Background: RV strain associates with mortality in pulmonary hypertension (PH) but time-resolved strain is not typically assessed. The aim was to evaluate phasic changes in RV strain using cardiac magnetic resonance (CMR) images. We hypothesized that phasic changes in ejection and filling RV strain significantly associate with outcomes in PH. Methods: Participants were identified from the Ohio State University CMR PH registry (n=96). RV endocardial areas were segmented from 4-chamber CMR Cine images. Time-resolved strains were calculated for RV global, free wall and septal strain. Ventricular dynamics were assessed during the ejection, early filling and late filling cardiac phases to quantify phasic changes in function. RV contractility, afterload and diastolic stiffness were quantified using the single-beat method. Outcomes were evaluated at one year. Results: In this retrospective, single-center study, 96 participants with and without pulmonary hypertension were included. Cohort was predominately female (n=53, 55%) with elevated mean pulmonary arterial pressure (38[26-48] mmHg) and reduced RV function (RVEF: 42[31-54] %, TAPSE of 19[15-23] cm). Filling strain patterns described changes in ventricular dynamics but did not associate with RV dilation or other measures characteristic of RV dysfunction. In comparison, decreased free wall strain and increased diastolic stiffness both associated with RV dysfunction but there were no significant differences in strain patterns. Participants with strain pattern 3, decreased free wall strain or increased Eed had increased one-year mortality. When investigated together, participants with decreased free wall strain, RVEF and increased Eed had greatly reduced one-year survival. Conclusions: Assessment of phasic changes in ventricular function does provide additional pathophysiological information but assessment of strain patterns alone are not sufficient for identifying reduced function. Deep phenotyping using a combination of RV strain and diastolic stiffness is highly selective of participants with increased one-year mortality.

The authors have declared no competing interest.

Research reported in this manuscript was supported by Department of Internal Medicine and the Division of Cardiovascular Medicine at The Ohio State University.

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The study was approved by The Ohio State University?s Institutional Review Board and informed consent was waived (IRB# 2021H0394).

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