ABNORMALITIES OF CARDIOCYTES IN REGIONS BORDERING FIBROUS SCARS OF DOGS WITH HEART-FAILURE

Progressive deterioration of left ventricular function is a characteri stic feature of the heart failure state and is often speculated to res ult from ongoing loss of viable myocytes. We previously showed that in dogs with chronic heart failure, cardiocyte death through apoptosis o ccurs in the border region of fibrous scars (old infarcts). In the pre sent study we examined the structural integrity of cardiocytes in regi ons bordering fibrous scars using transmission electron microscopy. Mo rphometric studies were performed using left ventricular tissue obtain ed from ten dogs with chronic heart failure produced by intracoronary microembolizations. Mitochondrial number increased significantly with proximity to the scar, while mitochondrial size decreased leading to a gradual decrease in mitochondrial volume fraction. Severe injury to m itochondria was present in only 5% of organelles in myocytes far from the scar but increased markedly to 28-41% in myocytes adjacent to or i ncorporated within the scar. Similarly, severe myofibrillar abnormalit ies were present in only 3% of myocytes that were far from the scar bu t increased significantly to 12-73% in myocytes adjacent to or incorpo rated within the scar. These results indicate that in dogs with chroni c heart failure, constituent myocytes of left ventricular regions bord ering fibrous scars manifest heterogeneity in the extent of degenerati on. The extent of degeneration is greatest in myocytes closest to the scar and least in myocytes far from the scar. We postulate that this w avefront of myocyte degeneration is a dynamic process that may lead to progressive expansion of the scar through loss of viable myocytes and ultimately may contribute, in part, to the progressive left ventricul ar dysfunction that characterizes the heart failure state. (C) 1997 El sevier Science Ireland Ltd.