1. The epidemiology and pathophysiology of coronary artery disease
The term cardiovascular disease covers a heterogeneous group of clinical syndromes that affects the heart and the circulatory system. Coronary artery disease (or ischemic heart disease) accounts for the greatest portion of cardiovascular diseases, and alone caused 8.2 million deaths globally in 2013 [1, 2], therefore it is the major cause of death worldwide. It remains responsible for about 30-35% of all deaths in individuals over the age of 35, although both the prevalence and morbidity rates of coronary artery disease have declined in the developed countries over the past three decades due to prevention and modern pharmacological and invasive treatment possibilities. It has …show more content…
It is caused predominantly by atherosclerosis, an accumulation of fatty deposits on the inner linings of arteries. Although coronary artery disease has also some non-atherogenic forms (e.g. arteritis, congenital coronary artery anomalies, embolism of coronary arteries, spasm of arteries or diseases of coagulation system), almost all myocardial infarctions develop from coronary atherosclerosis, generally with superimposed coronary thrombosis. [4].
During the evolution of atherosclerotic plaques, especially vulnerable (lipid-laden) plaques, a plaque disruption can occur, which exposes substances that promote platelet activation and aggregation, thrombin generation and ultimately thrombus formation [5]. This thrombus interrupts blood flow and can result in a severe disproportion between oxygen supply and demand and - if this imbalance is persistent – consequently myocardial necrosis. Myocardial infarction (MI) can be transmural and subendocardial (nontransmural). Both forms cause significant alterations in the structure and function of residual myocardium …show more content…
Myocardial infarction is followed by a complex and interrelated sequence of events. The histological evaluation of MI shows several stages. The coagulation necrosis mostly occurs in the central region of infarcts, and results in the stretching of myofibrils, many with nuclear pyknosis, vascular congestion, and healing by phagocytosis of necrotic muscle cells. The contraction band necrosis (or coagulative myocytolysis) results from severe ischemia followed by reperfusion. It is characterized by hypercontracted myofibrils (increased Ca2+ influx into dying cells) with contraction bands, marked vascular congestion, and healing by lysis of muscle cells. It occurs in the periphery of large infarcts and to a greater extent in non-transmural than in transmural infarcts. Finally, the severe prolonged ischemia (without necrosis) can cause myocyte vacuolization (often termed myocytolysis), hydropic, vascular, and fatty degeneration. Apoptosis (programmed cell death) is an additional pathway of myocyte death after ischaemia. In contrast to coagulation necrosis, myocytes undergoing apoptosis exhibit shrinkage of cells, fragmentation of DNA, and phagocytosis [7,
The term cardiovascular disease covers a heterogeneous group of clinical syndromes that affects the heart and the circulatory system. Coronary artery disease (or ischemic heart disease) accounts for the greatest portion of cardiovascular diseases, and alone caused 8.2 million deaths globally in 2013 [1, 2], therefore it is the major cause of death worldwide. It remains responsible for about 30-35% of all deaths in individuals over the age of 35, although both the prevalence and morbidity rates of coronary artery disease have declined in the developed countries over the past three decades due to prevention and modern pharmacological and invasive treatment possibilities. It has …show more content…
It is caused predominantly by atherosclerosis, an accumulation of fatty deposits on the inner linings of arteries. Although coronary artery disease has also some non-atherogenic forms (e.g. arteritis, congenital coronary artery anomalies, embolism of coronary arteries, spasm of arteries or diseases of coagulation system), almost all myocardial infarctions develop from coronary atherosclerosis, generally with superimposed coronary thrombosis. [4].
During the evolution of atherosclerotic plaques, especially vulnerable (lipid-laden) plaques, a plaque disruption can occur, which exposes substances that promote platelet activation and aggregation, thrombin generation and ultimately thrombus formation [5]. This thrombus interrupts blood flow and can result in a severe disproportion between oxygen supply and demand and - if this imbalance is persistent – consequently myocardial necrosis. Myocardial infarction (MI) can be transmural and subendocardial (nontransmural). Both forms cause significant alterations in the structure and function of residual myocardium …show more content…
Myocardial infarction is followed by a complex and interrelated sequence of events. The histological evaluation of MI shows several stages. The coagulation necrosis mostly occurs in the central region of infarcts, and results in the stretching of myofibrils, many with nuclear pyknosis, vascular congestion, and healing by phagocytosis of necrotic muscle cells. The contraction band necrosis (or coagulative myocytolysis) results from severe ischemia followed by reperfusion. It is characterized by hypercontracted myofibrils (increased Ca2+ influx into dying cells) with contraction bands, marked vascular congestion, and healing by lysis of muscle cells. It occurs in the periphery of large infarcts and to a greater extent in non-transmural than in transmural infarcts. Finally, the severe prolonged ischemia (without necrosis) can cause myocyte vacuolization (often termed myocytolysis), hydropic, vascular, and fatty degeneration. Apoptosis (programmed cell death) is an additional pathway of myocyte death after ischaemia. In contrast to coagulation necrosis, myocytes undergoing apoptosis exhibit shrinkage of cells, fragmentation of DNA, and phagocytosis [7,