Pulmonary arterial load and ventricular–arterial coupling in pulmonary hypertension

Pulmonary hypertension (PH), defined by increased pulmonary artery (PA) pressure, is a disorder of the pulmonary vasculature. Because of the increased afterload, the right ventricle (RV) function deteriorates, eventually determining poor clinical outcomes. The heart-independent arterial load is increased in PH (for example, pulmonary vascular resistance and arterial elastance increase approximately fourfold), altering the load-independent heart function (for example, RV end-systolic elastance—quantifying RV contractility augments two- to fourfold) to maintain the coupling of the RV to the pulmonary arterial system (RV–PA coupling). If the RV is not successful in coupling to the PA, the RV needs to dilate to maintain cardiac output (CO). However, dilatation is detrimental because larger RV volume further increases RV wall stress/tension and thereby myocardial oxygen consumption. Understanding the pathophysiology of the RV–PA coupling will improve the interpretation of clinical data, mostly given as the load-dependent heart function (CO and RV ejection fraction).