Left ventricular dysfunction in pulmonary arterial hypertension is primarily driven by chronic underfilling and ventricular interdependence rather than intrinsic myocardial disease.
Left ventricular dysfunction in PAH, driven by ventricular interdependence and chronic underfilling, is an underrecognized component that may improve risk stratification.
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. Central figure. Conceptual Models of Left Ventricular Dysfunction in PAH Several mechanisms have been proposed to explain LV dysfunction in PAH. The most compelling and consistently supported is chronic underfilling: progressive RV pressure overload displaces the interventricular septum. It increases pericardial constraint, limiting LV diastolic filling and reducing pulmonary venous return, impairing LV mechanics despite preserved intrinsic myocardial function 1. A second hypothesis suggests that sustained low mechanical workload induces structural atrophy, as evidenced by reduced LV mass and chamber dimensions 2,3. A third, less established hypothesis proposes secondary intrinsic myocardial remodeling in advanced disease, whereby sarcomeric, metabolic, and molecular alterations may contribute to impaired contractility beyond loading abnormalities 4.While evidence exists for each, structural and molecular changes likely represent downstream consequences of prolonged ventricular interdependence rather than primary myocardial disease. Abbreviations: CMR: Cardiac magnetic resonance; Ea: Arterial elastance; Ees: End-systolic elastance; LARS: Left atrial reservoir strain; LV: Left ventricle; LV-GLS: Left ventricular global longitudinal strain; LVEDVI: Left ventricular end-diastolic volume index; LVOT-VTI: Left ventricular outflow tract velocity time integral; PA: Pulmonary artery; PAH: Pulmonary arterial hypertension; PASP: Pulmonary artery systolic pressure; RA: Right atrium; RAP: Right atrial pressure; RV: Right ventricle; RVEDVI: Right ventricular end-diastolic volume index; RVEF: Right ventricular ejection fraction; RVOT-VTI: Right ventricular outflow tract velocity time integral; TAPSE: Tricuspid annular plane systolic excursion.
Cabada-García et al. (Fri,) conducted a review in Pulmonary arterial hypertension. Ventricular interdependence and left ventricular underfilling was evaluated. Left ventricular dysfunction in pulmonary arterial hypertension is primarily driven by chronic underfilling and ventricular interdependence rather than intrinsic myocardial disease.