Coronary atherosclerotic heart disease

Introduction to coronary atherosclerotic heart disease Coronary atherosclerotic heart disease is called coronary heart disease. It is the most common type of heart disease. It refers to myocardial dysfunction and/or organic disease caused by coronary artery stenosis and insufficient blood supply. It is also called ischemia. Cardiomyopathy. The occurrence of coronary heart disease is closely related to the degree and number of coronary atherosclerotic stenosis. At the same time, suffering from diseases such as hypertension and diabetes, as well as obesity and bad habits, are the main factors that induce the disease. Recent studies have shown that hypertriglyceridemia is also an independent risk factor for coronary heart disease, high-density lipoprotein has a protective effect on coronary heart disease, and its value is reduced to coronary heart disease, the ratio of high-density lipoprotein cholesterol to total cholesterol < 0.15, a valuable predictor of coronary atherosclerosis, recent studies have found that elevated serum alpha-lipoprotein [Lp ()] (> 0.3g / L) is also an independent risk factor for coronary heart disease. basic knowledge The proportion of illness: 0.032% Susceptible people: no specific population Mode of infection: non-infectious Complications: sudden death, arrhythmia, cardiogenic shock, heart failure, ischemic cardiomyopathy, mitral valve prolapse syndrome, sick sinus syndrome

Causes of coronary atherosclerotic heart disease

High blood pressure (50%):

It is an important risk factor for coronary heart disease. Hypertensive patients with coronary heart disease are four times more likely to have normal blood pressure. 60% to 70% of patients with coronary heart disease have hypertension, and the shear stress and sidewall pressure change when arterial pressure is increased Intimal damage, and elevated blood pressure, promotes the infiltration of plasma lipids into the blood vessel cells, thus causing platelet accumulation and smooth muscle cell proliferation, resulting in atherosclerosis.

Hyperlipidemia (15%):

Recent studies have shown that hypertriglyceridemia is also an independent risk factor for coronary heart disease, high-density lipoprotein has a protective effect on coronary heart disease, and its value is reduced to coronary heart disease, the ratio of high-density lipoprotein cholesterol to total cholesterol < 0.15, a valuable predictor of coronary atherosclerosis, recent studies have found that elevated serum alpha-lipoprotein [Lp ()] (> 0.3g / L) is also an independent risk factor for coronary heart disease.

Diabetes (10%):

It is an important risk factor for coronary heart disease. The risk of coronary heart disease is 2 times higher than that of normal people. The risk of coronary heart disease in women with diabetes is 3 times higher than that of male patients, and heart failure, stroke and death are prone to occur. In blood glucose, the increase in glycosylated low-density lipoprotein in the blood inhibits the degradation metabolism of the low-density lipoprotein receptor pathway, and hyperglycemia also damages the intima of the blood vessel, and diabetes often has abnormal lipid metabolism. Therefore, diabetics are prone to coronary heart disease.

1. Age This disease is more common in people over the age of 40. The occurrence of atherosclerosis can begin in children, and the incidence of coronary heart disease increases with age.

2. Gender males are more common, the ratio of male to female incidence is about 2:1, because estrogen has anti-atherosclerosis, so the incidence of women after menopause increases rapidly.

3. Family history has coronary heart disease, diabetes, hypertension, family history of hyperlipidemia, the incidence of coronary heart disease increased.

4. Individual type A personality (strong competition, competitive) There is a high prevalence of coronary heart disease, and people with excessive mental stress are also susceptible to disease, which may be related to the long-term high concentration of catecholamines in the body.

5. Smoking is an important risk factor for coronary heart disease. The prevalence of coronary heart disease in smokers is 5 times higher than that of non-smokers, and is proportional to the amount of smoking. The blood carbon monoxide hemoglobin is increased in smokers, and nicotine in blood vessels shrinks blood vessels, resulting in arteries. The wall is deficient in oxygen and causes arterial damage.

6. Obesity and exercise are too small 1 standard body weight (kg) = height (cm) -105 (or 110), 2 body mass index = body weight (kg) / (height m) 2, more than standard body weight 20% or body mass index > 24 Obesity, although obesity is not as important as high blood pressure, hyperlipidemia, diabetes, but obesity can indirectly affect coronary heart disease by promoting the development of these three factors, exercise can regulate and improve vascular endothelial function, and promote already suffering In patients with coronary heart disease, the establishment of coronary collateral circulation, the amount of exercise is less likely to cause obesity, so the importance of treating obesity and increasing the amount of exercise should be fully recognized.

7. Other

(1) drinking: long-term high-drinking high-alcohol liquor has damage to the function of heart, blood vessels, liver and other organs, which can cause alcoholic cardiomyopathy, cirrhosis, and hypertension; and moderately drink low-quality colored wine (for example) Wine) can reduce the risk of coronary heart disease, because drinking alcohol can increase the concentration of high-density lipoprotein.

(2) Oral contraceptives: long-term oral contraceptives can increase blood pressure, increase blood lipids, abnormal glucose tolerance, and at the same time change the coagulation mechanism and increase the chance of thrombosis.

(3) Eating habits: eating high calorie, high animal fat, high cholesterol, high sugar diet is prone to coronary heart disease, and other changes in the intake of trace elements.

Coronary heart disease is the abbreviation of coronary atherosclerotic heart disease, and atherosclerosis is the cells of the arterial wall, extracellular matrix, blood components (especially monocytes, platelets and LDL), local hemodynamics, environment And the results of the interaction of a variety of complex factors such as heredity, it should be noted that the existence of risk factors for coronary heart disease does not mean coronary heart disease.

Pathogenesis

1. Mechanism of atherosclerosis Atherosclerosis can occur in elastic arteries and large and medium-sized muscles (such as coronary arteries and cerebral arteries). Atherosclerotic lesions have the following characteristics: 1 focal lesions often Occurred in the bifurcation of the arteries, 2 lesions begin with functional changes in endothelial cells (EC), the most important cells of the 3 lesions are smooth muscle cells (SMC), and SMC migrates from the media to the intima and proliferates and synthesizes more cells. External connective tissue, 4 monocytes and/or macrophages also play an important role in the formation and regression of atherosclerotic lesions. 5 lesions have different lipids inside and outside the cell, mainly cholesterol. There are a lot of lipids in the cell called foam cells, the latter mainly from macrophages, but also from smooth muscle cells.

At present, it is widely believed that the mechanism of atherosclerosis is the result of the interaction of a variety of complex factors, among which the "injury reaction hypothesis" has been recognized, that is, the atherosclerotic lesion begins with the damage of endothelial cells, this hypothesis Can be summarized as the following process:

(1) Changes in endothelial cells in vulnerable areas: Unlike endothelial cells in non-vulnerable areas, endothelial cells are easily formed into atherosclerotic regions in the shape of round stones, mononuclear cells and/or giants. The phagocytes easily reach the subcutaneous space through the endothelium, thereby initiating the process of atherosclerosis.

(2) When there is an increase in lipoprotein levels: easy to produce foam cells Low-density lipoprotein (LDL) and other proteins pass through endothelial cells into the subendothelial space where LDL is oxidized to oxidized LDL (Ox-LDL), the latter Lead to endothelial cell damage, while also stimulating endothelial cells and smooth muscle cells to secrete chemokines that regulate monocyte/macrophage entry. Monocyte chemokines (MCP-1) are the most important chemokines. First, it attracts monocytes in the blood from the endothelial cells to the subendothelial space, and then is activated into macrophages, absorbing Ox-LDL, and turning into cholesteryl ester-rich foam cells.

(3) Lipid formation: When monocytes, LDL continue to enter, while the mid-membrane SMC migrates to the intimal space, the lipoprotein forms a fatty streak. At this time, the endothelial cells above the fat streaks may be underneath. The foam cells are squeezed out, making the endothelial cells thin and thin.

(4) Transitional lesions (pre-atherosclerosis): Ox-LDL toxic effects cause foam cell necrosis, release a large amount of lipids and lysosomal enzymes, or because the amount of Ox-LDL exceeds the ability of macrophages to ingest, Lead to the cholesteryl ester-rich lipid core and cholesterol crystals in the subendothelial space, Ox-LDL also causes damage and/or death of endothelial cells and smooth muscle cells, the inner lining of the intima begins to break, and smooth muscle cells in the intima (including The middle membrane migrates to the endometrium) to proliferate and synthesize a large amount of connective tissue, at which time the arterial wall is thickened, but the vascular lumen is not yet restricted.

(5) Mature fiber plaque: that is, atherosclerosis, when the intima is thickened, the middle membrane is thinned, the outer membrane is fibrotic, the blood vessels are narrowed, and the smoother muscle cells in the thickened intima are more Embedded in a tight collagen matrix and capillaries to form a fibrous cap; the lipid core can be seen at the edge of the plaque; the fibrous cap and lipid core can have calcification, after the formation of atherosclerotic lesions, depending on the lesion, size, blood vessels The degree of stenosis may appear corresponding to atherosclerotic manifestations, such as aortic atherosclerosis, coronary atherosclerosis, cerebral atherosclerosis, renal atherosclerosis, mesenteric atherosclerosis, lower extremity atherosclerosis, and the like.

2. The pathogenesis of coronary heart disease whether coronary atherosclerosis occurs in coronary heart disease, to some extent depends on the degree of vascular stenosis caused by coronary atherosclerosis, pathologically often according to the cross section of the most severe part of the stenosis, Four-level classification: Grade I, lumen stenosis area 25%; Grade II, lumen stenosis area is 26% to 50%; Grade III, 51% to 75%; Grade IV, 76% to 100%, Generally, grade I to II atherosclerosis does not cause significant reduction in coronary blood flow. Except for coronary artery spasm, there is no direct effect on the onset of coronary heart disease. Therefore, although there is coronary atherosclerosis, there is no clinical crown. The manifestation of heart disease, or although there is "coronary heart disease performance" is not caused by coronary heart disease, and those with grade III or higher stenosis are directly related to the occurrence of coronary heart disease.

Recent studies have shown that the presence or absence of coronary heart disease, in addition to the degree of coronary stenosis, more important depends on the stability of atherosclerotic plaque, arterial atherosclerosis, especially in the elderly and severe plaque, easy There is a large amount of calcium salt deposition, and normal arteries do not undergo calcification; although the degree of calcification is not proportional to the severity of atherosclerosis, especially the degree of stenosis, it can be observed from vascular ultrasound that calcified plaques are generally relatively stable. The problem is that some calcified plaques, or when the plaque develops into a thick calcified cap, which tends to cause rupture of coronary atherosclerotic plaque, hemorrhage and subsequent vascular lumen when the stress between the adjacent membrane increases. The formation of thrombosis leads to the occurrence of "acute coronary syndrome", unstable angina, myocardial infarction and even sudden death. Pathologically, plaque rupture often occurs at the junction of calcified and non-calcified atherosclerotic lesions.

Atherosclerotic lesions that do not cause symptoms may have occurred very early in life, but once the lesion plaque rapidly expands, it can lead to the occurrence of acute coronary artery disease, which occurs in the development of "acute coronary syndrome". It plays an important role, and plaque enlargement is especially rapid in people with coronary heart disease risk factors (such as hypercholesterolemia). Therefore, active control of coronary heart disease risk factors is an important measure to prevent coronary heart disease.

In some patients, the occurrence of coronary heart disease is caused by coronary artery spasm. However, in most cases, coronary atherosclerosis is accompanied by the following factors:

(1) Neurological factors: coronary arteries are rich in alpha receptors, sympathetic excitation, exercise, cold compression test can induce coronary spasm; secondly, vasomotor receptors, vagus nerve excitation can also induce coronary spasm, In this case, atropine can be used to fight.

(2) Humoral factors: The balance of prostacyclin (PGI2) and thromboxane (TXA2) also directly affects the contractile state of coronary artery: PGI2 is synthesized by vascular endothelial cells, which has obvious vasodilator effect, and TXA2 is platelet aggregation. When released, there is a strong contraction of blood vessels. When PGI2 is lowered and (or) TXA2 is increased, it can cause coronary sputum, 2 serotonin and other vasoactive substances released during platelet aggregation, in the occurrence of coronary contraction or spasm It also plays a certain role, 3 the role of serum calcium and magnesium ions: calcium ions increase, when hydrogen ions decrease, calcium ions enter the cells more, increase coronary tension and coronary vasospasm; excessive ventilation, intravenous alkaline Drugs cause blood alkalosis can induce coronary spasm; magnesium deficiency can also cause coronary contraction.

(3) The atherosclerotic blood vessels have obvious contractile reactivity to various vasoconstrictive substances. This is caused by cholesterol promoting the flow of extracellular calcium ions into the cells. In addition, when the endothelial damage is reduced, the synthesis of PGI2 is decreased, and the TXA2 is increased. The endothelial-derived relaxing factor synthesized by endothelial cells is decreased, thereby inhibiting the vasoconstriction of vasoconstrictors such as ADP, serotonin and thrombin. Recently, it has been observed that acetylcholine relaxes the coronary artery with normal endothelial function. The atherosclerotic blood vessels contract.

In short, the mechanism of coronary spasm is multifaceted, and endothelial injury is currently considered to be the most important predisposing factor for coronary spasm.

3. The pathophysiological basis of coronary heart disease on the basis of coronary atherosclerotic lesions, myocardial oxygen supply and oxygen demand imbalance, is the pathophysiological basis of myocardial ischemia and hypoxia, leading to coronary heart disease.

(1) Determining factors of myocardial oxygen consumption: The available oxygen in the coronal circulation accounts for 75% of the required oxygen. It is used to produce high-phosphorus compounds. The myocardial oxygen consumption is mainly caused by myocardial tension and myocardial contraction. The three factors of force and heart rate are determined. The other three secondary factors are basal metabolism, electrical activation and myocardial fiber shortening, arterial systolic pressure, heart rate and ejection time, "three product" and left ventricular pressure curve contraction area and heart rate, ie The tension-time index is closely related; however, a simpler method is commonly used in clinical practice, that is, the "two product" of systolic blood pressure and heart rate is used as an indicator of myocardial oxygen consumption. For example, when the threshold value of angina pectoris is observed, this index is commonly used.

(2) Determining factors of myocardial oxygen supply: the muscle of the heart, that is, the myocardium, is only about 25% of the oxygen directly contained in the blood contained in the atrioventricular cavity. The oxygen required by the myocardium mainly depends on the coronary artery. The blood flow is supplied, so the coronary blood flow is the most important factor affecting myocardial oxygen supply. When the person is at rest, the oxygen intake of the myocardium from the coronary blood is close to the maximum, and it is difficult to increase the oxygen demand. More oxygen in the coronary blood can only be provided by increasing the amount of blood in the coronary arteries. Under normal circumstances, the coronary circulation has a large reserve, vigorous exercise, and the coronary artery is dilated during hypoxia, and the blood flow can be increased to rest. 4 to 7 times; coronary atherosclerotic stenosis and occlusion are the main reasons limiting the transmission of oxidized blood to the myocardium. In addition, mechanical activity of cardiac contraction and relaxation, metabolism of cardiomyocytes, neurohumoral fluid and various vascular activities Substances are involved in the regulation of coronary blood flow.

(3) imbalance of myocardial oxygen supply and oxygen demand: any cause of myocardial oxygen supply and / or oxygen demand exceeds the body compensation range, will lead to imbalance of supply and demand of myocardial oxygen, resulting in myocardial ischemia, Among them, coronary heart disease caused by coronary atherosclerosis is the most common myocardial ischemia, so it should be noted that the so-called "myocardial ischemia" is the most common coronary heart disease, but it is not equal to coronary heart disease; coronary heart disease and ischemia Sexual heart disease is synonymous.

(4) The effect of myocardial ischemia on the heart: When myocardial ischemia, glycolysis becomes the main source of ATP. At this time, in addition to the increase in the amount of lactic acid, the contraction and diastolic function of the heart are affected by insufficient energy. Heavier ischemia (including acute severe ischemia around acute myocardial infarction or myocardial reperfusion after coronary reperfusion) and longer duration, reversible damage to the myocardium, recovery with blood supply, myocardial structure, metabolism and The function is slowly recovered, and it takes hours, days or even weeks. The myocardium in this state is called stunned myocardium. In patients with coronary heart disease, in order to adapt to blood flow below normal, some myocardium can "Automatically" lowers the oxygen consumption to ensure that the supply and demand of myocardial oxygen reaches a new level, and the myocardial function recovers with the recovery of blood supply, such as a viable myocardium with neither myocardial infarction nor ischemic symptoms. Called hibernating myocardium.

It is generally believed that this is a protective mechanism of the myocardium. Once the blood supply is improved, the myocardial function can be completely restored. When coronary atherosclerotic stenosis produces myocardial ischemia, metabolites can stimulate coronary dilatation to increase blood flow. The phenomenon of "reactive hyperemia" gradually decreases with the increase of stenosis, and disappears completely until the degree of coronary stenosis is >90%. At the same time, chronic ischemia can promote the establishment of collateral circulation, and these compensatory mechanisms are beneficial to maintain myocardial Oxygen supply and demand balance, the patient can have no myocardial ischemia for a long time, only when myocardial oxygen consumption is significantly increased, coronary blood flow and collateral blood flow is insufficient to maintain this balance, myocardial ischemia occurs On the basis of atherosclerosis, rapid plaque rupture and/or hemorrhage, paralysis and acute or incomplete thrombotic occlusion, causing acute coronary syndrome, clinical manifestations of instability Angina pectoris, acute myocardial infarction or sudden death.

Coronary atherosclerotic heart disease prevention

1. Primary prevention for people who do not have coronary heart disease, intervention of coronary heart disease susceptibility factors to prevent the occurrence of coronary heart disease, this work is a very difficult task, starting from children, adolescents should start coronary heart disease Prevention work is carried out.

Recognized risk factors for coronary heart disease include men, with a family history of premature coronary heart disease (parents, brothers with a defined myocardial infarction or sudden death at age 55), smoking (currently smoking cigarettes 10 / d), high blood pressure, Diabetes, HDL-C concentration is still <0.9mmol / L (35mg / dl), there is a clear history of cerebrovascular or peripheral vascular occlusion, severe obesity (overweight 30%), susceptible to many coronary heart disease Among the factors, some are unchangeable factors, such as: age, gender, family history of cardiovascular and cerebrovascular diseases; others are changeable factors, such as: high blood pressure, high blood fat, high blood sugar, smoking, eating habits, obesity, etc. Therefore, in order to prevent the occurrence of coronary heart disease, we should actively control the "changeable factors", control weight, moderate exercise, quit smoking, low-fat and low-salt diet is an important health care measure, effective control of hypertension, hyperlipidemia and diabetes is more urgent The task of taking positive preventive measures can significantly reduce the incidence of coronary heart disease.

2. Secondary prevention for people with coronary heart disease, to prevent the development of the disease and sudden death, for those who have not had myocardial infarction, should actively prevent the occurrence of myocardial infarction.

For the secondary prevention of patients with myocardial infarction, the following aspects should be included: health education for patients and their families; targeted measures for risk factors for coronary heart disease to prevent the progression of coronary artery disease; drug or surgery for prevention and treatment of myocardium Ischemia, left ventricular dysfunction or severe arrhythmia; those who are at high risk for re-infarction or sudden death should minimize the risk factors.

The meaning of the "ABC program" in the first and second stage of prevention and treatment of coronary heart disease proposed in recent years can be summarized as follows:

AAspirine (aspirin) means that anticoagulant and antiplatelet drugs should be used in the prevention and treatment of coronary heart disease. Some clinicians believe that it also contains the use of angiotensin converting enzyme inhibitor (ACEI).

B (beta) - Blocker (beta blocker); C - Cholesterol, which means lowering cholesterol.

Coronary atherosclerotic heart disease complications Complications sudden cardiac arrhythmia cardiogenic shock heart failure ischemic cardiomyopathy mitral valve prolapse syndrome sick sinus syndrome

Coronary heart disease can have sudden cardiac death, arrhythmia, heart failure, cardiogenic shock, ischemic cardiomyopathy, mitral valve prolapse and other complications.

1. Sudden cardiac death Sudden cardiac death is the most common cause of coronary heart disease, accounting for more than 3/4, 50% to 70% of all deaths from coronary heart disease are sudden death. Epidemiological data reported by Lown in the United States show that each year, sudden cardiac death 400,000, an average of 1 case of sudden cardiac death occurred, 80% of which are caused by coronary heart disease, many patients with coronary heart disease usually have no symptoms, sudden death is the first clinical manifestation, accounting for about 20% of coronary heart disease sudden death, The prevalence of coronary heart disease in the general northern provinces and cities in China is significantly higher than that in the south.

2. Arrhythmia Arrhythmia can be the only symptom of ischemic heart disease, can occur a variety of rapid and slow arrhythmia, but the clinically common coronary heart disease arrhythmia mainly pre-systolic (atrial and ventricular), atrial flutter Dynamic and atrial fibrillation, non-sustained ventricular tachycardia and conduction system disorders caused by sick sinus syndrome, varying degrees of atrioventricular block and bundle branch block.

3. Heart failure is mainly due to coronary atherosclerosis, long-term lack of myocardial blood supply caused by stenosis, myocardial tissue dystrophies and atrophy, resulting in scattered or diffuse myocardial fibrosis and ventricular remodeling, most patients have myocardial History of infarction or history of angina pectoris, heart failure gradually occurs, most of which first develop left ventricular failure, followed by right heart failure, the corresponding clinical symptoms of total heart failure.

4. Ischemic cardiomyopathy refers to myocardial damage caused by acute (reversible) or chronic myocardial ischemia caused by coronary heart disease, manifested as ventricular systolic or diastolic dysfunction, often due to coronary atherosclerotic stenosis caused by scattered Or caused by diffuse myocardial fibrosis.

5. Mitral valve prolapse mitral valve prolapse syndrome is higher in the incidence of coronary heart disease, physical and chemical analysis of 76 cases, 14 cases (18.4%) clinically have this syndrome, mainly due to the supply of anterior external papillary muscles or After the arterial stenosis of the posterior papillary muscles, the insufficiency of blood supply and contraction of the anterior or posterior papillary muscles is caused.

Coronary atherosclerotic heart disease symptoms Common symptoms fatigue chest pain sudden chest tightness laminar hematoma chest tightness suffocation qi stun dyspnea dyspnea cardiac arrest

The disease is divided into five clinical types.

1. Asymptomatic coronary heart disease Also known as occult coronary heart disease, including atypical symptoms, true asymptomatic and history of coronary heart disease but asymptomatic, the incidence of asymptomatic coronary heart disease is unclear in the population, in the Framingham study, About 1/4 of patients with myocardial infarction have no clinical symptoms before onset. Although these patients are asymptomatic, there are myocardial ischemia changes in ECG during rest or stress test, including ST-segment depression, T-wave low-level or inversion, etc., pathology There was no obvious histomorphological change in the myocardium. There was no significant difference between the prognosis and the symptomatic coronary heart disease. The prognosis depends on the severity of myocardial ischemia and the degree of left ventricular function.

2. Angina pectoris coronary heart disease patients with clinical myocardial ischemia caused by paroxysmal precordial pain, pathological examination of myocardial no tissue changes, refer to the World Health Organization "ischemic heart disease nomenclature and diagnostic criteria", Combined with clinical features, angina pectoris is divided into the following types.

(1) angina pectoris: often in sports, fatigue, emotional or other increase in myocardial oxygen consumption, the pain in the precordial area, and quickly relieved after taking or sublingual nitroglycerin.

1 Initial angina pectoris: also known as recent angina pectoris, that is, the first occurrence of exertional angina in the last month; also includes patients with stable angina pectoris, has not had pain in the precordial area for several months, is now recurring, time is not up to 1 Months.

2 stable angina pectoris: recurrent angina pectoris, and no significant change in nature, lasted 1 to 3 months, the frequency, extent, time limit of angina pectoris and the degree of fatigue induced pain, and significant response to nitroglycerin.

3 worsening angina pectoris: also known as increased angina pectoris, that is, stable angina pectoris, increased angina pectoris and seizure frequency in the last 3 months, prolonged pain time and frequent changes in predisposing factors, often caused by low myocardial oxygen consumption Angina pectoris, suggesting a progressive deterioration of the condition.

(2) Spontaneous angina pectoris: There is no obvious relationship between the onset of angina pectoris and the increase of myocardial oxygen consumption. The pain is heavier and longer, and it is not easy to be relieved by sublingual nitroglycerin. The ECG often has a transient ST-T wave. Change, but not with serum enzyme changes.

1 lying angina pectoris: often occurs in the middle of the night when sleeping, may be due to dreams, nighttime blood pressure fluctuations or supine position to increase venous return, causing cardiac insufficiency, resulting in coronary perfusion and increased myocardial oxygen consumption, severe cases can develop For myocardial infarction or sudden cardiac death.

2 variant angina pectoris: usually at a fixed time of day and night, spontaneous episodes of precordial pain, angina pectoris, seizures, electrocardiogram, ST-segment elevation, and ST-segment depression in the dorsal lead, often accompanied by severe ventricular Arrhythmia or atrioventricular block.

3 intermediate syndrome: also known as coronary dysfunction or angina pectoris, patients often have spontaneous angina during rest or sleep, and severe pain, can last up to 30min, but no myocardial infarction ECG and serum enzymes Variety.

4 post-infarction angina pectoris: spontaneous recurrent angina pectoris within 1 to 3 months after the onset of acute myocardial infarction, usually infarct-related coronary recanalization (incomplete obstruction) or collateral circulation, resulting in "incomplete obstruction "The still surviving but ischemic myocardium causes angina pectoris, and post-infarction angina can also be caused by multiple coronary lesions.

Initial sensation, deteriorating and spontaneous angina are collectively referred to as unstable angina.

(3) mixed angina pectoris: angina pectoris occurs during rest and fatigue, often due to severe or narrow coronary stenosis, resulting in sudden and transient reduction of coronary blood flow, the latter may be due to a large epicardium Excessive sensitivity of the coronary arteries, increased tension in the subcapsular atherosclerotic plaque, platelet thrombosis temporarily blocked blood vessels, vasoconstriction and obstruction combined with changes in vascular tone at small vessels.

3. Myocardial infarction coronary heart disease is a serious clinical manifestation of coronary heart disease. The basic cause is plaque rupture, bleeding, vasospasm, platelet adhesion, aggregation, clotting factor involvement, thrombosis. Formation and vascular lumen obstruction, causing myocardial ischemic necrosis, clinical manifestations of persistent severe precordial pain, accompanied by typical electrocardiogram and serum enzyme concentration sequence changes, according to ECG findings, acute myocardial infarction can be divided into transmural, Q Wave myocardial infarction and subendocardial, non-penetrating, no Q-wave myocardial infarction, the former showed abnormalities, persistent pathological Q wave or QS wave and ST segment linear back up, the latter showed no pathological Q Waves have ST-segment elevation or depression and T-wave inversion. Sometimes the pain in the precordial area can be mild or even absent, while other symptoms are mainly manifested as heart failure, shock, syncope, and arrhythmia.

In the recovery period of acute myocardial infarction, some patients may present with spontaneous chest pain, sometimes accompanied by ECG changes, such as increased serum enzymes, may be an extension of acute myocardial infarction, such as no new serum enzyme changes, some cases can be Diagnosis is post-infarction syndrome, some are spontaneous angina pectoris. Other diagnostic methods are helpful to establish a definitive diagnosis. The ST segment of acute myocardial infarction is rapidly decreased or the pathological Q wave self-resolved during recovery. Regarding coronary recanalization, ventricular function was less impaired. Conversely, ST-segment elevation after 2 weeks of acute myocardial infarction often showed severe abnormalities in wall motion in the infarcted area or bulging in the infarct area, and ventricular aneurysm formation.

4. Heart failure and arrhythmia coronary heart disease, also known as myocardial sclerosis type coronary heart disease, this type of coronary heart disease is caused by myocardial necrosis or long-term blood supply deficiency, resulting in fibrous tissue hyperplasia, its clinical features are gradually increased heart, heart failure occurs And arrhythmia, often referred to as ischemic cardiomyopathy, it must be noted that the majority of patients with ischemic cardiomyopathy have a history of myocardial infarction and angina pectoris, indicating that these patients have severe coronary lesions, only a few patients can be no significant The symptoms of angina or history of myocardial infarction are confirmed by coronary angiography in these patients.

5. Sudden-type coronary heart disease refers to natural occurrence and unexpected death. The World Health Organization stipulates that the death of the person within 6 hours after the onset is sudden death. Most authors claim to be 1h, but others claim that the death within 24h after the onset also belongs to sudden death. More than half of the sudden cardiac deaths are caused by coronary heart disease. On the basis of atherosclerosis, coronary artery spasm or coronary circulatory obstruction leads to acute myocardial ischemia, causing local ECG instability and transient severe arrhythmia. (especially ventricular fibrillation), because this type of patient can survive after timely rescue, the World Health Organization believes that this type is called "primary cardiac arrest coronary heart disease" is appropriate.

Sudden-type coronary heart disease occurs in the winter, patients are generally young, can suddenly occur in a variety of occasions, half of patients are asymptomatic before birth, most patients have no prodromal symptoms before onset, some patients have aura symptoms of myocardial infarction.

Examination of coronary atherosclerotic heart disease

The biochemical examination of coronary heart disease varies according to different clinical types, and generally includes:

Laboratory inspection

1. The performance of serum hyperlipoproteinemia (cholesterol, triglyceride, LDL-C increased), blood sugar increased.

2. If myocardial infarction occurs, abnormalities in serum myocardial enzyme test (creatine kinase, lactate dehydrogenase, glutamate oxaloacetate transaminase increase; especially CK-MB increase, LDH1/LDH2>1, etc.) may have diagnostic value. .

3. Serum myoglobin and troponin can be increased during myocardial infarction.

Film degree exam

1. Electrocardiogram reflects the electrical activity of the heart, and has a high sensitivity and important diagnostic significance in the diagnosis of arrhythmia, myocardial ischemia, myocardial infarction (position, extent, depth, etc.) of coronary heart disease.

2. Dynamic electrocardiogram Because DCG can continuously record the electrocardiogram of patients in daily life without the influence of receptor position, it can capture short-term arrhythmia and transient myocardial ischemia that cannot be recorded by patients with conventional electrocardiogram. Symptoms Myocardial ischemia, angina pectoris, arrhythmia diagnosis and evaluation of drug efficacy play an important role.

3. Electrocardiogram exercise test This test increases the cardiac load by exercise and increases the oxygen consumption of the heart. When the exercise reaches a certain load, the myocardial blood flow of patients with coronary artery stenosis does not increase with the amount of exercise, that is, myocardial ischemia occurs, in the electrocardiogram. Corresponding changes have occurred in the diagnosis of asymptomatic myocardial ischemia; the prognostic evaluation of acute myocardial infarction is meaningful.

4. Cardiac drug load test Some drugs such as dipyridamole, adenosine, dobutamine can increase heart rate, increase myocardial oxygen consumption or "coronary blood stealing" induces myocardial ischemia, causing angina or The ST segment of the electrocardiogram is changed. Using the characteristics of these drugs, the drug load test is performed on those who are suspected of having coronary heart disease but cannot be exercised due to frail or physical defects, thereby improving the diagnosis rate.

5. Transesophageal atrial pacing load test The electrode catheter is placed at the level of the left atrium of the esophagus near the heart. The pulsed pacing atrium is issued by a programmed cardiac stimulator to accelerate the heart rhythm, thereby increasing the oxygen consumption of the heart and inducing myocardial ischemia.

6. X-ray films can show pulmonary congestion, pulmonary edema and cardiac-left ventricular enlargement secondary to myocardial ischemia and/or myocardial infarction, and have important implications for disease assessment and prognosis assessment, for some mechanical concurrency Symptoms such as ventricular aneurysm, interventricular septal perforation (rupture), and diagnosis of dysfunction or fracture of the papillary muscles are also helpful.

7. Coronary angiography (including left ventricular angiography) is still a reliable method for diagnosing coronary heart disease, selecting indications for surgical and interventional treatment of patients with coronary heart disease, using a catheter according to the coronary anatomy, inserting and delivering the catheter through the peripheral artery. To the coronary artery opening, the contrast agent is directly injected into the left and right coronary arteries, showing the anatomy of the coronary artery and its branches, the lesion site and the extent of the lesion.

8. Cardiac CT, magnetic resonance imaging, multi-slice spiral CT coronary angiography MRI is a non-invasive technique for the diagnosis of coronary stenosis (>50%) and CABG vascular occlusion, the choice of indications for coronary stenosis intervention and intervention Both the follow-up after surgical treatment and the observation of its efficacy have preliminary and good value.

9. Echocardiography is an indispensable means of diagnosing coronary heart disease. It is widely used in clinical diagnosis, intraoperative observation, postoperative and drug treatment evaluation in terms of simple, non-invasive and reproducible.

10. Nuclide imaging myocardial perfusion imaging is the most valuable non-invasive method for screening coronary angiography. Negative myocardial perfusion imaging can basically exclude coronary lesions, simple myocardial ischemia, visible in myocardial imaging of the load. There is a significant radioactive sparse (reduced) or defect area in the myocardial segment distributed along the coronary artery. On the resting imaging, the local part is radioactively filled, which proves that the myocardial segment is ischemic. Coronary angiography, to determine the location of coronary stenosis, to determine the treatment plan, in addition, this test also for the diagnosis of myocardial infarction, myocardial infarction with ventricular aneurysm; assessment of viable myocardium, evaluation of revascularization and coronary heart disease prognosis Etc. is also an important means of inspection.

Diagnosis and diagnosis of coronary atherosclerotic heart disease

Diagnostic criteria

1. Classification criteria of the World Health Organization (WH0) Over the past 20 years, there have been many clinical classification methods for coronary heart disease. The most common application is the standard set by the World Health Organization (WHO) in 1979. According to its standards, Coronary heart disease is divided into the following five types:

(1) Primary cardiac arrest: refers to primary cardiac arrest caused by unstable ECG. Most of the primary cardiac arrest is ventricular fibrillation. Failure to recover may cause sudden death. Previous diagnosis of coronary heart disease may have No, if there is no witness in the event of sudden death, the diagnosis is speculative.

(2) angina:

1 labor-type angina pectoris: refers to the short-term chest pain episodes induced by exercise or other increase in myocardial oxygen consumption, rest or nitroglycerin can be quickly relieved, labor-type angina is divided into three types:

A. Initial labor angina: refers to the duration of labor-type angina within 1 month.

B. Stabilizing labor-type angina: refers to the stable course of labor-type angina for more than 1 month.

C. Deterioration of labor-type angina: refers to the number of chest pain episodes induced by the same level of labor, the severity and duration of sudden increase.

2 self-style angina pectoris: it is characterized by no significant relationship between the onset of chest pain and the increase of myocardial oxygen demand. Compared with labor-type angina pectoris, this pain generally lasts longer, is more severe, and is not easily relieved by nitroglycerin. Characteristic changes in enzymes, ECG often have temporary ST-segment depression or T-wave changes. Self-style angina can occur alone or in combination with labor-type angina. Some patients with spontaneous angina have temporary ST-segment elevation at the onset. , called varicose angina.

Initial labor-type angina, worsening labor-type angina and spontaneous angina are often referred to as "unstable angina", and these reports use these specific names.

(3) Myocardial infarction:

1 acute myocardial infarction: its clinical diagnosis is often based on medical history, ECG and serum enzyme changes.

A. History: A typical medical history is severe and persistent chest pain. Sometimes the medical history is not typical. The pain may be mild or not. It may be mainly symptoms of other systems, such as toothache or right flank pain.

B. Electrocardiogram: The affirmative change is an abnormality, a persistent Q wave or Qs wave, and an evolutionary damage current lasting more than one day. When these affirmative changes occur in the electrocardiogram, the diagnosis can be made only by the electrocardiogram, and others. Cases, electrocardiography is an affirmative change, including: static damage current, T wave symmetry inversion, a pathological Q wave in a single ECG recording, conduction disorder.

C. Serum enzymes: Affirmative changes include sequence changes in serum enzyme concentrations, or initial and subsequent reductions, which must be closely related to the specific enzyme and the onset of symptoms and the timing of taking blood samples. The increase in the enzyme (CPK-MB) is also considered to be a positive change, and the uncertainty change is the increase in concentration at the beginning, but without the subsequent decrease, the curve of enzyme activity cannot be obtained.

D. Affirmative Acute Myocardial Infarction: If a positive electrocardiographic change and/or a positive enzyme change occurs, a clear acute myocardial infarction can be diagnosed, with a typical or atypical history.

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