Right Ventricular Failure

This comprehensive NEJM review describes the anatomy, pathophysiology, diagnosis, and treatment of right ventricular (RV) failure. Historically underappreciated, the RV plays a pivotal prognostic role in conditions such as pulmonary arterial hypertension (PAH), left heart failure, and ARVC. RV failure arises from abnormalities in preload, afterload, contractility, or lusitropy often overlapping. Acute RV failure may stem from infarction or pulmonary embolism, while chronic overload induces hypertrophy, fibrosis, and ventriculoarterial uncoupling. Metabolic shifts include reduced β-oxidation and increased glycolysis, potentially maladaptive. Obesity and insulin resistance aggravate RV dysfunction via inflammation, lipotoxicity, and hemodynamic effects. Diagnosis requires echocardiography, cardiac MRI, and catheterization to assess pressures, volumes, and RV-pulmonary arterial coupling. Management targets optimization of volume status, reduction of afterload (with pulmonary vasodilators in PAH), and augmentation of contractility using inotropes or mechanical support. New therapies aim to address fibrosis, contractility, and metabolic remodeling.

This comprehensive NEJM review describes the anatomy, pathophysiology, diagnosis, and treatment of right ventricular (RV) failure. Historically underappreciated, the RV plays a pivotal prognostic role in conditions such as pulmonary arterial hypertension (PAH), left heart failure, and ARVC. RV failure arises from abnormalities in preload, afterload, contractility, or lusitropy often overlapping. Acute RV failure may stem from infarction or pulmonary embolism, while chronic overload induces hypertrophy, fibrosis, and ventriculoarterial uncoupling. Metabolic shifts include reduced β-oxidation and increased glycolysis, potentially maladaptive. Obesity and insulin resistance aggravate RV dysfunction via inflammation, lipotoxicity, and hemodynamic effects. Diagnosis requires echocardiography, cardiac MRI, and catheterization to assess pressures, volumes, and RV-pulmonary arterial coupling. Management targets optimization of volume status, reduction of afterload (with pulmonary vasodilators in PAH), and augmentation of contractility using inotropes or mechanical support. New therapies aim to address fibrosis, contractility, and metabolic remodeling.