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(Circulation. 2004;110:4-6.)
© 2004 American Heart Association, Inc.

Editorial

Widespread Targets for Friendly Fire in Acute Coronary Syndromes

Erling Falk, MD, PhD

From the Department of Cardiology, Cardiovascular Research Unit, Aarhus University Hospital (Skejby), Aarhus, Denmark.

Correspondence to Erling Falk, MD, PhD, Department of Cardiology, Cardiovascular Research Unit, Aarhus University Hospital (Skejby), DK-8200 Aarhus N, Denmark. E-mail Erling.Falk@iekf.au.dk

Key Words: Editorials • atherosclerosis • myocardial infarction • heart failure • remodeling

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

Transfer of lymphocytes between healthy inbred rats is harmless to the myocardium. If, however, the lymphocytes are donated by a rat that has survived a myocardial infarction (MI), the healthy myocardium of the recipient rat is attacked and myocytes are executed by the transferred lymphocytes, and the damage caused by the infiltrating lymphocytes seems to be directly related to the size of the infarct in the donors.¹ Furthermore, cytotoxic CD8+ T lymphocytes obtained after MI are able to recognize and kill healthy cardiomyocytes in vitro.¹ These observations indicate that MI may immunize the victim against its own myocardium, resulting in subsequent autoimmune-mediated damage of the surviving myocytes. Whether such friendly fire by lymphocytes against viable myocardium does occur in humans after MI is not known but is not unlikely.

See p 46

MI Development and Healing

A wealth of information exists on the role of inflammation and friendly fire in myocardial ischemia-reperfusion injury.^2,3 Myocardial necrosis induces inflammation mediated by the nonspecific (innate) immune system, involving endothelial activation and leakage (expression of adhesion molecules and contraction), complement activation, and recruitment of neutrophils followed by monocytes/macrophages, lymphocytes, plasma cells, eosinophils, and mast cells.^2–4 How and why cells belonging to the adaptive immune system (lymphocytes and plasma cells), specialized to handle foreign microbial invaders, participate remains a mystery. T cells by far outnumbered B cells in a canine model of myocardial ischemia and reperfusion,⁵ but virtually no data exist on the phenotypes of the infiltrating lymphocytes in human MI. The purpose of the short-lived presence of neutrophils . . . [Full Text of this Article]

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