diastolic heart failure

Diastolic heart failure results from impaired ventricular relaxation (lusitropy) and increased myocardial stiffness, leading to elevated left ventricular end-diastolic pressure (LVEDP) despite normal or near-normal ejection fraction. This causes backward transmission of pressure into the pulmonary circulation, resulting in pulmonary congestion and dyspnea. Common etiologies include long-standing hypertension (causing concentric left ventricular hypertrophy), hypertrophic cardiomyopathy, restrictive cardiomyopathy (e.g., amyloidosis, sarcoidosis, hemochromatosis), constrictive pericarditis, and normal aging with myocardial fibrosis. Diabetes mellitus, obesity, and coronary artery disease are also strongly associated with HFpEF.

Pathophysiologically, the ventricle has a normal stroke volume and EF, but requires higher filling pressures to achieve adequate preload due to decreased compliance. Echocardiography typically shows normal EF with evidence of diastolic dysfunction: abnormal E/A ratio on mitral inflow Doppler, reduced e' velocity on tissue Doppler, and elevated E/e' ratio (correlating with LV filling pressure). Left atrial enlargement is often present due to chronically elevated LA pressure.

Clinically, patients present similarly to systolic heart failure with exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema, but with a normal EF on imaging. BNP/NT-proBNP levels are elevated, though sometimes less dramatically than in HFrEF. Physical exam may reveal an S4 gallop (reflecting atrial contraction against a stiff ventricle), in contrast to the S3 gallop typically heard in systolic (HFrEF) heart failure.

Management is more limited in evidence base compared to HFrEF; it focuses on treating underlying causes (blood pressure control, rate control in atrial fibrillation), diuretics for volume overload, and management of comorbidities like obesity and diabetes. SGLT2 inhibitors have shown benefit in reducing hospitalizations in HFpEF. Unlike HFrEF, medications such as ACE inhibitors, ARBs, and beta-blockers have not shown consistent mortality benefit in pure diastolic heart failure, although they are often used to control hypertension, a major underlying cause.

This distinction between HFpEF and HFrEF is high-yield for boards, particularly regarding echocardiographic findings, S3 vs S4 gallops, and the differing therapeutic approaches.