Abstract
Abstract Low blood pressure in heart failure is often treated as a simple barrier to therapy, but this approach is too crude. The same clinic blood pressure may reflect successful unloading and tolerated neurohormonal blockade in one patient, but low output, venous congestion, autonomic failure, or infiltrative disease in another. Recent heart failure data have clarified that low systolic blood pressure is consistently associated with risk across chronic and acute heart failure, particularly when accompanied by poor perfusion or advanced disease. At the same time, low blood pressure does not automatically justify withdrawal of guideline-directed therapy, as patients receiving higher or increasing doses of heart failure medication may still derive benefit. In this Perspective, we argue that hypotension in heart failure should be approached as a precision phenotype rather than a threshold problem. A practical framework based on symptoms, orthostatic response, congestion, perfusion, ventricular phenotype, rhythm, and disease substrate can distinguish tolerated low blood pressure from depletion, frailty-related orthostasis, right-sided circulatory failure, infiltrative disease, and advanced low-output heart failure. The biological meaning may also differ across heart failure syndromes: in HFrEF, progressive hypotension may indicate declining circulatory reserve, whereas in a patient with preserved ejection fraction it should prompt a search for structural, valvular, pulmonary vascular, right-sided, or infiltrative disease. This conceptual framework may help preserve life-saving therapy when appropriate, avoid preventable harm, and identify patients who require escalation; prospective validation is still needed.