Beyond the right ventricle: left heart involvement in pulmonary arterial hypertension.

Authors

María José Cabada-García, Jahir Rodríguez-Rivera, Jathniel Panneflek, Salma Andrade-Leal, Ana Lucía Martínez-Rodríguez, Enrique Paredes-Gutiérrez, Humberto De Leon-Gutierrez, Andres Gerardo Peña-Bladé, Raul Monjaras-Alvarado, Jesús Antonio Morón-Mosso, Alejandra Torres, Daniel Aguirre, María José Serrano, Carlos Jerjes Sanchez-Ramirez, Pedro Gutiérrez-Fajardo, Alicia Ramirez-Rivera, Carlos Jerjes-Sanchez

Published in

Heart failure reviews. Volume 31. Issue 1. Jun 19, 2026. Epub Jun 19, 2026.

Abstract

Pulmonary arterial hypertension (PAH) is characterized by progressive remodeling of the pulmonary vasculature, leading to increased pulmonary vascular resistance and chronic right ventricular (RV) pressure overload. As RV dysfunction develops, ventricular interdependence alters the structural and functional relationship between the right and left ventricles. Although normal left-sided filling pressures define PAH, growing evidence indicates that left ventricular (LV) mechanics may be substantially affected. Leftward septal displacement, pericardial constraint, and reduced pulmonary venous return contribute to chronic underfilling of the left atrium and LV, impairing ventricular geometry and contractile dynamics despite preserved intrinsic myocardial function. However, secondary myocardial remodeling in advanced disease remains debated. These alterations may lead to subclinical or overt LV dysfunction and represent an underrecognized component of PAH pathobiology. Imaging markers such as LV global longitudinal strain, LV outflow tract velocity-time integral, and left atrial strain have emerged as potential indicators of left-sided involvement and may provide additional prognostic information. In this narrative review, we summarize current evidence on the pathobiological mechanisms linking RV dysfunction to left-sided cardiac alterations and discuss the role of ventricular interdependence in the coupling of the pulmonary circulation. Understanding this interaction may help redefine PAH as a progressive biventricular syndrome and may improve risk stratification and clinical assessment.

PMID:
42319624
Bibliographic data and abstract were imported from PubMed on 19 Jun 2026.

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