Abstract
Hospitalization for acute heart failure syndromes (AHFS) heralds a grim prognosis: More than one third of patients will be dead or rehospitalized within 90 days postdischarge.1 Although total hospitalizations for AHFS have decreased over the past decade, rehospitalization rates have not.2,3 With 1 million hospitalizations annually at an estimated cost exceeding $20 billion, AHFS is a major public health problem.4 Article see p 17 One of the possible contributors to these poor outcomes is our approach to patients with AHFS in the emergency department (ED). Approximately 80% of hospitalized patients initially present to the ED, highlighting the pivotal role of the ED in initial AHFS management.5 Yet there are no class I, level A guideline recommendations for the initial pharmacological treatment of AHFS.6 ED treatment today is largely the same as it was 40 years ago and is similar across all patients with AHFS despite the heterogeneity of patients in terms of precipitant, presentation (eg, pulmonary edema, hypertension), phenotype (eg, reduced or preserved ejection fraction), or etiology (ischemic versus nonischemic).6a,7–9 This management approach and lack of progress is not the fault of frontline caregivers; rather it reflects our limited understanding of the pathophysiology of AHFS and the need for further research, especially in the ED setting. In this issue of Circulation: Heart Failure , Drexler et al10 address the hypothesis that ED patients with AHFS with an underlying ischemic etiology have a distinct pathophysiology compared to patients with AHFS with a nonischemic etiology. Specifically, they tested whether higher brain natriuretic peptide and troponin levels are present in patients with AHFS with an ischemic etiology versus nonischemic etiology due to greater hemodynamic stress and myocyte damage. The authors contextualize their study by suggesting that knowledge of the etiology …
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