Decongestion in chronic heart failure

Abstract

Congestion drives symptoms and adverse outcomes in heart failure (HF), and loop diuretics remain the cornerstone of decongestion. Yet randomized trials of diuretic strategies and other acute decongestive approaches have not shown mortality benefit, while mechanistic studies demonstrate rapid neurohormonal activation after acute loop diuretic administration. In chronic HF, observational data consistently associate higher loop diuretic requirements—particularly above ∼40 mg/day furosemide equivalent or with dose escalation—with worse prognosis across HF phenotypes, though confounding by disease severity is likely. Decongestion needs vary across the HF trajectory: early guideline-directed therapy provides intrinsic decongestive effects, whereas advanced HF is marked by diuretic resistance and renal vulnerability. Preload-dependent states (notably cardiac amyloidosis and selected HFpEF phenotypes) require especially careful titration to avoid hypovolemia and low output, and robust protocol-level trial evidence is lacking. Contemporary randomized data do not demonstrate superiority of torsemide over furosemide. Small trials and systematic reviews suggest that in carefully selected, stable, non-congested patients, diuretic withdrawal or reduction can be feasible, with ∼25–35% requiring re-initiation within 1–3 months and consistent lowering of renin activity; however, clinical outcome benefit remains unproven. Overall, evidence supports maintaining euvolemia with the lowest effective diuretic dose and considering monitored deprescribing in appropriate low-risk patients.