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European Heart Journal 1995 16(Supplement N):37-45; doi:10.1093/eurheartj/16.suppl_N.37
Copyright © 1995 by the European Society of Cardiology.
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© 1995 The European Society of Cardiology

Myocardial infarction and the myocyte IGF1 autocrine system

P. Anversa, K. Reiss, J. Kajstura, W. Cheng, P. Li, E. H Sonnenblick* and G. Olivetti

Department of Medicine, New York Medical College Valhalla, New York, USA
* Albert Einstein College of Medicine Bronx, New York, USA

Correspondence: Piero Anversa, MD, Department of Medicine, New York Medical College Vosburgh Pavilion, Room 302, valhalla, New York 10595 U.S.A.

To determine the effects of acute myocardial infarction on the extent and distribution of mural stress on surviving myocardial tissue, coronary artery occlusion was surgically produced in rats. Following haemodynamic measurements in vivo, the characteristics of cardiac anatomy were determined and found to consist of an increase in mid-chamber luminal diameter and a decrease in wall thickness. The combination of these phenomena resulted in an eight-fold increase in diastolic wall stress on the remaining viable portion of the wall and severe impairment of left and right ventricular performance. Since insulin-like growth factor-I (IGF1) and its receptor (IGF1 R) are required for cell growth in vitro, the possibility was raised that an autocrine IGF1–IGF1 R system may be present in vivo and may become activated in viable ventricular myocytes shortly after infarction. Therefore, the unaffected myocytes of the left ventricle were enzymatically dissociated and the expression of IGF1 R and IGF1 mRNAs were measured at 12 h and at 1, 2–3, and 7 days after surgery. The level of IGF1 R mRNAs increased at 12 h and remained elevated at 1 and 2–3 days following coronary artery ligation. In addition, an increased level of IGF1 R protein was found on these cells. This phenomenon was coupled with the enhanced expression of IGF1 mRNA in the muscle cells at all points. Thus, the marked elevation in ventricular loading after coronary occlusion may activate the IGF1–IGF1 R autocrine system of the unaffected cells, modulating the cellular growth processes implicated in short-term ventricular remodelling of the infarcted heart.

Key Words: Myocardial infarction • wall stress • IGFI1-IGFIR1R system • myocyte growth • ventricular remodelling


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