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(Circulation. 2004;109:440-442.)
© 2004 American Heart Association, Inc.

Focused Perspective

Acute Heart Failure Complicating Acute Coronary Syndromes

A Deadly Intersection

Eric J. Velazquez, MD; Marc A. Pfeffer, MD, PhD

From the Division of Cardiology, Department of Medicine, Duke University Medical Center and Duke Clinical Research Institute, Durham, NC (E.J.V.), and Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (M.A.P.).

Correspondence to Marc A. Pfeffer, MD, PhD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail mpfeffer@rics.bwh.harvard.edu

Key Words: Focused Perspectives • heart failure • coronary disease • myocardial infarction

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Patients manifesting symptomatic pulmonary congestion during an acute myocardial infarction have long been recognized to be at heightened risk of both short- and long-term mortality.^1–3 Acute heart failure (AHF) complicates acute myocardial infarction as a result of a complex interaction of structural, hemodynamic, neurohormonal, and genetic maladaptations. Abrupt myocyte loss leading to contractile dysfunction and AHF is an obvious mechanism, and the extent of biomarker elevation correlates with prognosis and the range of functional recovery.⁴ In those without extensive myocyte necrosis, postischemic left ventricular systolic dysfunction (LVSD) leading to AHF can result from transient myocardial stunning or hibernation depending on the extent of coronary reperfusion.⁵ Ventricular remodeling can increase wall stress to viable regions that may be relatively underperfused, furthering ischemia and adding to this cycle. Ischemia-induced impairment in myocardial relaxation can increase left ventricular filling pressures irrespective of global systolic function and lead to AHF. Furthermore, ischemia can also precipitate acute mitral regurgitation in some patients, contributing to the risk of pulmonary congestion. Recent data also suggest that AHF potentiates apoptosis in and outside the infarct zone,⁶ which focuses attention beyond mechanics, hemodynamics, and perfusion to alterations in signaling pathways and genetic expression. Regardless of which processes dominate in individual patients, it is clear that the intersection of AHF and myocardial infarction remains deadly even in the current era of acute reperfusion.⁷

See p 494

In this issue of Circulation, the Global Registry of Acute Coronary Events (GRACE) investigators⁸ expand on our understanding of the interrelation between AHF . . . [Full Text of this Article]

Related Article:

Determinants and Prognostic Impact of Heart Failure Complicating Acute Coronary Syndromes: Observations From the Global Registry of Acute Coronary Events (GRACE)

Philippe Gabriel Steg, Omar H. Dabbous, Laurent J. Feldman, Alain Cohen-Solal, Marie-Claude Aumont, José López-Sendón, Andrzej Budaj, Robert J. Goldberg, Werner Klein, Frederick A. Anderson, Jr for the Global Registry of Acute Coronary Events (GRACE) Investigators
Circulation 2004 109: 494-499. [Abstract] [Full Text]

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