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Collagenous Proteins in Scar Tissue Subsequent to Myocardial Infarction

1996; Springer Nature; Linguagem: Inglês

10.1007/978-1-4613-1235-2_25

2542-8373

Ian Dixon, V. Pelouch, Rajat Sethi, Naranjan S. Dhalla,

Venous Thromboembolism Diagnosis and Management

A significant body of evidence from observations in clinical and experimental models has accumulated to demonstrate that a progressive loss of intrinsic contractility occurs in surviving myocardium after large transmural myocardial infarction, and the degree of cardiac pump dysfunction in viable tissue has been correlated to the size of the initial infarct [1–4]; however, no common biochemical defect has been identified to explain the loss of cardiac function [5]. Previous work indicates that structural and biochemical remodeling of surviving cardiac tissue is characterized by concentric and eccentric hypertrophy of myocytes and altered biochemical characteristics of myosin protein [4,6–9]. Furthermore, defective sarcolemmal and sarcoplasmic reticular membrane functions have been described both in the clinical setting and in experimental models of heart failure, including the rat model of congestive heart failure following myocardial infarction [5]. Indeed, many previous investigative efforts that have addressed the pathology of myocardial infarction have been directed at mechanisms to explain the loss of contractility in surviving myocardium of infarcted hearts. The extracellular matrix has been suggested to play a role in the pathogenesis of heart failure, and recent work from this laboratory has revealed that the collagen, a major component of the matrix, is altered in remaining viable myocardium [10].