Ventricular remodeling following acute myocardial infarction: The role of altered collagen homeostasis

Abstract

Ventricular remodeling following myocardial infarction, characterized by detrimental changes on ventricular size, shape and function, is considered to be one of the most powerful predictors of adverse outcomes after myocardial infarction [1,2]. Recently, McGavigan et al. [3] have evaluated the role of impaired collagen homeostasis in predicting the development of early ventricular remodeling following acute myocardial infarction. Fifty-one patients with acute myocardial infarction have been included in this study. Twenty-three of these patients had normal left ventricular wall motion index and 28 have had abnormal wall motion index. C-propeptide for type-I collagen (PICP) andC-telopeptide for type-I collagen (CITP) have been measured as the markers of collagen synthesis and degradation, respectively. Patients who manifested early left ventricular remodeling following acute myocardial infarction have increased degradation and reduced synthesis of collagen, favoring net collagen breakdown. Both groups with normal and abnormalwall motion index have shown to have increased in PICP and CITP over time. However mean admission of CITP levels, indicating collagen degradation, has been detected to be significantly higher in patients with abnormal wall motion index. In contrary, admission of PICP levels, indicating collagen synthesis, has been shown to be significantly lower in abnormal wall motion index group. In addition admission of CITP levels had a positive correlation with wall motion index. CITPN3.2 ng/ml has been reported to