Pathophysiology of acute heart failure syndrome: a knowledge gap

Although much remains unknown regarding the pathophysiology of acute heart failure (AHF), precipitating events are thought to involve a complex set of interactions between the heart, kidneys, and peripheral vasculature. In addition to these interactions, which are considered the primary abnormalities in patients with AHF, several other organ systems may also be affected and contribute to disease progression. Currently available scientific literature suggests that the natural history and pathophysiology of AHF consists of two phases: (1) an "initiation phase" involving a series of triggering events, and (2) an "amplification phase," in which multiple mechanisms contribute to worsening HF and exacerbate end-organ damage. Biomarkers of cardiac, renal, pulmonary, and other organ function have been identified during episodes of AHF, including brain natriuretic peptide, troponin I, and troponin T; biomarkers associated with AHF have proven to be useful tools for studying the pathophysiology of the syndrome, predicting clinical outcomes, and identifying patient management strategies. Despite considerable advances in recent years, AHF continues to be a leading cause of hospitalization and death in patients with chronic HF. Moreover, AHF remains a major healthcare issue exacting a considerable cost burden. Addressing this ongoing unmet need requires prioritizing efforts to better understand the natural history and pathophysiology of AHF; only then can targeted therapies be developed to prevent rehospitalization in patients with AHF, or at least alter the trajectory of disease progression toward improved clinical outcomes.