Mechanisms of subcellular remodelling in post-infarct heart failure.

Abstract

Occlusion of a coronary artery results in myocardial ischemia and subsequent myocardial infarction. Whenever the infarct size is more than 30% of the ventricular wall, the remaining myocardium attempts to compensate for the loss of muscle mass by changing the size and shape of cardiocytes in addition to developing cardiac hypertrophy, cardiac dilatation and congestive heart failure. This remodeling of the heart is associated with changes in the extracellular matrix including collagen proteins and is most probably due to the activation of both sympathetic nervous system and renin-angiotensin system as well as increased formation of various growth factors. Alterations in contractile function of the infarcted heart are associated with remodelling of the sarcoplasmic reticulum with respect to Ca(2+)-pump and Ca(2+)-release channels as well as contractile and regulatory proteins of the myofibrils. Myocardial infarction has also been shown to result in remodelling of the sarcolemmal membrane with respect to Ca(2+)-channels, Ca(2+)-transport systems, cardiac receptors and signal transduction mechanisms. Although information regarding remodelling of mitochondria in the infarcted heart is limited, alterations in energy yielding and Ca(2+)-accumulating systems are suspected. Accordingly, it is suggested that changes in cardiac contractile dysfunction due to myocardial infarction are associated with remodeling of both extracellular matrix and subcellular organelles in the heart.