x1qEAAAAASUVORK5CYII=","orcid":"","institution":"Beth Israel Deaconess Medical Center, Harvard Medical School","correspondingAuthor":true,"prefix":"","firstName":"Connie","middleName":"W.","lastName":"Tsao","suffix":""}],"badges":[],"createdAt":"2024-03-29 23:29:11","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-4189960/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-4189960/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1007/s10554-024-03159-y","type":"published","date":"2024-06-23T00:33:35+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":58874421,"identity":"37b40595-3d6d-44b6-8ffd-42dab52e3e6f","added_by":"auto","created_at":"2024-06-23 00:33:39","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":583040,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-4189960/v1/230a5cf2-bfe8-4f1a-91ff-eae789afb0ce.pdf"},{"id":54014294,"identity":"e78d5cad-eb7e-4ffd-8601-778db82eac4c","added_by":"auto","created_at":"2024-04-03 11:43:57","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":16235,"visible":true,"origin":"","legend":"","description":"","filename":"SupplementalTable.docx","url":"https://assets-eu.researchsquare.com/files/rs-4189960/v1/2ea7846388261e1cca96681a.docx"}],"financialInterests":"Competing interest reported. Dr. Mitchell is the owner of Cardiovascular Engineering, Inc., a company that develops and manufactures devices to measure vascular stiffness, and is a consultant to and receives honoraria from Novartis, Merck, Servier, and Philips. All other authors report no disclosures.","formattedTitle":"Subclinical Association of Aortic Stiffness with Cardiac Structure and Function in African- Americans: the Jackson Heart Study","fulltext":[{"header":"INTRODUCTION","content":"\u003cp\u003eAortic stiffness, a result of fibrosis and degenerative changes that reduce the elasticity of the vascular walls, plays a crucial role in cardiovascular hemodynamics by increasing the afterload encountered by the left ventricle (LV). [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e] [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e] The stiffness of the aorta can be determined non-invasively by pulse wave velocity (PWV), a measure obtainable via various imaging techniques, including cardiovascular magnetic resonance (CMR).[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e] Prior prospective studies in mostly white populations have established PWV as an independent predictor of coronary heart disease, heart failure, and stroke in healthy individuals. [\u003cspan additionalcitationids=\"CR5 CR6\" citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e7\u003c/span\u003e]\u003c/p\u003e \u003cp\u003eAortic stiffness is associated with adverse cardiovascular remodeling including LV hypertrophy as well as systolic dysfunction.[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e] Both LV mass and ventricular strain are markers of cardiovascular structure and function, correlating with heart failure risk and independent predictors of cardiovascular and all-cause mortality.[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e9\u003c/span\u003e] Additionally, LV hypertrophy has been shown to carry a relatively greater adverse prognostic significance for survival from coronary artery disease in African Americans (AA) than whites.[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e11\u003c/span\u003e] Yet, the vast majority of data on ventricular-vascular relations are derived from studies done on whites, leading to a gap in our understanding of these relationships in AA, who constitute a group particularly vulnerable to CVD.\u003c/p\u003e \u003cp\u003eIn the Multi-Ethnic Study of Atherosclerosis (MESA), higher regional PWV at the aortic arch was associated with adverse LV remodeling and worse mid-LV cavity systolic Eulerian strain circumferential strain (Ecc).[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e12\u003c/span\u003e] However, these data represent associations in focal areas of the aorta and LV, and little is understood of the relations and patterns of association of PWV along the length of the aorta and among other regions of the LV. Furthermore, the variability of these associations across different races, important due to differences in LV structure in whites and AA, have not been well studied. The Jackson Heart Study is a community-based study of AA in the U.S. with meticulous phenotyping including CMR assessment of aortic stiffness and both regional and global LV function, offering the opportunity to study these subclinical relations in detail. We hypothesized that increased PWV across the aortic arch (AA-PWV) and ascending and descending thoracic aorta (T-PWV) are associated with adverse LV remodeling and systolic dysfunction detected by strain across the LV in individuals without prevalent CV. We sought to study these associations between measures of vascular stiffness and early metrics of ventricular dysfunction in healthy AA.\u003c/p\u003e"},{"header":"METHODS","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStudy Population and Clinical Covariates\u003c/h2\u003e \u003cp\u003eThe Jackson Heart Study (JHS) is a longitudinal community cohort study of cardiovascular disease in AA in the Jackson, Mississippi, U.S., tri-county area, with study design previously described.[\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e14\u003c/span\u003e] Enrolled participants in the study received 3 serial examinations: (Exam 1, 2000\u0026ndash;2004; Exam 2, 2005\u0026ndash;2008; and Exam 3, 2009\u0026ndash;2013). Demographic information, medical history, phlebotomy, and blood pressure were collected at each examination. Participants (n\u0026thinsp;=\u0026thinsp;1,685) underwent cardiovascular magnetic resonance (CMR) imaging at Exams 2 (n\u0026thinsp;=\u0026thinsp;264) and Exam 3 (n\u0026thinsp;=\u0026thinsp;1,421). After exclusions for prevalent CVD (n\u0026thinsp;=\u0026thinsp;59), clinical covariates (n\u0026thinsp;=\u0026thinsp;143), LV structure or function measures (n\u0026thinsp;=\u0026thinsp;9) and missing aortic stiffness variables (n\u0026thinsp;=\u0026thinsp;424), data for a total of 1,050 individuals were available for analysis.\u003c/p\u003e \u003cp\u003eClinical covariates were taken at Examination 3, with serum samples obtained after an overnight fast. Diabetes was defined as fasting plasma glucose\u0026thinsp;\u0026ge;\u0026thinsp;126 mg/dl, random blood glucose\u0026thinsp;\u0026gt;\u0026thinsp;200 mg/dl, the use of hypoglycemic agents, or physician diagnosis. Hypertension was defined as SBP\u0026thinsp;\u0026ge;\u0026thinsp;140 mm Hg, DBP\u0026thinsp;\u0026ge;\u0026thinsp;90 mm Hg, or the use of antihypertensive medications.\u003c/p\u003e \u003cp\u003e The study protocol was approved by the institutional review board of Jackson State University, Tougaloo College, and the University of Mississippi Medical Center. All participants provided written informed consent.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec4\" class=\"Section2\"\u003e \u003ch2\u003eCMR Imaging\u003c/h2\u003e \u003cp\u003eCMR was performed on a 1.5 T Siemens Espree (Siemens, Erlangen, Germany). Electrocardiographically-gated steady-state free precession images were obtained to quantify LV geometry and systolic function (TrueFISP, repetition time [TR] 45.5 ms, echo time [TE] 1.1 ms, flip angle 78\u0026deg; to 82\u0026deg;, 8-mm slice thickness, matrix 109\u0026times;192, and field of view 400 mm). By convention, papillary muscles were included in the LV volumes and excluded from LV mass. [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e15\u003c/span\u003e] CMR structure and function were assessed using Cardiac Image Modeler software (University of Auckland, New Zealand). [\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e16\u003c/span\u003e] CMR tagged images were acquired at the base, mid-cavity, and apex of the LV using a cine radiofrequency grid\u0026ndash;tagging sequence (field of view 400 mm, slice thickness 8 mm, 192\u0026times;256 matrix, TR 60 ms, TE 4 s, and FA of 12\u0026deg; [Siemens sequence: Tl2d1r5]). Tagging analysis on LV short axis images was performed using harmonic phase software (Diagnasoft, Morrisville, NC).[\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e17\u003c/span\u003e] Global peak circumferential strain was calculated as the average peak circumferential systolic Eulerian strain (Ecc) of the base, mid-cavity, and apical segments of the left ventricle.\u003c/p\u003e \u003cp\u003eProspective ECG-gated phase contrast images at the proximal ascending and descending aorta level of the pulmonary artery bifurcation, and at the level of the abdominal aorta 2 cm above its bifurcation were obtained for calculation of pulse wave velocity of the aortic arch (AA-PWV) and full ascending and descending thoracic aorta (T-PWV), respectively. The following image acquisition parameters were used: TR 76.55, TE 3.14, flip angle 15, matrix 108x192, FOV 360, slice thickness 8 mm in the thorax and 4 mm between the diaphragm and aortic bifurcation. The transit time between the regions of the aorta were calculated as the average time difference using the least squares estimate between all data points on the upslope of the ascending and descending aortic flow curves during systole, after peak flow normalization. PWV was calculated as the distance between the phase-contrast acquisitions divided by the transit time, as previously described, using custom designed MATLAB-based software (MIMP).[\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e18\u003c/span\u003e] Intraclass correlation coefficient for interobserver reliability based on 96 scans that were analyzed as new scans after relabeling (to blind analysts) was 0.95, 0.88, 0.85, and 0.96 for LV end-diastolic volume (LVEDV), LV end-systolic volume, LV stroke volume, and LV mass (LVM) indexed to body surface area (LVMI), respectively. The intraclass correlation coefficient for HARP Ecc measures was 0.78 (and for PWV analyses was 0.82) in repeated, blinded analyses of 96 scans.[\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e18\u003c/span\u003e]\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec5\" class=\"Section2\"\u003e \u003ch2\u003eStatistical Analysis\u003c/h2\u003e \u003cp\u003eContinuous variables were reported either as mean (standard deviation) or median (interquartile range, IQR) and categorical variables were reported as count (percentage). Skewed cardiac measures for LV mass (positive) and ejection fraction (negative) were log and second power transformed, respectively. PWV was inverse-transformed and multiplied by -1000 to restore the direction of effect. Unsymmetrical winsorization was leveraged to replace the top 2 percentile (n\u0026thinsp;=\u0026thinsp;20) of aortic pulse wave velocity values to 30 meters/second. The dependent variables were measures of LV function and geometry, including LVMI, LVM/LVEDV ratio, ejection fraction (EF), and global and regional Ecc at the base, midwall, and apex. AA-PWV and T-PWV were independent variables.\u003c/p\u003e \u003cp\u003eMultivariable (MV) linear regression analysis was used to assess the association between aortic stiffness measured by PWV and the outcomes of LV remodeling and dysfunction. We estimated two sets of models: 1) adjusting for age and sex, 2) multivariable (MV) model adjusting for age, sex, height, weight, mean arterial pressure, heart rate, total/HDL cholesterol, diabetes mellitus, and use of antihypertensive and lipid lowering medications. Continuous variables were standardized to a mean of 0, SD 1 to facilitate comparisons. Logistic regression was used to examine the association of PWV with abnormal LV structure and function, defined by as LV measures\u0026thinsp;\u0026gt;\u0026thinsp;90th percentile of the study sample values for LVMI, LV mass/LVEDV, and Ecc measures, and \u0026lt;\u0026thinsp;10th percentile of the study sample values for EF. Multivariable models included adjustment for the same CVD risk factors as linear regression models. Secondarily, we evaluated for age (by median) and sex interactions in the relations between aortic stiffness and measures of LV structure and function. We report standardized beta coefficients as the standard deviation unit numerical change in the dependent (LV structure and function) variable per standard deviation unit change of the independent (aortic stiffness) variable. A 2-tailed Bonferroni-corrected \u003cem\u003eP\u003c/em\u003e value of 0.05/10 tests\u0026thinsp;=\u0026thinsp;0.005 was used as the threshold for statistical significance. All risk factors were chosen \u003cem\u003ea priori\u003c/em\u003e. Statistical analyses were performed using SAS version 9.4 (SAS Institute, Cary, NC).\u003c/p\u003e \u003c/div\u003e"},{"header":"RESULTS","content":"\u003cdiv id=\"Sec7\" class=\"Section2\"\u003e\n\u003ch2\u003eBaseline Characteristics of Participants\u003c/h2\u003e\n\u003cp\u003eBaseline characteristics of the 1,050 JHS participants in this study are presented in Table\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e. Participants, of whom 63% were women, were middle-aged and had an elevated mean body mass index. Over one-fifth of participants had diabetes, nearly 1/3 used lipid-lowering medications, and the majority used antihypertensive medications. Participants did not have elevated PWV and had normal mean LV systolic function reflected by ejection fraction and Ecc. Comparison of characteristics of individuals included and excluded in the study are reported in the \u003cstrong\u003eSupplemental Table\u003c/strong\u003e. Excluded individuals were similar in age, but with greater CVD risk factors including higher prevalence of diabetes and use of anti-hypertensive and lipid lowering medications, slightly higher PWV, and similar to slightly more favorable measures of LV function.\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003ctable id=\"Tab1\" border=\"1\"\u003e\u003ccaption\u003e\n\u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\n\u003cdiv class=\"CaptionContent\"\u003e\n\u003cp\u003eCharacteristics of the study sample (n\u0026thinsp;=\u0026thinsp;1050)\u003c/p\u003e\n\u003c/div\u003e\n\u003c/caption\u003e\n\u003cthead\u003e\n\u003ctr\u003e\n\u003cth colspan=\"2\" align=\"left\"\u003e\n\u003cp\u003eCharacteristics\u003c/p\u003e\n\u003c/th\u003e\n\u003c/tr\u003e\n\u003c/thead\u003e\n\u003ctbody\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eAge, yrs\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e59 (10)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eWomen\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e658 (63)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eBody mass index, mg/dL\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e32 (6)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eSystolic blood pressure, mm Hg\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e126 (18)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eDiastolic blood pressure, mm Hg\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e76 (10)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eHeart rate, beats/min\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e63 (10)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eTotal to HDL cholesterol ratio\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e3.6 (1.1)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eTriglyceride, mg/dL\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e95 (55)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003ePlasma Glucose, mg/dL\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e102 (30)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eDiabetes Mellitus\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e224 (21)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eUse of hypertensive medications\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e634 (60)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eUse of hyperlipidemia medications\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e321 (31)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd colspan=\"2\" align=\"left\"\u003e\n\u003cp\u003e\u003cstrong\u003eCMR variables\u003c/strong\u003e\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eAortic arch PWV, m/s\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e7.4 (5.9)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eThoracic PWV, m/s\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e6.5 (2.6)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eLV mass index, g/m\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e66 (16)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eLV end-diastolic volume, mL\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e125 (33)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eLV Mass to LVEDV ratio\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e1.1 (0.3)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eEjection fraction, %\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e61 (9)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eStroke volume, mL\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e75 (21)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eLV Global circumferential strain (Ecc), %\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-15.8 (2.4)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eBase\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-15.7 (2.9)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eMid\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-15.8 (3.2)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eApex\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-16.1 (2.9)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd colspan=\"2\" align=\"left\"\u003e\n\u003cp\u003eData reported as n (%) for categorical variables and mean (SD) for continuous variables\u003c/p\u003e\n\u003cp\u003eAbbreviations: HDL\u0026thinsp;=\u0026thinsp;High Density Lipoprotein. LV: left ventricular. LVEDV\u0026thinsp;=\u0026thinsp;LV end diastolic volume. CMR\u0026thinsp;=\u0026thinsp;cardiovascular magnetic resonance.\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003c/tbody\u003e\n\u003c/table\u003e\n\u003c/div\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e\n\u003ch2\u003e\u0026nbsp;\u003c/h2\u003e\n\u003cdiv id=\"Sec9\" class=\"Section3\"\u003e\n\u003cdiv id=\"Sec10\" class=\"Section4\"\u003e\n\u003ch2\u003eAssociation of LV Structure and Function with Aortic Stiffness\u003c/h2\u003e\n\u003cp\u003eThe age- and sex- and MV-adjusted associations of aortic stiffness with LV structure are presented in Table\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e. In MV models, AA-PWV and T-PWV were associated with LVMI (\u0026beta;\u0026thinsp;=\u0026thinsp;0.089, 95% CI 0.026\u0026ndash;0.152, p\u0026thinsp;=\u0026thinsp;0.005 and \u0026beta;\u0026thinsp;=\u0026thinsp;0.096 95% CI\u0026thinsp;=\u0026thinsp;0.034\u0026ndash;0.158, p\u0026thinsp;=\u0026thinsp;0.002). There was no association of AA-PWV or T-PWV with LVM/LVEDV (p\u0026thinsp;=\u0026thinsp;0.09, p\u0026thinsp;=\u0026thinsp;0.37, respectively).\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003ctable id=\"Tab2\" border=\"1\"\u003e\u003ccaption\u003e\n\u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e\n\u003cdiv class=\"CaptionContent\"\u003e\n\u003cp\u003eContinuous associations of aortic stiffness with LV structure\u003c/p\u003e\n\u003c/div\u003e\n\u003c/caption\u003e\n\u003cthead\u003e\n\u003ctr\u003e\n\u003cth align=\"left\"\u003e\u0026nbsp;\u003c/th\u003e\n\u003cth colspan=\"3\" align=\"left\"\u003e\n\u003cp\u003eLVMI (g/m\u003csup\u003e2\u003c/sup\u003e)\u003c/p\u003e\n\u003c/th\u003e\n\u003cth colspan=\"3\" align=\"left\"\u003e\n\u003cp\u003eLVM/LVEDV Ratio\u003c/p\u003e\n\u003c/th\u003e\n\u003c/tr\u003e\n\u003c/thead\u003e\n\u003ctbody\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eR\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e\u0026szlig; (95% CI)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eP-value\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eR\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e\u0026szlig; (95% CI)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eP-value\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd colspan=\"7\" align=\"left\"\u003e\n\u003cp\u003e\u003cstrong\u003eAortic Arch PWV (m/s)\u003c/strong\u003e\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eAge/sex-adjusted\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.28\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.122 (0.060, 0.185)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.0001\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.12\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.073 (0.004, 0.142)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.037\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eMV-adjusted\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.34\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.089 (0.026, 0.152)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.005\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.25\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.057 (-0.009, 0.123)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.091\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd colspan=\"7\" align=\"left\"\u003e\n\u003cp\u003e\u003cstrong\u003eThoracic Aorta PWV (m/s)\u003c/strong\u003e\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eAge/sex-adjusted\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.13\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.128 (0.067, 0.188)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e\u0026lt;\u0026thinsp;0.0001\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.12\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-0.007 (-0.074, 0.060)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.84\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eMV-adjusted\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.34\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.096 (0.034, 0.158)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.002\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.25\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-0.030 (-0.095, 0.035)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.37\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003c/tbody\u003e\n\u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003ePWV: Pulse wave velocity; LV: left ventricle. LVMI: LV mass indexed to body surface area. LVM/LVEDV: LV Mass to End Diastolic Volume Ratio. MV model adjusted for age, sex; weight, height, mean arterial pressure, heart rate, diabetes, total to HDL ratio, blood pressure medications and antilipidemia medications.\u003c/p\u003e\n\u003cp\u003eThe multivariable-adjusted associations of aortic stiffness with LV function are presented in Table\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e3\u003c/span\u003e. AA-PWV and T-PWV were not associated with global peak LV Ecc (p\u0026thinsp;=\u0026thinsp;0.012 and 0.13, respectively, for age- and sex-adjusted and MV-adjusted models). However, AA-PWV and T-PWV were associated with worse (more positive) Ecc at the LV base, but not mid or apical segments (AA-PWV: \u0026beta;\u0026thinsp;=\u0026thinsp;0.126 per SDU, 95% CI\u0026thinsp;=\u0026thinsp;0.054\u0026ndash;0.198, p\u0026thinsp;=\u0026thinsp;0.0007; T-PWV: \u0026beta;\u0026thinsp;=\u0026thinsp;0.108 per SDU, 95% CI\u0026thinsp;=\u0026thinsp;0.037\u0026ndash;0.180, p\u0026thinsp;=\u0026thinsp;0.0029). In analyses relating PWV to dichotomized LV structure or functional measures, there was a borderline association of AA-PWV and T-PWV to elevated (\u0026gt;\u0026thinsp;90th percentile) LV basal Ecc (HR 2.36, 95% CI 1.27\u0026ndash;4.38, p\u0026thinsp;=\u0026thinsp;0.006 for AA-PWV; T-PWV results were similar (p\u0026thinsp;=\u0026thinsp;0.006). There was no significant association of PWV with other dichotomous measures of LV structure or function (LVMI, LVM/EDV, EF, or regional Ecc of the mid-ventricle or apex). There were no significant age and sex interactions in the associations between AA-PWV and T-PWV with measures of LV structure or function.\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003cdiv class=\"colspec\" align=\"left\"\u003e\u0026nbsp;\u003c/div\u003e\n\u003ctable id=\"Tab3\" border=\"1\"\u003e\u003ccaption\u003e\n\u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e\n\u003cdiv class=\"CaptionContent\"\u003e\n\u003cp\u003eContinuous associations of aortic stiffness with LV systolic function\u003c/p\u003e\n\u003c/div\u003e\n\u003c/caption\u003e\n\u003cthead\u003e\n\u003ctr\u003e\n\u003cth rowspan=\"3\" align=\"left\"\u003e\u0026nbsp;\u003c/th\u003e\n\u003cth colspan=\"2\" rowspan=\"2\" align=\"left\"\u003e\n\u003cp\u003eEjection Fraction\u003c/p\u003e\n\u003cp\u003e(%)\u003c/p\u003e\n\u003c/th\u003e\n\u003cth colspan=\"2\" rowspan=\"2\" align=\"left\"\u003e\n\u003cp\u003eLV global Ecc\u003c/p\u003e\n\u003cp\u003e(%)\u003c/p\u003e\n\u003c/th\u003e\n\u003cth colspan=\"6\" align=\"left\"\u003e\n\u003cp\u003eLV regional Ecc (%)\u003c/p\u003e\n\u003c/th\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003cth colspan=\"2\" align=\"left\"\u003e\n\u003cp\u003eBase\u003c/p\u003e\n\u003c/th\u003e\n\u003cth colspan=\"2\" align=\"left\"\u003e\n\u003cp\u003eMid\u003c/p\u003e\n\u003c/th\u003e\n\u003cth colspan=\"2\" align=\"left\"\u003e\n\u003cp\u003eApex\u003c/p\u003e\n\u003c/th\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003eR\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e\n\u003c/th\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003e\u0026szlig; (95% CI)\u003c/p\u003e\n\u003c/th\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003eR\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e\n\u003c/th\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003e\u0026szlig; (95% CI)\u003c/p\u003e\n\u003c/th\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003eR\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e\n\u003c/th\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003e\u0026szlig; (95% CI)\u003c/p\u003e\n\u003c/th\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003eR\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e\n\u003c/th\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003e\u0026szlig; (95% CI)\u003c/p\u003e\n\u003c/th\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003eR\u003csup\u003e2\u003c/sup\u003e\u003c/p\u003e\n\u003c/th\u003e\n\u003cth align=\"left\"\u003e\n\u003cp\u003e\u0026szlig; (95% CI)\u003c/p\u003e\n\u003c/th\u003e\n\u003c/tr\u003e\n\u003c/thead\u003e\n\u003ctbody\u003e\n\u003ctr\u003e\n\u003ctd colspan=\"11\" align=\"left\"\u003e\n\u003cp\u003e\u003cstrong\u003eAortic Arch PWV (m/s)\u003c/strong\u003e\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eModel 1\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.04\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-0.098\u003c/p\u003e\n\u003cp\u003e(-0.170, -0.026)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.07\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.090\u003c/p\u003e\n\u003cp\u003e(0.019, 0.161)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.07\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.129*\u003c/p\u003e\n\u003cp\u003e(0.059, 0.200)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.04\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.011\u003c/p\u003e\n\u003cp\u003e(-0.061, 0.083)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.04\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.084\u003c/p\u003e\n\u003cp\u003e(0.012, 0.156)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eModel 2\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.07\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-0.086\u003c/p\u003e\n\u003cp\u003e(-0.160, -0.011)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.17\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.091\u003c/p\u003e\n\u003cp\u003e(0.021, 0.162)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.13\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.126*\u003c/p\u003e\n\u003cp\u003e(0.054, 0.198)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.10\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.015\u003c/p\u003e\n\u003cp\u003e(-0.058, 0.089)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.10\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.087\u003c/p\u003e\n\u003cp\u003e(0.014, 0.160)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd colspan=\"11\" align=\"left\"\u003e\n\u003cp\u003e\u003cstrong\u003eThoracic Aorta PWV (m/s)\u003c/strong\u003e\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eModel 1\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.031\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-0.060\u003c/p\u003e\n\u003cp\u003e(-0.130, 0.010)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.07\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.054\u003c/p\u003e\n\u003cp\u003e(-0.015,0.123)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.06\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.105*\u003c/p\u003e\n\u003cp\u003e(0.036, 0.175)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.04\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-0.029\u003c/p\u003e\n\u003cp\u003e(-0.099, 0.041)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.04\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.066\u003c/p\u003e\n\u003cp\u003e(-0.004, 0.136)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003ctr\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003eModel 2\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.06\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-0.042\u003c/p\u003e\n\u003cp\u003e(-0.116, 0.031)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.07\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.054\u003c/p\u003e\n\u003cp\u003e(-0.015,0.123)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.13\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.108*\u003c/p\u003e\n\u003cp\u003e(0.037, 0.180)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.10\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e-0.030\u003c/p\u003e\n\u003cp\u003e(-0.102, 0.043)\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.10\u003c/p\u003e\n\u003c/td\u003e\n\u003ctd align=\"left\"\u003e\n\u003cp\u003e0.063\u003c/p\u003e\n\u003cp\u003e(-0.009, 0.135)\u003c/p\u003e\n\u003c/td\u003e\n\u003c/tr\u003e\n\u003c/tbody\u003e\n\u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003e* p\u0026thinsp;\u0026lt;\u0026thinsp;0.005\u003c/p\u003e\n\u003cp\u003ePWV: Pulse wave velocity; Ecc. = Global circumferential Peak systolic strain; EDV\u0026thinsp;=\u0026thinsp;End-Stage Diastolic Volume Ratio; Model 1: Age- and Sex-Adjusted Model; Model 2: Adjusted for age, sex; weight, height, mean arterial pressure, heart rate, diabetes, total to HDL ratio, blood pressure medications and antilipidemic medications\u003c/p\u003e\n\u003c/div\u003e\n\u003c/div\u003e\n\u003c/div\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eIn this study of 1,050 AA in the community without prevalent CVD, aortic stiffness was associated with subclinical measures of adverse cardiac structural remodeling measured by CMR. The present study elaborates on prior work by exploring the ventricular-vascular associations at distinct segments of the LV and aorta in individuals free of CVD, enhancing our understanding of the relationship between subclinical aortic stiffness and ventricular dysregulation. Greater aortic stiffness measured by either AA-PWV or T-PWV was associated with higher LV mass. Notably, while aortic stiffness was not associated with LVEF or worse global Ecc, PWV had a stronger association with less favorable LV strain at the base, but not mid-LV or apical segments. Our findings are consistent with the growing evidence demonstrating the connection between dysfunction of the aorta and LV structural and functional remodeling that may underlie preclinical CVD, including heart failure in AA.\u003c/p\u003e \u003cp\u003eThe proximal aorta located immediately distal to the LV, buffers LV afterload, and progressive loss of the elasticity of this segment may create impairment to LV contractility. Greater aortic stiffness and associated higher pressure pulsatility and wave reflection that returns earlier during systole, collectively result in greater workload for the LV.[\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e19\u003c/span\u003e] In this study, we found that the association of LV strain with aortic stiffness was not uniform and varied by segments. Aortic stiffness was associated with unfavorable circumferential strain of the basal segments, perhaps indicating excessive afterload on these areas. The underlying anatomy and physiology of the LV underscores the importance of our findings: the LV base contains a greater proportion of circumferential fibers compared to distal segments,[\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e20\u003c/span\u003e] and the basal segments generate the most stroke volume of all segments in the LV. Such dynamics over time lead to consequences that include LV hypertrophy and declines in systolic and diastolic function, as has been observed in hypertension. Unfavorable ventricular-vascular interactions may perpetuate with the constellation of adverse LV structural and functional remodeling begetting further hemodynamic abnormalities leading to greater aortic stiffness, ultimately leading to adverse CVD events. Because the base of the LV generates the most stroke volume compared to the distal LV segments, functional decline of this region may explain greater susceptibility to development of clinical CVD, including heart failure, in AA.\u003c/p\u003e \u003cp\u003eOur study results add to the prior literature on the relationship between aortic stiffness and LV structure and function that has been primarily demonstrated in non-AA samples. Several groups, including the Framingham Heart Study (FHS), MESA, and AGES-Reykjavik have reported similar associations of aortic stiffness assessed with CMR or carotid femoral PWV with LV mass and mass index.[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e21\u003c/span\u003e, \u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e22\u003c/span\u003e] Variability in the type and location of the systolic function measure, across cohort studies contribute to differences in, and preclude direct comparison of, the associations of aortic stiffness with LV systolic function. Similar to our study, the FHS reported that carotid femoral PWV was not associated with fractional shortening, a surrogate of LVEF,[\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e21\u003c/span\u003e] but was associated with worse echocardiographic global longitudinal strain,[\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e23\u003c/span\u003e] though circumferential strain was not measured. Using CMR, MESA investigators reported an association of aortic arch PWV with LVEF and LV Ecc as assessed in the mid-ventricle, but did not evaluate the associations of global aortic stiffness or additional segments of LV Ecc.[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e12\u003c/span\u003e]\u003c/p\u003e \u003cp\u003eAdditionally, underlying differences in the study samples likely also contribute to differences between our collective study results. In the present study, we excluded individuals with CVD in order to study subclinical ventricular-vascular associations, whereas the sample in MESA included individuals with angina, myocardial infarction, and heart failure. Though the mean values of CMR LV structure and function measures are similar between participants in our study and MESA, notably our study sample was also younger with a greater proportion of women, which may have influenced detection of associations. Additionally, though MESA included non-white participants, only one-quarter of the study participants were AA and study results of aortic stiffness-LV structure and function were not reported by race/ethnicity.[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e12\u003c/span\u003e] Including over 1000 AA, our study is among the largest to study ventricular\u0026ndash;vascular associations of both regional and global aortic and LV function in AA free of CVD. Given the vulnerability of AA to elevated LV mass and associated morbidity,[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e24\u003c/span\u003e] and outcomes including CVD and HF,[\u003cspan additionalcitationids=\"CR26\" citationid=\"CR33\" class=\"CitationRef\"\u003e25\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e27\u003c/span\u003e] our findings highlight additional pathophysiological associations that may underlie these risks. Future investigation of the effect of modulating arterial stiffness may identify its impact on reversing LV remodeling.\u003c/p\u003e \u003cdiv id=\"Sec12\" class=\"Section2\"\u003e \u003ch2\u003eStrengths and Limitations\u003c/h2\u003e \u003cp\u003eThough AA individuals face higher CVD risks than those of other race/ethnicities, they are a relatively understudied group. The strengths of this study include the large community dwelling cohort, study of individuals free of CVD, detailed imaging, and extensive phenotyping of clinical risk factors to study subclinical disease. Our analysis of LV circumferential strain on CMR using tagging is highly reproducible and allows comparison across other cohorts with similar data. We used Bonferroni correction to identify the key associations between aortic stiffness and LV structure and function, to lower the risk of inaccurate associations based upon multiple testing. However, the findings of this study must be interpreted within the context of its limitations. First, the relatively low temporal resolution of PWV transit across the aortic arch may have led to overestimation of PWV, though this is a caveat of all such CMR studies of this aortic region. Though Ecc was the predominant method for strain analysis at the time of CMR, the recent advent of commercially available feature tracking analysis applied post-hoc to cine CMR images allows additional study of myocardial strain in longitudinal and radial orientations and with greater ease, though variability in the latter techniques across vendors remains. Additionally, the study is observational and cannot determine a causal link between aortic stiffness and adverse LV remodeling and function. Further, the studied sample, compared to those excluded, had fewer CVD risk factors. Though this may limit the generalizability of this study to the population at large, it reinforces that observations of abnormal ventricular-vascular relations occur even in the healthier participants with subclinical disease. While the participants in this study represent a region within the U.S., the JHS represents the largest comprehensive study of CVD associations and cardiovascular imaging in Black Americans.\u003c/p\u003e \u003c/div\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eAortic stiffness is associated with subclinical regional LV systolic dysfunction in a large cohort of AA individuals free of prevalent CVD in the community. Our findings highlight that adverse ventricular-vascular remodeling occur beyond that accounted for CVD risk factors alone, and may provide the substrate on which clinical CVD including heart failure may develop. Future studies will be helpful to elucidate the temporal relationships of aortic stiffness on the pattern and progression of LV dysfunction and clarify the role of modulation of aortic stiffness on the prevention or regression of abnormal LV remodeling and function.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e \u003ch2\u003eDISCLOSURES\u003c/h2\u003e \u003cp\u003eDr. Mitchell is the owner of Cardiovascular Engineering, Inc., a company that develops and manufactures devices to measure vascular stiffness and is a consultant to and receives honoraria from Novartis, Merck, Servier, and Philips. All other authors report no disclosures.\u003c/p\u003e \u003c/p\u003e\u003cp\u003e\u003cstrong\u003eCompeting Interests\u003c/strong\u003e\u003cp\u003eDr. Mitchell is the owner of Cardiovascular Engineering, Inc., a company that develops and manufactures devices to measure vascular stiffness, and is a consultant to and receives honoraria from Novartis, Merck, Servier, and Philips. All other authors report no disclosures.\u003c/p\u003e\u003c/p\u003e\u003ch2\u003eFUNDING\u003c/h2\u003e \u003cp\u003eThe Jackson Heart Study (JHS) is supported and conducted in collaboration with Jackson State University (HHSN268201800013I), Tougaloo College (HHSN268201800014I), the Mississippi State Department of Health (HHSN268201800015I) and the University of Mississippi Medical Center (HHSN268201800010I, HHSN268201800011I and HHSN268201800012I) contracts from the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute for Minority Health and Health Disparities (NIMHD). CWT is partially supported by NIH R03 HL145195.\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eGFM, EF, CWT were the senior authors involved in the study design and critical revision of the manuscript. WGH, JJC, JGT, AO, RSV, JBM, MH, and EF contributed to data collection and analysis. SM was responsible for statistical analysis. MJ, IR, CWT drafted the manuscript. All authors participated in contributing to text and the content of the manuscript, including revisions and edits. All authors approve of the content of the manuscript.\u003c/p\u003e\u003ch2\u003eAcknowledgement\u003c/h2\u003e\u003cp\u003eThe authors wish to thank the staff and participants of the Jackson Heart Study.\u003c/p\u003e\u003ch2\u003eData Availability\u003c/h2\u003e\u003cp\u003eAll primary data related to this study is available upon reasonable request.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eCohn JN, Ferrari R, Sharpe N (2000) Cardiac remodeling\u0026ndash;concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling. Behalf of an International Forum on Cardiac Remodeling. J Am Coll Cardiol 35(3):569\u0026ndash;582 Epub 2000/03/15. 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N Engl J Med 360(12):1179\u0026ndash;1190. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1056/NEJMoa0807265\u003c/span\u003e\u003cspan address=\"10.1056/NEJMoa0807265\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003ePubMed PMID: 19297571; PubMed Central PMCID: PMCPMC2829671\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"the-international-journal-of-cardiovascular-imaging","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"caim","sideBox":"Learn more about [The International Journal of Cardiovascular Imaging](https://www.springer.com/journal/10554)","snPcode":"10554","submissionUrl":"https://submission.nature.com/new-submission/10554/3","title":"The International Journal of Cardiovascular Imaging","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false},"keywords":"Aortic stiffness, pulse wave velocity, left ventricle, strain, cardiovascular magnetic resonance","lastPublishedDoi":"10.21203/rs.3.rs-4189960/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-4189960/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eCardiovascular disease (CVD) morbidity and mortality are high among black adults. We aimed to study the granular subclinical relations of aortic stiffness and left ventricular (LV) function and remodeling in blacks, in whom limited data are available.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eMethods\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eIn the Jackson Heart Study, 1,050 U.S. community-dwelling black adults without CVD (mean age 59±10 years, 62% women) underwent 1.5T cardiovascular magnetic resonance. We assessed regional and global aortic stiffness and LV structure and function, including LV mass indexed to body surface area (LVMI), end-diastolic volume (LVEDV), ejection fraction (EF), and global and regional circumferential strain (Ecc).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eResults\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePhase contrast images of the cross-sectional aorta at the pulmonary artery bifurcation and abdominal aorta bifurcation were acquired to measure pulse wave velocity of the aortic arch (AA-PWV) and thoracic aorta (T-PWV). Results of multivariable-adjusted analyses are presented as SD unit change in LV variables per SD change in PWV variables. Higher AA-PWV and T-PWV were associated with greater LVMI: for T-PWV, β=0.10, 95% CI=0.03-0.16, p=0.002. Higher AA-PWV and T-PWV were associated with worse (more positive) Ecc at the LV base (for AA-PWV, β=0.13, 95% CI=0.05-0.20, p=0.0007), but not mid-LV or apex. AA-PWV and T-PWV were not associated with LV mass/LVEDV or EF.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eIn this cross-sectional study of blacks without CVD in the U.S., aortic stiffness is associated with subclinical adverse LV function in basal segments. Future studies may elucidate the temporal relationships of aortic stiffness on the pattern and progression of LV remodeling, dysfunction, and associated prognosis in blacks.\u003c/p\u003e","manuscriptTitle":"Subclinical Association of Aortic Stiffness with Cardiac Structure and Function in African- Americans: the Jackson Heart Study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-04-03 11:43:53","doi":"10.21203/rs.3.rs-4189960/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2024-05-04T15:27:08+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2024-05-02T03:39:16+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2024-04-23T17:53:58+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"993d1035-e2bb-454c-a6da-687bbfaaac19","date":"2024-04-16T23:32:09+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"a479ec96-718e-42d2-ad77-52fa2816a511","date":"2024-04-02T20:20:14+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2024-04-02T16:20:13+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2024-03-30T06:56:00+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2024-03-30T06:56:00+00:00","index":"","fulltext":""},{"type":"submitted","content":"The International Journal of Cardiovascular Imaging","date":"2024-03-29T23:20:49+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"the-international-journal-of-cardiovascular-imaging","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"caim","sideBox":"Learn more about [The International Journal of Cardiovascular Imaging](https://www.springer.com/journal/10554)","snPcode":"10554","submissionUrl":"https://submission.nature.com/new-submission/10554/3","title":"The International Journal of Cardiovascular Imaging","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false}}],"origin":"","ownerIdentity":"06237c89-cb04-4ff1-92dc-2c4b14e29217","owner":[],"postedDate":"April 3rd, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2024-06-23T00:33:35+00:00","versionOfRecord":{"articleIdentity":"rs-4189960","link":"https://doi.org/10.1007/s10554-024-03159-y","journal":{"identity":"the-international-journal-of-cardiovascular-imaging","isVorOnly":false,"title":"The International Journal of Cardiovascular Imaging"},"publishedOn":"2024-06-23 00:33:35","publishedOnDateReadable":"June 23rd, 2024"},"versionCreatedAt":"2024-04-03 11:43:53","video":"","vorDoi":"10.1007/s10554-024-03159-y","vorDoiUrl":"https://doi.org/10.1007/s10554-024-03159-y","workflowStages":[]},"version":"v1","identity":"rs-4189960","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-4189960","identity":"rs-4189960","version":["v1"]},"buildId":"qtupq5eGEP_6zYnWcrvyt","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}