A detailed analysis of the causes of myocardial infarction:
(1) etiology and pathogenesis
The main cause is coronary atherosclerosis (even coronary artery embolism, inflammation, congenital malformation, spasm and coronary artery occlusion), resulting in severe lumen stenosis and insufficient myocardial blood supply, while collateral circulation is not fully established. On this basis, once the blood supply is further reduced or interrupted, myocardial infarction can occur after acute and persistent acute ischemia of the myocardium for more than 1 hours. The incidence of myocardial infarction increases with age, which is the highest in 65~79 years. Male patients were more than women before the age of 65, and the prevalence of amphoteric disease was gradually close to 1:1 after 65 years of age. Acute myocardial infarction is mainly caused by emotional excitement, mental stress, physical work and after eating. Myocardial infarction can occur not only in patients with frequent angina but also in the original asymptomatic. In patients with variant angina, repeated episodes of coronary artery spasm may also develop into acute myocardial infarction. The disease is more frequent in spring and winter. It is related to cold climate and large temperature change. It often occurs in quiet or sleep. It occurs most frequently from 6 in the morning to 12 noon.
Because of coronary arteriosclerosis in the elderly, coronary artery insufficiency leads to myocardial ischemia and hypoxia. The myocardium is necrotic due to irreversible structural changes caused by severe or complete interruption of blood supply. Most of the coronary artery occlusion caused by acute exacerbation, coronary atherosclerotic plaques or lesions of intimal rupture, hemorrhage, thrombosis, was soon completely blocked, such as the artery and other coronary collateral circulation between the original is not fully established, can lead to this artery should be serious myocardial ischemia induced by 1H is more durable. Myocardial necrosis. A few cases of coronary artery lumen without complete occlusion of coronary artery spasm, but persistent, the coronary blood flow decreased gradually, excitement, emotion and heavy physical labor, after the meal, the myocardial oxygen consumption increased, cardiac burden, long-term myocardial ischemia, the myocardial hypoxia induced coagulation necrosis, and the subendocardial myocardium and the ventricular wall and myocardial infarction. In the basis of atherosclerotic lesions of coronary artery stenosis on the occurrence of sudden cardiac output (hemorrhage, shock or severe arrhythmia), or left ventricular load surge (severe physical activity, emotional drama too excited, blood pressure rise or defecate), can also cause severe and persistent myocardial ischemia, myocardial necrosis caused by. During sleep, the tension of the vagus nerve increases and the coronary artery spasm; the operation injury of interventional therapy can aggravate the necrosis of myocardial ischemia.
Acute coronary syndrome (Acs) is a new concept proposed in recent years, the main pathogenesis is the rupture of unstable plaque, thus induce acute thrombosis formation, secondary mechanism is the contraction and spasm of coronary plaque rupture and induced intimal injury, can coexist with thrombosis, the incidence of ACS accounted for 10% to 20% reasons: Plaque both factors of rupture of the plaque itself, there are factors other than plaque. The factors of the plaque itself include the size of the fat nucleus under plaque, the degree of inflammation in the plaque, the thickness of the fibrous cap, and the amount of collagen in the plaque. A large lipid core plaques, is easily broken; if there is a large number of plaques in T cells and macrophages, macrophages release a large number of metalloproteinases. The thinning of the fibrous cap, plaque rupture; in addition, more collagen content in the fibrous cap, while plaque strength, is not easy to rupture: Plaque outside factors is a sudden change of heart rate and blood pressure and coronary arterial pressure, shear stress on plaque increased thrombosis mechanism relates to blood vessel wall, blood platelet, blood coagulation and fibrinolysis and blood flow. Platelet and coagulation factors are essential for thrombosis. Their activation is a manifestation of hypercoagulability. Fibrinolytic activity plays an important role in the outcome of thrombosis. According to the sT segment elevation, it is divided into sT segment elevation and non sT segment elevation ACS. The sT segment elevation of ACS mainly evolved into Q wave acute myocardial infarction (AM1), and a few also had acute non Q wave myocardial infarction. The non sT segment elevation of ACS mainly evolved into two major categories of non Q wave myocardial infarction and unstable angina pectoris, and acute non Q wave myocardial infarction could occur in a few cases. According to the new classification, myocardial infarction is classified according to the elevation of the sT segment of the electrocardiogram. The treatment and prognosis of different types of AMI are also different.