Keywords: acute myocardial infarction
More than 90% of patients with acute myocardial infarction ‘acute thrombosis with plaque rupture’ supply damaged area of artery occlusion (which had been due to atherosclerosis partial obstruction) the speculated atherosclerotic plaque at the intimal change induced platelet function abnormalities trigger thrombosis ‘about 2/3 of the patients had thrombosis autolysis’ ’24 hours later only 30% still thrombotic occlusion.
The vast majority of patients with acute myocardial infarction in coronary atherosclerosis, coronary atherosclerosis as a chronic lesions caused by coronary artery gradually narrow, unless the main coronary artery or three have severe coronary artery stenosis, coronary circulation fully conditions and time of collateral circulation, generally does not separate because of coronary plaque causing luminal atresia and acute myocardial infarction, therefore, tend to have a predisposing factor in the occurrence of acute myocardial infarction. Abroad reported approximately 90% to 95% transmural myocardial infarction is caused by coronary thrombosis reported in China was 73.1%. Thrombosis are not the starter factors of acute myocardial infarction, and coronary atherosclerotic plaque rupture, have a close association between platelet factor and coronary artery spasm.
Atherosclerotic plaque rupture and thrombosis: acute myocardial infarction often occurs in the presence of atherosclerotic plaque by coronary dominated area. Late atherosclerotic lesions often present lipid core, which is often caused by cholesterol crystals, composed of a large number of lipid-rich foam cells and cell debris, the core containing smooth muscle cells by a thin layer of collagen fibers and macrophages The composition of the fibrous cap covering. Containing the lipid rich plaques exposed to stress or coronary artery stenosis enhanced sharp change of the pressure or tension, and easily broken. Coronary atherosclerotic plaque rupture in acute myocardial infarction after death autopsy detection rate of 70% to 100%, and its surface is mostly associated with thrombosis. Plaque rupture surface thrombus, often constituted by the platelet and atherosclerotic plaque components, indicating that plaque rupture earlier than thrombosis occurred before.
Coronary artery spasm: often occurs in a narrow foundation of atherosclerotic lesions, a few may occur in morphologically normal coronary arteries. Endothelial cell dysfunction may appear earlier than clinical coronary heart disease symptoms, or CAG significant coronary artery stenosis few years before that exist. Complete coronary endothelial function, platelet activation and the release of the product, such as ADP, thromboxane A2 (TXA2) ,5-HT, PDGF, etc., as well as sports, acetylcholine (Ach) allows the vascular endothelium-dependent relaxation; while endothelial cell function when a failure occurs, the endothelium dependent vasodilation weakened, even into the vasoconstrictor effect. Pathological conditions after the activation of the endothelial cells, endothelin-1, AT Ⅱ vasoconstrictor substances increases the production of the above factors may be involved in coronary artery spasm occurred. Coronary artery spasm not only lead to aggravation of endothelial cell injury, and further increase in the degree of vascular stenosis, severe trigger plaque rupture, and even lead to coronary artery acute occlusion and acute myocardial infarction.
The role of platelets and coagulation factors in acute myocardial infarction: platelets play an important role in the incidence of atherosclerosis and coronary thrombosis. Coronary atherosclerotic lesions, intimal injury, plaque rupture and subendocardial collagen fibers exposed, can promote rapid platelet adhesion, aggregation, formation of platelet aggregation and release of platelet granule composition, formation of microthrombi. Its table mask sugar protein Ia, and Ib platelet activation activation, platelets start moving contacts from the important role; platelet membrane GP Ⅱ b / stage Ⅲ b receptor activation after exposure, become fibrin and von Willebrand factor such as the combination of parts, leading to platelet between the connection and the formation of platelet aggregates. Coronary atherosclerotic plaque lesions, especially when the plaque ruptures, its intimal thrombosis characteristics weakening or loss of product release platelet activation the TXA2 ,5-HT and platelet-derived growth factor (PDGF) addition to further promote platelet aggregation, and can still cause coronary artery spasm, resulting in thrombosis continue to progress.
Hypercoagulable state in some patients without atherosclerotic lesions lead to myocardial infarction, of certain acute myocardial infarction may lead to the dissolution of fibrinogen due to reduced plasma tissue plasminogen activator inhibitor increased. The urine of patients with acute myocardial infarction fibrinopeptide A concentration, indicating that thrombin acts on fibrinogen make up the original so that an increase in newly generated fibrin, provide evidence of increased activity of the coagulation system.
The role of neutrophils in acute myocardial infarction: neutrophils play an important role in the inflammatory response and healing process of acute myocardial infarction, and also directly involved in the acute phase of myocardial ischemia or promote myocardial cell injury. Neutrophils bulky, stiff, i.e. when the flow in the normal capillaries prone Coanda phenomenon in coronary perfusion pressure drop, this phenomenon is more significant, the initial few hours of myocardial ischemia, neutrophils the the ischemic myocardium gathering gradually increased clogging and aggravate myocardial ischemia can lead to myocardial capillary mechanical, and produce a variety of oxidation products and protein dissolving enzyme directly cause myocardial injury.
Myocardial ischemia – reperfusion period, neutrophils caused by mechanical blockage in the the myocardial microvascular gathering the main reason leading to myocardial no-reflow “phenomenon. Myocardial ischemia-reperfusion in animal experiments, vascular endothelial cell injury in reperfusion injury plays a major role, clearly showing endothelial cell injury neutrophil accumulation myocardial necrosis “when phase change.
Oxygen free radicals is another one of the mechanisms that lead to ischemic myocardial injury or necrosis, vascular endothelial cells and neutrophils are the main source of oxygen free radicals. Radical scavenger experiments can have a protective effect on oxygen free radical mediated injury in the ischemic myocardium occurs before reperfusion plasma neutrophil observe the “no-reflow" phenomenon can prevent reperfusion, and mitigate myocardial edema, reduce reperfusion arrhythmias, reduced myocardial necrosis area and reduce the role of the heart stunning.
Normal coronary myocardial infarction: the atherosclerotic lesion is the most common cause of coronal Chi pulse fixed narrow, and many non-atherosclerotic factors also can cause severe coronary artery stenosis, and can lead to unstable angina, Acute myocardial infarction or sudden cardiac death. Non-atherosclerotic lesions caused by the incidence of acute myocardial infarction, heart the adventitia main coronary artery is normal or near normal 4% to 7% of patients with acute myocardial infarction patients, approximately 50% to 60% for coronary spasm or (and ) thrombosis; 40% to 50% for other rare cause of congenital coronary anomaly, coronary extraluminal pressure (myocardial bridge), coronary thrombosis, coronary arteritis, aortic dissection and myocardial oxygen supply and demand Imbalance (such as carbon monoxide poisoning).