Pulmonary vascular resistance at hospital admission is associated with early mortality in patients with intermediate-to-high-risk acute pulmonary embolism

Pulmonary vascular resistance at hospital admission is associated with early mortality in patients with intermediate-to-high-risk acute pulmonary embolism | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Short Report Pulmonary vascular resistance at hospital admission is associated with early mortality in patients with intermediate-to-high-risk acute pulmonary embolism Leslie Marisol González-Hermosillo, Marlene Monserrat Juárez, and 9 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8950718/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Acute pulmonary embolism (PE) is a critical disease with a high 30-day mortality rate in intermediate-to-high-risk (IHR) patients. Herein, we prospectively enrolled 117 patients with IHR-PE and recorded demographic, clinical, and biochemical parameters from electronic records, as well as hemodynamic variables acquired by right-heart catheterization at hospital admission. After a 6-month follow-up, we retrospectively analyzed all variables and found that hemodynamic parameters increased significantly in patients who subsequently died within the first 30 days after discharge, especially pulmonary vascular resistance (PVR) (9.6 ± 3.3 versus 5.5 ± 3.1, p = 0.002, in non-survival and survival patients, respectively). In fact, PVR ≥ 6.55 Wood units (WU) at hospital admission was an accurate predictor of 30-day mortality, with an area under the receiver operating characteristic curve of 0.85 (95% Confidence Interval, 0.71–0.97; p = 0.007), a sensitivity of 100%, and a specificity of 70%. Our findings emphasize the urgency of assessing hemodynamic parameters in all IHR-PE patients, prompting discussion of the benefit-risk balance of right-heart catheterization in IHR-PE. Pulmonary vascular resistance pulmonary embolism 30-day mortality right-heart catheterization Figures Figure 1 Introduction Acute pulmonary embolism (PE) is a critical medical condition that occurs when a blood clot originating from deep vein thrombosis (DVT) obstructs one or more pulmonary arteries [1]. PE is the third cause of cardiovascular death worldwide, behind acute myocardial infarction and cerebrovascular accident [2]. Particularly, patients with intermediate-to-high-risk (IHR) PE show a 30-day mortality rate ranging from 9% to 25%, even on medical management [3]. Numerous studies have tried to explore the factors contributing to early mortality in patients with IHR-PE, where vascular remodeling, right ventricular (RV) dysfunction, and previous comorbidities appear to play central roles [4]. Elevated serum levels of cytokines and chemokines, such as transforming growth factor-beta 1 (TGF-b1) and interleukin (IL-) 8, are indicators of vascular remodeling [5]. Biochemical markers, such as natriuretic peptides and cardiac troponins, and hemodynamic parameters are crucial for assessing RV impairment [6, 7]. However, evidence regarding the most relevant clinical contributors to early mortality in IHR-PE remains uncertain. Therefore, we conducted an ambispective, longitudinal, 6-month cohort study in patients with IHR-PE to examine factors associated with 30-day mortality. Materials and Methods Patients and study design We invited women and men aged 18 years or older who attended the Department of Cardiorespiratory Emergencies at the General Hospital of Mexico after confirmation of IHR-PE according to the 2019 European Society of Cardiology (ESC) risk stratification guidelines [8]. All participants with a medical indication for right-heart catheterization (RHC) to conduct catheter-directed thrombolysis (CDT) agreed to participate in the study by signing the informed consent letter. We excluded patients with symptom onset more than one week ago, as well as pregnant or lactating women. We eliminated participants from the study if they expressed a willingness to leave, or patients for whom we could not collect demographic, clinical, biochemical, and hemodynamic parameters at hospital admission. The Institutional Ethics Committee, Research Committee, and Biosafety Committee of the General Hospital of Mexico approved the study under registration number DI/23/503/03/16, in accordance with the 1975 Declaration of Helsinki and its subsequent 2024 amendment. This ambispective, longitudinal, 6-month cohort study collected prospectively demographic, clinical, biochemical, and hemodynamic parameters at hospital admission from January 2017 to December 2024. After a 6-month follow-up, we retrospectively examined all data, with particular emphasis on those associated with 30-day mortality. Statistics We used the Chi-squared test and the Student T-test to compare data between survival and non-survival IHR-PE patients. We calculated the area under the receiver operating characteristic (ROC) curve (AUC) and 95% confidence interval (CI) for all variables, using the Youden Index to obtain optimal cut-off values, sensitivity, and specificity, adjusting for confounders by multiple regression analysis. We considered differences significant when p < 0.05 and reported data as mean ± standard deviation, absolute numbers, or percentages. We used GraphPad Prism 6.01 (GraphPad Software, La Jolla, CA 92037, USA), MDCalc (New York, NY 10003, USA), and R i386 3.5.2 (Microsoft Corp., Boston, MA, USA). Results At the end of follow-up, the 30-day mortality rate was 7.69% among the 117 enrolled patients (Table 1). After examining all variables registered at hospital admission, there were no differences in age, sex, body mass index (BMI), pulmonary embolism severity index (PESI) score, BOVA score, and right-to-left ventricular ratio (RV/LV) between survival and non-survival patients (Table 1). There were also no differences in oxygen therapy, mechanical ventilation, and the prevalence of comorbidities. Most laboratory variables did not show significant differences between survival and non-survival patients, except for serum lactate levels, which were significantly higher at admission in patients who did not survive during follow-up than in those who survived ( p = 0.021). Conversely, hemodynamic parameters exhibited the most significant changes, with higher values of systolic right ventricular pressure (sRVP), diastolic right ventricular pressure (dRVP), systolic pulmonary arterial pressure (sPAP), diastolic pulmonary arterial pressure (dPAP), and mean pulmonary arterial pressure (mPAP) in non-survival patients than in survival participants. In contrast, cardiac output (CO) decreased significantly in non-survivors compared with survivors. Pulmonary vascular resistance (PVR) at admission showed the greatest difference, increasing nearly 2-fold in patients who died compared with those who survived (9.60 ± 3.3 versus 5.5 ± 3.1, p = 0.002, respectively) (Table 1). Calculation of AUCs revealed that PVR ≥ 6.55 Wood units (WU) outperformed other variables by predicting 30-day mortality with an AUC of 0.85 (95% CI, 0.71-0.97; p = 0.007), a sensitivity of 100.0%, and a specificity of 70.0% (Fig. 1), independently of confounding variables such as sex and comorbidities. Discussion Herein, we provide compelling evidence that PVR is associated with an increased risk of early pulmonary deterioration leading to 30-day mortality in IHR-PE patients. Our findings highlight the importance of assessing hemodynamic parameters in IHR-PE patients upon hospital arrival, particularly PVR. PVR is a hemodynamic measure that reflects how difficult blood flows through the pulmonary circulation and is related to the resistance the right ventricle encounters in pumping blood into the lungs [9]. PVR integrates crucial hemodynamic factors into a single variable, including pulmonary arterial pressure and cardiac output, which allows it to capture both the severity of vascular obstruction and the impact on cardiac performance [10]. An increase in PVR may result from mechanical obstruction caused by the thrombus and pulmonary blood vessel vasoconstriction, leading to increased RV afterload and failure, and death [11]. A previous study showed that experimental increases in pulmonary arterial pressure in rabbits lead to vascular remodeling, characterized by increased collagen and elastin production in blood vessels [12]. In addition to vascular remodeling, increased pulmonary arterial pressure induces geometrical changes in cardiomyocytes, local inflammation, and fibrosis, collectively affecting myocardial contractility and RV function [13]. Altogether, this information suggests that increased PVR at disease onset may predispose the organism to early vascular and cardiac remodeling, thus increasing the chances of developing RV overload and failure, and death. At hospital admission, PVR could not only help assess 30-day mortality risk but also identify patients who may benefit from novel anti-inflammatory and anti-fibrotic drugs before vascular and cardiac remodeling aggravates [14, 15]. In this pilot study, we observed that PVR has an AUC greater than 0.85 for predicting early mortality in IHR-PE patients at hospital admission. Our findings may help expand the body of predictive tools to facilitate 30-day mortality risk assessment in PE [16], encouraging additional studies in larger patient cohorts to validate markers such as PVR in clinical practice. We must acknowledge that this study has certain limitations, including the sample size and the need for a catheterization laboratory, which may not be available in community hospitals or resource-constrained healthcare facilities. Moreover, we focused only on IHR, which limits the extrapolation of our findings to low-risk patient groups. Conclusion We found that PVR ≥ 6.55 WU at hospital admission is associated with early mortality and may represent an independent hemodynamic predictor of death in IHR-PE. An increase in PVR reveals that pulmonary artery pressures may play a role in aggravating early vascular and cardiac remodeling, leading to rapid disease worsening and mortality. These data highlight the importance of assessing hemodynamic parameters at hospital admission in IHR-PE patients, which may help healthcare professionals initiate more aggressive medical treatments to improve short-term survival. Declarations Competing interest Funding: No funding was received for conducting this study. Financial interest: The authors declare they have no financial interests. Non-financial interest: None. Ethics approval: The institutional Ethics Committee of the General Hospital of Mexico approved the study with the registration number DI/23/503/03/16 and supervised that all enrolled patients provided written informed consent. Conflict of interest : The authors declare they have no conflict of interests. References Pesavento R, Filippi L, Palla A, Visona A, Bova C, Marzolo M, et al. Impact of residual pulmonary obstruction on the long-term outcome of patients with pulmonary embolism. Eur Respir J. 2017;49(5). doi: 10.1183/13993003.01980-2016. Wendelboe AM, Raskob GE. Global Burden of Thrombosis: Epidemiologic Aspects. Circ Res. 2016;118(9):1340-7. doi: 10.1161/CIRCRESAHA.115.306841. Alabi FO, Ghaneie A, Koury I, Alkhateeb HA, Liu J, Guo M, et al. Management of intermediate high-risk pulmonary embolism: a single-center retrospective study. Front Cardiovasc Med. 2025;12:1483968. doi: 10.3389/fcvm.2025.1483968. Stam K, van Duin RWB, Uitterdijk A, Cai Z, Duncker DJ, Merkus D. Exercise facilitates early recognition of cardiac and vascular remodeling in chronic thromboembolic pulmonary hypertension in swine. Am J Physiol Heart Circ Physiol. 2018;314(3):H627-H42. doi: 10.1152/ajpheart.00380.2017. Yamada Y, Satoh T, Yaoita N, Yamada K, Chiba N, Komaru K, et al. Pathogenesis of Pulmonary Artery Remodeling: TGF-Beta Signaling and Inhibin Subunit Beta A in Group 1 and 2 Pulmonary Hypertension. Arterioscler Thromb Vasc Biol. 2026. doi: 10.1161/ATVBAHA.125.322506. Dursunoglu N, Dursunoglu D, Yildiz AI, Rota S. Evaluation of cardiac biomarkers and right ventricular dysfunction in patients with acute pulmonary embolism. Anatol J Cardiol. 2016;16(4):276-82. doi: 10.5152/akd.2014.5828. Hameed A, Condliffe R, Swift AJ, Alabed S, Kiely DG, Charalampopoulos A. Assessment of Right Ventricular Function-a State of the Art. Curr Heart Fail Rep. 2023;20(3):194-207. doi: 10.1007/s11897-023-00600-6. Konstantinides SV, Meyer G. The 2019 ESC Guidelines on the Diagnosis and Management of Acute Pulmonary Embolism. Eur Heart J. 2019;40(42):3453-5. doi: 10.1093/eurheartj/ehz726. Chemla D, Lau EM, Papelier Y, Attal P, Herve P. Pulmonary vascular resistance and compliance relationship in pulmonary hypertension. Eur Respir J. 2015;46(4):1178-89. doi: 10.1183/13993003.00741-2015. Maron BA, Kovacs G, Vaidya A, Bhatt DL, Nishimura RA, Mak S, et al. Cardiopulmonary Hemodynamics in Pulmonary Hypertension and Heart Failure: JACC Review Topic of the Week. J Am Coll Cardiol. 2020;76(22):2671-81. doi: 10.1016/j.jacc.2020.10.007. Smulders YM. Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. Cardiovasc Res. 2000;48(1):23-33. doi: 10.1016/s0008-6363(00)00168-1. Chow MJ, Zou Y, He H, McGowan FX, Zurakowski D, Zhang Y. Obstruction-induced pulmonary vascular remodeling. J Biomech Eng. 2011;133(11):111009. doi: 10.1115/1.4005301. Rosenkranz S, Howard LS, Gomberg-Maitland M, Hoeper MM. Systemic Consequences of Pulmonary Hypertension and Right-Sided Heart Failure. Circulation. 2020;141(8):678-93. doi: 10.1161/CIRCULATIONAHA.116.022362. Wang Y, Ma TT, Gao NN, Zhou XL, Jiang H, Guo R, et al. Effect of Tongxinluo on pulmonary hypertension and pulmonary vascular remodeling in rats exposed to a low pressure hypoxic environment. J Ethnopharmacol. 2016;194:668-73. doi: 10.1016/j.jep.2016.10.004. Nguyen QT, Nsaibia MJ, Sirois MG, Calderone A, Tardif JC, Fen Shi Y, et al. PBI-4050 reduces pulmonary hypertension, lung fibrosis, and right ventricular dysfunction in heart failure. Cardiovasc Res. 2020;116(1):171-82. doi: 10.1093/cvr/cvz034. Li S, Huang S, Feng Y, Mao Y. Development of a nomogram model to predict 30-day mortality in ICU cancer patients with acute pulmonary embolism. Sci Rep. 2025;15(1):9232. doi: 10.1038/s41598-025-93907-4. Table Table 1. Characteristics of the study participants . We prospectively enrolled patients with IHR-PE and registered demographic, clinical, laboratory, and hemodynamic variables at hospital admission. After completing the 6-month follow-up, we identified patients who survived or did not for a posterior retrospective comparison between groups, using the Student T-test or the Chi-squared test. We reported data as mean ± standard deviation or as percentages, considering significant differences when p < 0.05. Abbreviations: PESI, Pulmonary Embolism Severity Index; BMI, body mass index; RV/LV, right-to-left ventricular ratio; T2D, type 2 diabetes; SAH, systemic arterial hypertension; HFNC, high-flow nasal cannula; N-IMV, non-invasive mechanical ventilation; IMV, invasive mechanical ventilation; sRVP, systolic right ventricular pressure; dRVP, diastolic right ventricular pressure; sPAP, systolic pulmonary arterial pressure; dPAP, diastolic pulmonary arterial pressure; mPAP, mean pulmonary arterial pressure; CO, cardiac output; PVR, pulmonary vascular resistance. Variable Total patients n = 117 Survivors n = 108 Non-survivors n = 9 p -value Demographic and clinical data Age (years) 56.8 ± 16.1 56.7 ± 16.4 57.8 ± 15.4 0.440 Sex (female, %) 57.2 55.5 77.7 0.294 PESI score 107.5 ± 29.8 107.7 ± 29.3 106.2 ± 35.8 0.446 BOVA score 4.2 ± 1.3 4.3 ± 1.4 4.0 ± 1.0 0.309 BMI (kg/m 2 ) 32.2 ± 8.3 32.2 ± 6.8 32.5 ± 16.0 0.465 RV/LV 1.1 ± 0.4 1.1 ± 0.3 1.1 ± 0.5 0.811 Comorbidities T2D (%) 11.9 9.2 44.4 0.755 SAH (%) 36.7 35.1 55.5 Stroke history (%) 5.9 4.6 22.2 Oxygen therapy Nasal cannula (%) 72.6 72.2 77.7 0.601 HFNC (%) 6.8 6.4 11.1 Mechanical ventilation N-IMV (%) 2.5 1.8 11.1 0.583 IMV (%) 6.8 5.5 22.2 Laboratory and hemodynamic parameters Lactate (mmol/l) 1.93 ± 1.0 1.86 ± 1.0 2.46 ± 0.5 0.021 sRVP (mmHg) 51.9 ± 19.6 49.6 ± 18.1 67.3 ± 23.6 0.018 dRVP (mmHg) 6.0 ± 4.6 5.5 ± 4.3 9.0 ± 5.8 0.046 sPAP (mmHg) 52.2 ± 18.8 50.0 ± 17.6 66.3 ± 21.9 0.024 dPAP (mmHg) 21.2 ± 9.3 20.3 ± 9.0 27.1 ± 10.11 0.048 mPAP (mmHg) 33.8 ± 12.6 32.4 ± 11.6 43.1 ± 16.0 0.026 CO (l/min) 4.96 ± 1.5 5.1 ± 1.5 4.0 ± 1.5 0.040 PVR (WU) 6.1 ± 3.4 5.5 ± 3.1 9.6 ± 3.3 0.002 Additional Declarations No competing interests reported. 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(A) Lactate showed an AUC of 0.75 (95% CI, 0.59-0.91; p = 0.044), with a sensitivity of 83.33% and a specificity of 47.50%. (B) sRVP exhibited an AUC of 0.72 (95% CI, 0.48-0.96; p = 0.076), with values of sensitivity and specificity of 83.33% and 79.48%, respectively. (C) dRVP showed an AUC of 0.69 (95% CI, 0.47-0.90; p = 0.133), a sensitivity of 66.67%, and a specificity of 43.59%. (D) sPAP had an AUC of 0.72 (95% CI, 0.46-0.97; p = 0.085) and ranges of sensitivity and specificity of 50.0% and 64.1%, respectively. (E) dPAP showed an AUC of 0.67 (95% CI, 0.43-0.90; p = 0.181), with a sensitivity of 83.33% and a specificity of 38.46%. (F) mPAP exhibited an AUC of 0.69 (95% CI, 0.44-0.94; p = 0.128), with values of sensitivity and specificity of 66.67% and 46.15%, respectively. (G) CO showed an AUC of 0.72 (95% CI, 0.43-0.97; p = 0.079), a sensitivity of 83.33%, and a specificity of 71.79%. (H) PVR had the best prognostic performance with an AUC of 0.85 (95% CI, 0.71-0.97; p = 0.007) and ranges of sensitivity and specificity of 100.0% and 70.0%, respectively. We calculated AUC and 95% CI using the Youden Index to obtain optimal cut-off values, sensitivity, and specificity. Abbreviations: IHR-PE, intermediate-to-high-risk pulmonary embolism; AUC, area under the receiver operating characteristic curve; CI, confidence interval; sRVP, systolic right ventricular pressure; dRVP, diastolic right ventricular pressure; sPAP, systolic pulmonary arterial pressure; dPAP, diastolic pulmonary arterial pressure; mPAP, mean pulmonary arterial pressure; CO, cardiac output; PVR, pulmonary vascular resistance.\u003c/p\u003e","description":"","filename":"Figure1PVR.png","url":"https://assets-eu.researchsquare.com/files/rs-8950718/v1/6e7d735bc77520e84ac96310.png"},{"id":104405251,"identity":"71410311-582e-4ed8-8e6e-713833cb971b","added_by":"auto","created_at":"2026-03-11 12:22:17","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":4146269,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8950718/v1/a3dc6f33-b902-4782-9d97-a2eb519c4ba9.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Pulmonary vascular resistance at hospital admission is associated with early mortality in patients with intermediate-to-high-risk acute pulmonary embolism","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAcute pulmonary embolism (PE) is a critical medical condition that occurs when a blood clot originating from deep vein thrombosis (DVT) obstructs one or more pulmonary arteries [1]. PE is the third cause of cardiovascular death worldwide, behind acute myocardial infarction and cerebrovascular accident [2]. Particularly, patients with intermediate-to-high-risk (IHR) PE show a 30-day mortality rate ranging from 9% to 25%, even on medical management [3].\u003c/p\u003e\n\u003cp\u003eNumerous studies have tried to explore the factors contributing to early mortality in patients with IHR-PE, where vascular remodeling, right ventricular (RV) dysfunction, and previous comorbidities appear to play central roles [4]. Elevated serum levels of cytokines and chemokines, such as transforming growth factor-beta 1 (TGF-b1) and interleukin (IL-) 8, are indicators of vascular remodeling\u0026nbsp;[5]. Biochemical markers, such as natriuretic peptides and cardiac troponins, and hemodynamic parameters are crucial for assessing RV impairment\u0026nbsp;[6, 7].\u003c/p\u003e\n\u003cp\u003eHowever, evidence regarding the most relevant clinical contributors to early mortality in IHR-PE remains uncertain. Therefore, we conducted an ambispective, longitudinal, 6-month cohort study in patients with IHR-PE to examine factors associated with 30-day mortality.\u003c/p\u003e"},{"header":"Materials and Methods","content":"\u003cp\u003e\u003cem\u003ePatients and study design\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eWe invited women and men aged 18 years or older who attended the Department of Cardiorespiratory Emergencies at the General Hospital of Mexico after confirmation of IHR-PE according to the 2019 European Society of Cardiology (ESC) risk stratification guidelines [8]. All participants with a medical indication for right-heart catheterization (RHC) to conduct catheter-directed thrombolysis (CDT) agreed to participate in the study by signing the informed consent letter. We excluded patients with symptom onset more than one week ago, as well as pregnant or lactating women. We eliminated participants from the study if they expressed a willingness to leave, or patients for whom we could not collect demographic, clinical, biochemical, and hemodynamic parameters at hospital admission. The Institutional Ethics Committee, Research Committee, and Biosafety Committee of the General Hospital of Mexico approved the study under registration number DI/23/503/03/16, in accordance with the 1975 Declaration of Helsinki and its subsequent 2024 amendment. This ambispective, longitudinal, 6-month cohort study collected prospectively demographic, clinical, biochemical, and hemodynamic parameters at hospital admission from January 2017 to December 2024. After a 6-month follow-up, we retrospectively examined all data, with particular emphasis on those associated with 30-day mortality.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eStatistics\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eWe used the Chi-squared test and the Student T-test to compare data between survival and non-survival IHR-PE patients. We calculated the area under the receiver operating characteristic (ROC) curve (AUC) and 95% confidence interval (CI) for all variables, using the Youden Index to obtain optimal cut-off values, sensitivity, and specificity, adjusting for confounders by multiple regression analysis. We considered differences significant when \u003cem\u003ep\u003c/em\u003e \u0026lt; 0.05 and reported data as mean ± standard deviation, absolute numbers, or percentages. We used GraphPad Prism 6.01 (GraphPad Software, La Jolla, CA 92037, USA), MDCalc (New York, NY 10003, USA), and R i386 3.5.2 (Microsoft Corp., Boston, MA, USA).\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eAt the end of follow-up, the 30-day mortality rate was 7.69% among the 117 enrolled patients (Table 1). After examining all variables registered at hospital admission, there were no differences in age, sex, body mass index (BMI), pulmonary embolism severity index (PESI) score, BOVA score, and right-to-left ventricular ratio (RV/LV) between survival and non-survival patients (Table 1).\u003c/p\u003e\n\u003cp\u003eThere were also no differences in oxygen therapy, mechanical ventilation, and the prevalence of comorbidities. Most laboratory variables did not show significant differences between survival and non-survival patients, except for serum lactate levels, which were significantly higher at admission in patients who did not survive during follow-up than in those who survived (\u003cem\u003ep\u003c/em\u003e = 0.021).\u003c/p\u003e\n\u003cp\u003eConversely, hemodynamic parameters exhibited the most significant changes, with higher values of systolic right ventricular pressure (sRVP), diastolic right ventricular pressure (dRVP), systolic pulmonary arterial pressure (sPAP), diastolic pulmonary arterial pressure (dPAP), and mean pulmonary arterial pressure (mPAP) in non-survival patients than in survival participants. In contrast, cardiac output (CO) decreased significantly in non-survivors compared with survivors. Pulmonary vascular resistance (PVR) at admission showed the greatest difference, increasing nearly 2-fold in patients who died compared with those who survived (9.60 \u0026plusmn; 3.3 \u003cem\u003eversus\u003c/em\u003e 5.5 \u0026plusmn; 3.1, \u003cem\u003ep\u003c/em\u003e = 0.002, respectively) (Table 1).\u003c/p\u003e\n\u003cp\u003eCalculation of AUCs revealed that PVR \u0026ge; 6.55 Wood units (WU) outperformed other variables by predicting 30-day mortality with an AUC of 0.85 (95% CI, 0.71-0.97; \u003cem\u003ep\u003c/em\u003e = 0.007), a sensitivity of 100.0%, and a specificity of 70.0% (Fig. 1), independently of confounding variables such as sex and comorbidities.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eHerein, we provide compelling evidence that PVR is associated with an increased risk of early pulmonary deterioration leading to 30-day mortality in IHR-PE patients. Our findings highlight the importance of assessing hemodynamic parameters in IHR-PE patients upon hospital arrival, particularly PVR.\u003c/p\u003e\n\u003cp\u003ePVR is a hemodynamic measure that reflects how difficult blood flows through the pulmonary circulation and is related to the resistance the right ventricle encounters in pumping blood into the lungs [9]. PVR integrates crucial hemodynamic factors into a single variable, including pulmonary arterial pressure and cardiac output, which allows it to capture both the severity of vascular obstruction and the impact on cardiac performance [10]. An increase in PVR may result from mechanical obstruction caused by the thrombus and pulmonary blood vessel vasoconstriction, leading to increased RV afterload and failure, and death [11].\u003c/p\u003e\n\u003cp\u003eA previous study showed that experimental increases in pulmonary arterial pressure in rabbits lead to vascular remodeling, characterized by increased collagen and elastin production in blood vessels [12]. In addition to vascular remodeling, increased pulmonary arterial pressure induces geometrical changes in cardiomyocytes, local inflammation, and fibrosis, collectively affecting myocardial contractility and RV function [13]. Altogether, this information suggests that increased PVR at disease onset may predispose the organism to early vascular and cardiac remodeling, thus increasing the chances of developing RV overload and failure, and death. At hospital admission, PVR could not only help assess 30-day mortality risk but also identify patients who may benefit from novel anti-inflammatory and anti-fibrotic drugs before vascular and cardiac remodeling aggravates [14, 15].\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;In this pilot study, we observed that PVR has an AUC greater than 0.85 for predicting early mortality in IHR-PE patients at hospital admission. Our findings may help expand the body of predictive tools to facilitate 30-day mortality risk assessment in PE [16], encouraging additional studies in larger patient cohorts to validate markers such as PVR in clinical practice.\u003c/p\u003e\n\u003cp\u003eWe must acknowledge that this study has certain limitations, including the sample size and the need for a catheterization laboratory, which may not be available in community hospitals or resource-constrained healthcare facilities. Moreover, we focused only on IHR, which limits the extrapolation of our findings to low-risk patient groups.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eWe found that PVR ≥ 6.55 WU at hospital admission is associated with early mortality and may represent an independent hemodynamic predictor of death in IHR-PE. An increase in PVR reveals that pulmonary artery pressures may play a role in aggravating early vascular and cardiac remodeling, leading to rapid disease worsening and mortality. These data highlight the importance of assessing hemodynamic parameters at hospital admission in IHR-PE patients, which may help healthcare professionals initiate more aggressive medical treatments to improve short-term survival.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eCompeting interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eFunding: No funding was received for conducting this study.\u003c/p\u003e\n\u003cp\u003eFinancial interest: The authors declare they have no financial interests.\u003c/p\u003e\n\u003cp\u003eNon-financial interest: None.\u003c/p\u003e\n\u003cp\u003eEthics approval: The institutional Ethics Committee of the General Hospital of Mexico approved the study with the registration number DI/23/503/03/16 and supervised that all enrolled patients provided written informed consent.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflict of interest\u003c/strong\u003e: The authors declare they have no conflict of interests.\u003c/p\u003e"},{"header":" References","content":"\u003col\u003e\n \u003cli\u003ePesavento R, Filippi L, Palla A, Visona A, Bova C, Marzolo M, et al. Impact of residual pulmonary obstruction on the long-term outcome of patients with pulmonary embolism. Eur Respir J. 2017;49(5). doi: 10.1183/13993003.01980-2016.\u003c/li\u003e\n \u003cli\u003eWendelboe AM, Raskob GE. Global Burden of Thrombosis: Epidemiologic Aspects. Circ Res. 2016;118(9):1340-7. doi: 10.1161/CIRCRESAHA.115.306841.\u003c/li\u003e\n \u003cli\u003eAlabi FO, Ghaneie A, Koury I, Alkhateeb HA, Liu J, Guo M, et al. Management of intermediate high-risk pulmonary embolism: a single-center retrospective study. Front Cardiovasc Med. 2025;12:1483968. doi: 10.3389/fcvm.2025.1483968.\u003c/li\u003e\n \u003cli\u003eStam K, van Duin RWB, Uitterdijk A, Cai Z, Duncker DJ, Merkus D. Exercise facilitates early recognition of cardiac and vascular remodeling in chronic thromboembolic pulmonary hypertension in swine. Am J Physiol Heart Circ Physiol. 2018;314(3):H627-H42. doi: 10.1152/ajpheart.00380.2017.\u003c/li\u003e\n \u003cli\u003eYamada Y, Satoh T, Yaoita N, Yamada K, Chiba N, Komaru K, et al. Pathogenesis of Pulmonary Artery Remodeling: TGF-Beta Signaling and Inhibin Subunit Beta A in Group 1 and 2 Pulmonary Hypertension. Arterioscler Thromb Vasc Biol. 2026. doi: 10.1161/ATVBAHA.125.322506.\u003c/li\u003e\n \u003cli\u003eDursunoglu N, Dursunoglu D, Yildiz AI, Rota S. Evaluation of cardiac biomarkers and right ventricular dysfunction in patients with acute pulmonary embolism. Anatol J Cardiol. 2016;16(4):276-82. doi: 10.5152/akd.2014.5828.\u003c/li\u003e\n \u003cli\u003eHameed A, Condliffe R, Swift AJ, Alabed S, Kiely DG, Charalampopoulos A. Assessment of Right Ventricular Function-a State of the Art. Curr Heart Fail Rep. 2023;20(3):194-207. doi: 10.1007/s11897-023-00600-6.\u003c/li\u003e\n \u003cli\u003eKonstantinides SV, Meyer G. The 2019 ESC Guidelines on the Diagnosis and Management of Acute Pulmonary Embolism. Eur Heart J. 2019;40(42):3453-5. doi: 10.1093/eurheartj/ehz726.\u003c/li\u003e\n \u003cli\u003eChemla D, Lau EM, Papelier Y, Attal P, Herve P. Pulmonary vascular resistance and compliance relationship in pulmonary hypertension. Eur Respir J. 2015;46(4):1178-89. doi: 10.1183/13993003.00741-2015.\u003c/li\u003e\n \u003cli\u003eMaron BA, Kovacs G, Vaidya A, Bhatt DL, Nishimura RA, Mak S, et al. Cardiopulmonary Hemodynamics in Pulmonary Hypertension and Heart Failure: JACC Review Topic of the Week. J Am Coll Cardiol. 2020;76(22):2671-81. doi: 10.1016/j.jacc.2020.10.007.\u003c/li\u003e\n \u003cli\u003eSmulders YM. Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. Cardiovasc Res. 2000;48(1):23-33. doi: 10.1016/s0008-6363(00)00168-1.\u003c/li\u003e\n \u003cli\u003eChow MJ, Zou Y, He H, McGowan FX, Zurakowski D, Zhang Y. Obstruction-induced pulmonary vascular remodeling. J Biomech Eng. 2011;133(11):111009. doi: 10.1115/1.4005301.\u003c/li\u003e\n \u003cli\u003eRosenkranz S, Howard LS, Gomberg-Maitland M, Hoeper MM. Systemic Consequences of Pulmonary Hypertension and Right-Sided Heart Failure. Circulation. 2020;141(8):678-93. doi: 10.1161/CIRCULATIONAHA.116.022362.\u003c/li\u003e\n \u003cli\u003eWang Y, Ma TT, Gao NN, Zhou XL, Jiang H, Guo R, et al. Effect of Tongxinluo on pulmonary hypertension and pulmonary vascular remodeling in rats exposed to a low pressure hypoxic environment. J Ethnopharmacol. 2016;194:668-73. doi: 10.1016/j.jep.2016.10.004.\u003c/li\u003e\n \u003cli\u003eNguyen QT, Nsaibia MJ, Sirois MG, Calderone A, Tardif JC, Fen Shi Y, et al. PBI-4050 reduces pulmonary hypertension, lung fibrosis, and right ventricular dysfunction in heart failure. Cardiovasc Res. 2020;116(1):171-82. doi: 10.1093/cvr/cvz034.\u003c/li\u003e\n \u003cli\u003eLi S, Huang S, Feng Y, Mao Y. Development of a nomogram model to predict 30-day mortality in ICU cancer patients with acute pulmonary embolism. Sci Rep. 2025;15(1):9232. doi: 10.1038/s41598-025-93907-4.\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Table","content":"\u003cp\u003e\u003cstrong\u003eTable 1. Characteristics of the study participants\u003c/strong\u003e. We prospectively enrolled patients with IHR-PE and registered demographic, clinical, laboratory, and hemodynamic variables at hospital admission. After completing the 6-month follow-up, we identified patients who survived or did not for a posterior retrospective comparison between groups, using the Student T-test or the Chi-squared test. We reported data as mean \u0026plusmn; standard deviation or as percentages, considering significant differences when \u003cem\u003ep\u003c/em\u003e \u0026lt; 0.05. Abbreviations: PESI, Pulmonary Embolism Severity Index; BMI, body mass index; RV/LV, right-to-left ventricular ratio; T2D, type 2 diabetes; SAH, systemic arterial hypertension; HFNC, high-flow nasal cannula; N-IMV, non-invasive mechanical ventilation; IMV, invasive mechanical ventilation; sRVP, systolic right ventricular pressure; dRVP, diastolic right ventricular pressure; sPAP, systolic pulmonary arterial pressure; dPAP, diastolic pulmonary arterial pressure; mPAP, mean pulmonary arterial pressure; CO, cardiac output; PVR, pulmonary vascular resistance.\u003c/p\u003e\n\u003cdiv align=\"Left\"\u003e\n \u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eVariable\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eTotal patients\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003en\u003c/em\u003e\u003c/strong\u003e\u003cstrong\u003e\u0026nbsp;= 117\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eSurvivors\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003en\u003c/em\u003e\u003c/strong\u003e\u003cstrong\u003e\u0026nbsp;= 108\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eNon-survivors\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003en\u003c/em\u003e\u003c/strong\u003e\u003cstrong\u003e\u0026nbsp;= 9\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003ep\u003c/em\u003e\u003c/strong\u003e\u003cstrong\u003e-value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eDemographic and clinical data\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eAge (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e56.8 \u0026plusmn; 16.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e56.7 \u0026plusmn; 16.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e57.8 \u0026plusmn; 15.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.440\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSex (female, %)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e57.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e55.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e77.7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.294\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003ePESI score\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e107.5 \u0026plusmn; 29.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e107.7 \u0026plusmn; 29.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e106.2 \u0026plusmn; 35.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.446\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eBOVA score\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.2 \u0026plusmn; 1.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.3 \u0026plusmn; 1.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.0 \u0026plusmn; 1.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.309\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eBMI (kg/m\u003csup\u003e2\u003c/sup\u003e)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e32.2 \u0026plusmn; 8.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e32.2 \u0026plusmn; 6.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e32.5 \u0026plusmn; 16.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.465\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eRV/LV\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.1 \u0026plusmn; 0.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.1 \u0026plusmn; 0.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.1 \u0026plusmn; 0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.811\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eComorbidities\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eT2D (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e11.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e9.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e44.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\"\u003e\n \u003cp\u003e0.755\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eSAH (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e36.7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e35.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e55.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eStroke history (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e22.2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eOxygen therapy\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eNasal cannula (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e72.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e72.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e77.7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\"\u003e\n \u003cp\u003e0.601\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eHFNC (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e6.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e6.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e11.1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eMechanical ventilation\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eN-IMV (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e11.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\"\u003e\n \u003cp\u003e0.583\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eIMV (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e6.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e22.2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"5\"\u003e\n \u003cp\u003e\u003cstrong\u003eLaboratory and hemodynamic parameters\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eLactate (mmol/l)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.93 \u0026plusmn; 1.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.86 \u0026plusmn; 1.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.46 \u0026plusmn; 0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.021\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003esRVP (mmHg)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e51.9 \u0026plusmn; 19.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e49.6 \u0026plusmn; 18.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e67.3 \u0026plusmn; 23.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.018\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003edRVP (mmHg)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e6.0 \u0026plusmn; 4.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.5 \u0026plusmn; 4.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e9.0 \u0026plusmn; 5.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.046\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003esPAP (mmHg)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e52.2 \u0026plusmn; 18.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e50.0 \u0026plusmn; 17.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e66.3 \u0026plusmn; 21.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.024\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003edPAP (mmHg)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e21.2 \u0026plusmn; 9.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e20.3 \u0026plusmn; 9.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e27.1 \u0026plusmn; 10.11\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.048\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003emPAP (mmHg)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e33.8 \u0026plusmn; 12.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e32.4 \u0026plusmn; 11.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e43.1 \u0026plusmn; 16.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.026\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eCO\u0026nbsp;(l/min)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.96 \u0026plusmn; 1.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.1 \u0026plusmn; 1.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.0 \u0026plusmn; 1.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.040\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003ePVR (WU)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e6.1 \u0026plusmn; 3.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.5 \u0026plusmn; 3.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e9.6 \u0026plusmn; 3.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.002\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\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":"Pulmonary vascular resistance, pulmonary embolism, 30-day mortality, right-heart catheterization","lastPublishedDoi":"10.21203/rs.3.rs-8950718/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8950718/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eAcute pulmonary embolism (PE) is a critical disease with a high 30-day mortality rate in intermediate-to-high-risk (IHR) patients. Herein, we prospectively enrolled 117 patients with IHR-PE and recorded demographic, clinical, and biochemical parameters from electronic records, as well as hemodynamic variables acquired by right-heart catheterization at hospital admission. After a 6-month follow-up, we retrospectively analyzed all variables and found that hemodynamic parameters increased significantly in patients who subsequently died within the first 30 days after discharge, especially pulmonary vascular resistance (PVR) (9.6 ± 3.3 \u003cem\u003eversus\u003c/em\u003e 5.5 ± 3.1, \u003cem\u003ep\u003c/em\u003e= 0.002, in non-survival and survival patients, respectively). In fact, PVR ≥ 6.55 Wood units (WU) at hospital admission was an accurate predictor of 30-day mortality, with an area under the receiver operating characteristic curve of 0.85 (95% Confidence Interval, 0.71–0.97; \u003cem\u003ep\u003c/em\u003e = 0.007), a sensitivity of 100%, and a specificity of 70%. Our findings emphasize the urgency of assessing hemodynamic parameters in all IHR-PE patients, prompting discussion of the benefit-risk balance of right-heart catheterization in IHR-PE.\u003c/p\u003e","manuscriptTitle":"Pulmonary vascular resistance at hospital admission is associated with early mortality in patients with intermediate-to-high-risk acute pulmonary embolism","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-03-10 13:18:17","doi":"10.21203/rs.3.rs-8950718/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":"0255b5e9-1123-464c-954c-068cd62ec402","owner":[],"postedDate":"March 10th, 2026","published":true,"recentEditorialEvents":[{"type":"decision","content":"Revision requested","date":"2026-04-30T14:53:56+00:00","index":"","fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-04-30T15:08:49+00:00","versionOfRecord":[],"versionCreatedAt":"2026-03-10 13:18:17","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8950718","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8950718","identity":"rs-8950718","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}