Heart Failure: HFrEF vs HFpEF

Heart failure (HF) is a clinical syndrome in which the heart cannot deliver enough cardiac output to meet metabolic demand — or can do so only at the cost of elevated filling pressures. Boards divide HF by left ventricular ejection fraction (LVEF), measured on echocardiography:

• HFrEF (reduced, EF ≤40%) — a systolic problem: the ventricle cannot contract. The chamber dilates (eccentric hypertrophy) and stroke volume falls.
• HFpEF (preserved, EF ≥50%) — a diastolic problem: a stiff, thick ventricle cannot relax and fill. EF looks normal, but filling pressures are high.
• HFmrEF (mildly reduced, EF 41–49%) bridges the two.

Both share the same maladaptive neurohormonal cascade — RAAS and sympathetic activation — which initially compensates but ultimately drives remodeling, congestion, and progression. This is why the mortality-reducing drugs all block that cascade.

Foundational therapy for HFrEF is the "four pillars" of guideline-directed medical therapy (GDMT), each independently proven to reduce mortality:

1. ARNI (sacubitril–valsartan) — preferred over an ACEi/ARB
2. Beta-blocker — only carvedilol, metoprolol succinate, or bisoprolol have mortality data; start when euvolemic, never during acute decompensation
3. MRA — spironolactone or eplerenone
4. SGLT2 inhibitor — dapagliflozin or empagliflozin

Add hydralazine + isosorbide dinitrate in self-identified Black patients or those intolerant of ACEi/ARB. Loop diuretics (furosemide) treat congestion only. Devices: ICD for primary prevention of sudden death if EF ≤35% despite ≥3 months of GDMT; CRT if EF ≤35% + LBBB + QRS ≥150 ms.

For HFpEF: control blood pressure, rate-control AFib, relieve volume with diuretics, treat comorbidities — and add an SGLT2 inhibitor, the first class with clear benefit here.