Role of complement factors and their inhibitors in the myocardial infarction

Abstract

Cardiovascular diseases and ischemic heart disease in particular with its extreme form -myocardial infarction, are responsible for approximately 40% of deaths in Poland and worldwide and therefore constitute one of the main problems of contemporary medicine. Despite widespread information, e.g. in the media, and multiple scientific publications, many aspects of these disorders remain unclear. Multiple factors can exacerbate ischemic heart disease, resulting in myocardial infarction: complete occlusion of an artery by a clot resulting from a ruptured atherosclerotic plaque [1]; an embolus originating from thrombi formed on the left ventricular valves; sudden increase of myocardial oxygen demand with coexisting impairment of coronary reserve; arteritis [2,3]. At the current stage of development of biomedical sciences, the disease progression is thought to be modulated by multiple immunological, biochemical and biophysical factors determined by genetic and environmental circumstances [4].Damage of the barrier between cardiomyocyte cytoplasm and extracellular environment resulting from ischemia is an important factor for the involvement of immunological mechanisms. Synthesis of ATP that is required for preservation of integrity of the cellular membrane and lysosomal membranes, is reduced, resulting in sarcolemmal damage. The mechanism of ionic exchange is disturbed, what results in inhibition of metabolite removal with subsequent accumulation of lactate, phosphate, ammonium and sodium ions in the cardiomyocytes. Increased osmotic pressure results in edema and cardiomyocyte rupture. Increased sarcolemmal permeability is also caused by the presence of superoxide and hydroxyl free radicals in higher amounts in the ischemic myocardium with simultaneous reduction of contents of inactivators [5]. The surface of all myocardial cells undergoes modification as a result of expression of adhesion molecules. Adhesion molecules are expressed at the border between the endothelium and necrotic cardiomyocytes, both on the surface of the endothelium as well as in the plasma, as soluble adhesion molecules [6]. Platelet endothelial cell adhesion molecule-1 (PECAM-1), also known as CD31, is also expressed on endothelial cells. These molecules are located on side surfaces of endothelial cells but also exist on peripheral blood

Clinical immunology Possible role of complement factors and their inhibitors in the myocardial infarction: an immunohistochemical study

“…Despite widely available information and numerous research reports, many aspects of these disorders remain unclear. At the current state of development of biomedical sciences it is believed that dynamics of development of cardiovascular diseases are modulated by many immunological, biochemical and biophysical factors of genetic and environmental nature [ 4 ].…”