INTRODUCTION
Echocardiography remains a fundamental clinical imaging tool for the assessment of the right heart ventricle (RV). Conventional echocardiographic parameters used in daily clinical practice that evaluate RV systolic function include tricuspid annular plane systolic excursion (TAPSE), the maximum velocity of the tricuspid lateral annulus during systole or the S wave (S’) and RV fractional area change (RVFAC) (1). All these echocardiographic parameters have well known limitations (2). Assessment of right ventricular free wall longitudinal strain (RV-FWS) by two-dimensional echocardiographic speckle tracking analysis has overcome some of these limitations and has emerged as a feasible and reproducible parameter to evaluate RV systolic function (3,4). RV-FWS has demonstrated good prognostic value in different clinical scenarios such as heart failure, and congenital heart disease (3). Nonetheless, RV-FWS and RA global longitudinal strain (RA-GS) have not been fully explored in a broad variety of pathologies (5,6,7,8. In patients with pulmonary hypertension, RV-FWS has been shown to be a potential predictor of major cardiovascular events. Moreover, its validation has been assessed with gold-standard methods such as cardiac magnetic resonance imaging (CMR) (9). However, to date, the diagnostic and predictive value of RV-FWS and RA-GS in pulmonary hypertension has not been fully explored. The use of right heart strain parameters in a clinical setting could broaden the stratification and overall, bring relevant information for care providers in patients with pulmonary hypertension. Furthermore, the evaluation of the long-standing effect of increased systolic pulmonary arterial pressure (sPAP) and myocardial fibrosis of the right heart chambers could support the hypothesis that myocardial deformation should be promptly tested in early stages of patients with pulmonary hypertension. Therefore, this study aims to assess the relationship and diagnostic performance of RV and RA strain to detect and evaluate sPAP parameters and stratify pulmonary hypertension categories. Furthermore, we extracted post-mortem sample biopsies to measure the degree of myocardial fibrosis in 12 patients classified with severe pulmonary hypertension to establish the association of increased sPAP with fibrosis.