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(Circulation. 2003;108:1167.)
© 2003 American Heart Association, Inc.

Clinician Update

Myocardial Replacement Therapy

Tomasz Siminiak, MD, PhD, FESC; Maciej Kurpisz, MD, PhD

From the University School of Medical Sciences, Department of Cardiology, District Hospital (T.S.), and the Institute of Human Genetics, Polish Academy of Sciences (M.K.), Pozna, Poland.

Correspondence to Prof Tomasz Siminiak, MD, PhD, FESC, FACC, University School of Medical Sciences, Department of Cardiology, District Hospital, ul. Juraszow 7/19, PL 60- 479 Pozna, Poland. E-mail tomasz.siminiak@usoms.poznan.pl

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

	Introduction

 
Case Presentation: A 56-year-old farmer who experienced a transmural anterior myocardial infarction (MI) 3 years ago was referred for evaluation of progressive dyspnea and fatigue. During the acute phase of MI, he was treated with fibrinolysis, as primary angioplasty was not available at his local hospital. Angiography performed 3 months after MI revealed occlusion of the left anterior descending artery with diffuse changes distal to the occluded segment. An attempt at percutaneous recanalization had failed. Despite treatment with ß-blockers and angiotensin-converting enzyme inhibitors, serial echocardiograms performed by his local cardiologist had shown a large dyskinetic area and subsequently progressive dilatation and remodeling of the left ventricle. The patient is currently presenting with New York Heart Association class III symptoms and a history of several recent episodes of pulmonary edema.

	Rationale for Myocardial Replacement Therapy

 
The development of postinfarction congestive heart failure in survivors of the acute phase of MI is related to myocardial cell loss in the area supplied by the infarct-related artery and the subsequent formation of a scar. As the most important strategies during the acute phase of MI, primary angioplasty and fibrinolysis are aimed at the restoration of blood flow to minimize necrosis. In addition, late revascularization procedures may enable recovery of contractility, but only in areas of the hibernating myocardium that contain a minimal number of viable, reversibly injured myocytes. In patients with a large myocardial necrotic area resulting from acute MI, and especially when the necrotic zone is weakly supplied by collaterals, the loss of cardiomyocytes results in the formation . . . [Full Text of this Article]

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