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.