Why the study?
High-output heart failure remains under-examined in the literature with limited clinician recognition, and failure to differentiate it from other heart failure forms can lead to deleterious vasodilator use.
This review highlights the distinct pathophysiology of high-output heart failure and proposes a novel diagnostic algorithm to prevent potentially deleterious management with standard guideline-directed vasodilator therapies.
Warrants caution with vasodilators in possible high-output HF; leaves open prospective validation of the algorithm.
Heart failure (HF) poses a significant medical challenge, affecting millions of adults in the United States. High-output heart failure (HOHF) is a distinct subtype characterized by elevated cardiac output exceeding 8 L/min or a cardiac index >4 L/min/m². Patients with HOHF often present similarly to those with heart failure with reduced ejection fraction and heart failure with preserved ejection fraction. However, the underlying pathophysiology differs; triggered by a progressive decline in systemic vascular resistance, the ensuing elevation of cardiac output eventually leads to left ventricular remodeling and HF. Failure to differentiate HOHF from other variant forms of HF has implications for management, particularly relating to the use of vasodilator medications with potentially deleterious consequences, ensuing from the unrestrained adoption of societal guideline-directed medical therapy recommendations. Despite its clinical importance, HOHF remains under-examined in literature, with limited recognition and understanding among clinicians. This review aims to provide a comprehensive analysis of knowledge surrounding HOHF, exploring its definition, etiopathology, and underlying pathophysiological mechanisms. Recognizing the challenges in diagnosing HOHF, we propose a novel diagnostic algorithm tailored to address the subtleties of this often-misdiagnosed variant of HF.
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Shafi et al. (2025) studied this question.
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