Key result
Dynamic diuretic adjustment optimizes heart failure care through rapid escalation and careful post-euvolemia deprescribing.
Why the study?
Long-term diuretic exposure without objective congestion may cause significant adverse effects, raising questions regarding optimal intensity, duration, and monitoring of diuretic therapy in cardiovascular disease.
Diuretic therapy in heart failure should be dynamic and phenotype-dependent, with prompt escalation for congestion and careful deprescribing once euvolemia is achieved to avoid adverse effects.
Supports cautious dynamic diuretic titration in HF to minimize risks; hypothesis-generating for deprescribing strategies pending prospective trials.
Diuretics remain indispensable for the treatment of congestion in cardiovascular disease, particularly in acute and chronic heart failure. Their principal clinical value is rapid symptom relief, reduction in filling pressures and facilitation of decongestion; however, a mortality benefit has not been consistently demonstrated. This distinction is clinically important because long-term diuretic exposure in patients without objective congestion may promote hypotension, renal dysfunction, electrolyte instability, neurohormonal activation, falls, cognitive impairment and avoidable polypharmacy. The challenge is therefore not whether diuretics should be used, but how intensively, for how long and under which monitoring strategy. In this narrative review, we summarize the pharmacology of major diuretic classes, the mechanisms of diuretic resistance, and the clinical consequences of potassium, sodium and magnesium disorders. We also discuss drug interactions, frailty, chronic kidney disease, pregnancy, heart failure with preserved ejection fraction and the emerging role of sodium–glucose cotransporter 2 inhibitors and adjunctive proximal-tubule strategies. A practical approach is proposed: use loop diuretics promptly when congestion is present, reassess response with symptoms, weight, urine output, renal function, electrolytes and congestion markers, and reduce or discontinue therapy once euvolemia is achieved and maintained. Deprescribing should be individualized, gradual and reversible, with explicit thresholds for restarting treatment. Optimized diuretic care requires the same discipline applied to disease-modifying heart failure therapy: phenotype recognition, dose minimization, close follow-up and avoidance of treatment inertia.
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Paraskevaidis et al. (2026) conducted a review in Heart failure. Diuretics was evaluated. Diuretic therapy in heart failure requires dynamic adjustment, with prompt escalation for congestion and gradual deprescribing once euvolemia is achieved to avoid adverse effects.
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