LETTER TO THE EDITOR
Toward a redefinition of ischemic cardiomyopathy: is it an indivisible entity?
Alexander Tenenbaum, MD, PhDa,
Enrique Z. Fisman, MDa and
Michael Motro, MDa
a Cardiac Rehabilitation Institute,Chaim Sheba Medical Center,Tel-Hashomet 52621,Israel
altenen{at}yahoo.com
We read with great interest the article by Felker et al. (1) in which the investigators raised an important question regarding definitions of ischemic cardiomyopathy (CMP). Based on prognostic differences, the researchers proposed a new definition of ischemic cardiomyopathy that reclassifies cases with single-vessel disease as nonischemic patients.
However, the magnitude of this problem seems considerably deeper. Conventionally, the pathogenesis of ischemic CMP is described as sequelae of single or recurrent myocardial infarctions (MIs), with loss of functioning myocytes, development of fibrosis and subsequent left ventricular (LV) dysfunction and remodeling. In contrast, in 1989 Atkinson and Virmani (2) described congestive heart failure due to severe coronary artery disease (CAD) without MI in 26% of consecutive necropsies with ischemic CMP. Its pathogenesis in absence of MI was unclear at that time. They presumed that although this type of coronary CMP may comprise a subset of ischemic CMP, it may also represent idiopathic-dilated CMP with coincidental CAD.
Recent investigations have elucidated the pathogenesis of ischemic CMP in absence of MI, suggesting that LV function impairment is related to progression of CAD and does not require a distinct coronary event, such as MI with enzymatic elevation (3). Hibernation subsequent to severe CAD represents a precarious balance between perfusion and tissue viability that cannot be maintained indefinitely; small but multiple foci of myocardial necrosis will ultimately occur if blood flow is not increased (4). At onset of heart failure, myocyte apoptosis occurs (5) contributing to the progression of ventricular dysfunction. In patients with severe CAD, production and release of endothelin, angiotensin II and activation of neurohormonal systems lead to direct stimulation of interstitial fibrosis, contributing to the pathophysiology of heart failure (6,7).
Thus, two distinct types of ischemic CMP could be separated: ischemic post-MI CMP and ischemic non–post-MI CMP. These entities have dissimilar prevalence, incidence, natural history and could require a dissimilar therapeutic approach.
Obviously, the majority of ischemic non–post-MI CMP is found among patients with severe CAD, LV dysfunction and congestive heart failure in absence of history of MI. Unfortunately, Felker et al. (1) did not report the proportion of patients with ischemic CMP but without history of MI in their population. It would be of interest to disclose these data.
The main pitfall in the differential diagnosis between ischemic post-MI and non–post-MI cardiomyopathies in the clinical setting is related to cases with silent MI in the past. For clinical research purposes, we propose that patients without a history of MI with severe diffuse CAD on coronary angiography and significant global LV dysfunction in absence of regional wall motion abnormalities and/or scars on echocardiography should be considered as bearing ischemic non–post-MI CMP. The recognition of this entity as a different type of ischemic CMP is important for clinical trials and population-based studies aiming to determinate the prevalence, natural history and optimal therapeutic strategies for patients with ischemic non–post-MI CMP.
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References
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1. Felker GM, Shaw LK, O’Connor CM. A standardized definition of ischemic cardiomyopathy for use in clinical research. J Am Coll Cardiol. 2002;39:210–218[Abstract/Free Full Text]
2. Atkinson JB, Virmani R. Congestive heart failure due to coronary artery disease without myocardial infarction: clinicopathologic description of an unusual cardiomyopathy. Hum Pathol. 1989;20:1155–1162[Medline]
3. Gheorghiade M, Bonow RO. Chronic heart failure in the United States: A manifestation of coronary artery disease. Circulation. 1998;97:282–289[Free Full Text]
4. Schwarz ER, Schaper J, vom Dahl J, et al. Myocyte degeneration and cell death in hibernating human myocardium. J Am Coll Cardiol. 1996;27:1577–1585[Abstract]
5. Olivetti G, Abbi R, Quaini F, et al. Apoptosis in the failing human heart. N Engl J Med. 1997;336:1131–1141[Abstract/Free Full Text]
6. Colucci WS. Myocardial endothelin: does it play a role in myocardial failure? Circulation. 1996;93:1069–1072[Free Full Text]
7. Cohn JN. The management of chronic heart failure. N Engl J Med. 1996;335:490–498[Free Full Text]
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