New Hemodynamic Insights in Pulmonary Vascular Disease and Heart Failure with Preserved Ejection Fraction

Purpose of review Patients often present with a mixed phenotype of pulmonary vascular disease and heart failure with preserved ejection fraction (HFpEF). Identifying the exact hemodynamic culprits in such cases has important therapeutic implications. This review discusses the hemodynamic characterization and treatment options in patients with pulmonary vascular disease, HFpEF, and their combination. Recent findings The threshold for pulmonary hypertension (PH) has been lowered toward a mean pulmonary arterial pressure (mPAP) > 20 mmHg at rest. Exercise-induced PH is defined as mPAP > 30 mmHg during exercise with a mPAP/cardiac output slope > 3 mmHg/L/min. A blunted pulmonary vasodilatory reserve is observed early on in HFpEF, before an elevated pulmonary vascular resistance or right ventricular remodeling is evident. Long-term exposure to elevated left heart filling pressures in HFpEF induces hemangiomatosis-like endothelial cell proliferation and smooth muscular hypertrophy, predominantly at the venous side of the pulmonary circulation. Enhanced ventricular interdependence because of pericardial constraint may play an important role in the pathophysiology of HFpEF, especially when pulmonary vascular disease is present. Summary Established and emerging treatment strategies for pulmonary vascular disease and HFpEF should target drivers of the underlying disease process and subsequent organ damage. Careful hemodynamic characterization is vital to guide treatment decisions.