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Background: The right ventricular free wall longitudinal strain to pulmonary arterial systolic pressure (RVFWLS/PASP) ratio is an emerging echocardiographic index for evaluating right ventricular–pulmonary artery (RV-PA) coupling. This study aimed to evaluate its prognostic significance and incremental value in risk stratification for patients with pulmonary arterial hypertension (PAH). Methods: We conducted a retrospective–prospective cohort study of 149 adult PAH patients (87 idiopathic PAH and 62 connective tissue disease-associated PAH). RVFWLS was measured via speckle tracking echocardiography, and PASP was estimated using Doppler. The primary endpoint was event-free survival, defined as the first occurrence of all-cause mortality, lung transplantation, or rehospitalization for right heart failure. Kaplan–Meier and multivariate Cox regression analyses were performed to identify independent predictors. Results: During a median follow-up of 32 months, 78 primary events occurred. Patients in the lower RVFWLS/PASP group (<0.246%/mmHg) exhibited significantly worse exercise capacity, higher NT-proBNP levels, and poorer hemodynamics compared with the higher group (≥0.246%/mmHg) (all p < 0.001). The event-free survival rate for the composite endpoint was significantly lower in the group with reduced RVFWLS/PASP compared with that observed in the higher RVFWLS/PASP group (log-rank p < 0.05). Multivariate Cox regression analysis demonstrated RVFWLS/PASP ≥ 0.246%/mmHg was independently predictive of reduced risk for the primary endpoint (HR = 0.46, 95%CI 0.23–0.93, p < 0.05). Moreover, RVFWLS/PASP facilitated additional risk stratification among patients classified as low risk based on established models (FPHN, COMPERA 2.0, and REVEAL Lite 2). Conclusions: RVFWLS/PASP is a robust, independent determinant of long-term prognosis in patients with PAH. As a noninvasive measure of RV-PA coupling, it provides significant incremental value for clinical risk assessment and treatment monitoring.
Published in: Journal of Cardiovascular Development and Disease
Volume 13, Issue 4, pp. 151-151
DOI: 10.3390/jcdd13040151