Coronary atherosclerotic heart disease
Risk factors
The cause of this disease is not fully understood, and extensive studies have shown that coronary heart disease is a multifactorial disease, caused by multiple factors acting at different points. These factors are called predisposing factors or risk factors and they are
(i) Age The disease is mostly seen in middle-aged and elderly people over 40 years of age, and progresses more rapidly after 49 years of age, but in some autopsies of young adults, their arteries have been found to have early atherosclerotic lesions, suggesting that the lesions have already started at this time.
(B) Gender The disease is more common in men, with a male to female ratio of about 2:1. Women often develop the disease after menopause, when estrogen decreases and blood high-density lipoprotein (HDL) also decreases.
(C) Lipids Abnormal blood lipid content, such as high total cholesterol, triglycerides, low-density lipoprotein (IDL) or very low-density lipoprotein (VLDL), and low high-density lipoprotein (HDL), especially its subgroup II (HDLU), are prone to the disease. In recent years, it is believed that the decrease of apolipoprotein A (apo A) and the increase of apolipoprotein B (apo B) are also causative factors. Recently, increased Lp(a) has been suggested as an independent causative factor.
(iv) Blood pressure Increased blood pressure is closely related to the disease. Fifty to 70% of patients with coronary atherosclerosis have hypertension, and the number of hypertensive patients suffering from this disease is four times higher than that of those with normal blood pressure. Both systolic and diastolic blood pressure increases are important.
(E) Smoking The incidence of the disease and death rate is 2-6 times higher in smokers compared with nonsmokers, and is proportional to the number of cigarettes smoked per day. Passive smoking also increases the risk of coronary heart disease.
(vi) Diabetes mellitus The incidence of this disease is two times higher in diabetic patients than in those with meta-diabetes mellitus, and hypoglycemic patients with this disease are quite common.
(G) weight Obese people who are over the standard weight (10% overweight for light, 20% for medium, 30% for severe obesity) are susceptible to this disease, especially those who gain weight rapidly.
(H) occupation engaged in physical activity less, mental activity, often have a sense of urgency of the work, more likely to get this disease.
(ix) Diet A high-calorie diet containing more animal fat, cholesterol, sugar and salt can lead to dyslipidemia, obesity, hypertension and diabetes mellitus, which are factors that predispose to the disease.
(J) Heredity If a family member has the disease at a younger age, the chances of the next of kin getting the disease can be 5 times higher than those without family history. Familial hyperlipidemia due to autosomal dominant inheritance is often a factor in predisposing these family members to the disease.
(xi) Other Micro-elements chromium, manganese, zinc, vanadium, selenium intake is reduced, lead, cadmium, cobalt intake is increased; impatient, aggressive and competitive temperament, type A personality who is preoccupied with work and does not pay attention to rest and forces himself to strive for achievement; the presence of hypoxia, antigen-antibody complexes, vitamin C deficiency, reduced activity of enzymes in the arterial wall and other factors that can increase vascular factors that increase permeability are considered to predispose to the disease.
Classification of ischemic heart disease ISFC/WHO
(i) Primary cardiac arrest Primary cardiac arrest is an abrupt event, presumed to be caused by electrocardiographic instability; there is no basis for an alternative diagnosis1. If resuscitation is not performed or fails, primary cardiac arrest is sudden death ②. Evidence of previous ischemic heart disease may or may not be available; if no one saw the death when it occurred, the diagnosis is speculative.
(II) Angina pectoris
1, exertional angina Exertional angina is characterized by brief episodes of chest pain induced by exercise or other conditions that increase myocardial oxygen demand, and the pain often disappears rapidly after rest or sublingual nitroglycerin. Exertional angina can be divided into three categories: (1) primary exertional angina: the duration of exertional angina is less than 1 month; (2) stable exertional angina: the duration of exertional angina is stable for more than 1 month; (3) worsening exertional angina: the number, severity and duration of chest pain attacks induced by the same degree of exertion are suddenly aggravated.
①Disability occurring in the early stage of proven myocardial infarction is not included, but should be considered as death due to myocardial infarction.
②The definition of sudden death was purposely omitted from this report. Because sudden death is the result of cardiac arrest.
2, spontaneous angina Spontaneous angina is characterized by episodes of chest pain that are not significantly related to an increase in myocardial oxygen demand. Compared with exertional angina, this pain is generally longer in duration and more severe, and is not easily relieved by nitroglycerin. No changes in serum cardiac enzymes are seen. Some transient ST-segment depression or T-wave changes are often seen on the ECG. Spontaneous angina may occur alone or in combination with exertional angina.
Patients with spontaneous angina can have different clinical presentations depending on the frequency, duration and degree of pain episodes. Sometimes, patients may have episodes of chest pain of longer duration, similar to myocardial infarction, but without characteristic changes in electrocardiogram and enzymes.
Some patients with spontaneous angina present with episodes of transient ST-segment elevation, often referred to as variant angina1. However, this name cannot be applied when this ECG pattern is recorded in the early stages of myocardial infarction.
Initial exertional angina, worsening angina and spontaneous angina are often referred to as “unstable angina”. In this report, these respective specific names are chosen.
(C) myocardial infarction
1, acute myocardial infarction The clinical diagnosis of acute myocardial infarction is often made based on the history, electrocardiogram and serum enzyme changes.
History: The typical history is the presence of severe and persistent chest pain. Sometimes, the history is atypical and the pain can be mild or even absent and can be dominated by other symptoms.
ECG: The definite changes in the ECG are the presence of abnormal, persistent Q or QS waves and evolving injury currents lasting more than l days. When these definite changes are present on the ECG, the diagnosis can be made on the basis of the ECG alone. In other cases, the ECG shows uncertain changes, including: (i) stationary injury current; (ii) symmetrical inversion of the T wave; (iii) a pathological Q wave in a single ECG recording; and (iv) conduction disturbance.
Serum enzymes: ① Definite changes include serial changes in serum enzyme concentrations, or an initial increase and subsequent decrease. Such changes must be associated with the specific enzyme and the time interval between symptom onset and the taking of a blood sample. Elevation of cardiac-specific isoenzymes is considered a definite change. ② Uncertain change is an increase in concentration at the beginning but not accompanied by a subsequent decrease, and a curve of enzyme activity cannot be obtained.
1. Definite acute myocardial infarction A definite acute myocardial infarction can be diagnosed if there are definite electrocardiographic changes and/or definite enzyme changes, and the history can be typical or atypical.
2.Probable acute myocardial infarction When serial and uncertain ECG changes persist for more than 24 hours with or without enzyme uncertainty changes, both can be diagnosed as possible acute myocardial infarction, and the medical history can be typical or atypical.
In recovery from acute myocardial infarction, certain patients may present with spontaneous chest pain, sometimes to be accompanied by ECG changes without new enzyme changes, in some cases diagnosed as Dressler’s post-infarction syndrome, in some patients with spontaneous angina, and in others with recurrent or possibly extended acute myocardial infarction. Other diagnostic measures may be helpful in establishing a definitive diagnosis.
2. Obsolete myocardial infarction Obsolete myocardial infarction is often diagnosed based on definitive ECG changes without a history of acute myocardial infarction and enzyme changes. If there are no legacy ECG changes, the diagnosis can be made based on earlier typical ECG changes or based on previous positive serum enzyme changes.
(iv) Heart failure in ischemic heart disease Heart failure in ischemic heart disease can occur for a variety of reasons; it can be a complication of acute myocardial infarction or earlier myocardial infarction, or it can be precipitated by an angina attack or arrhythmia. In patients with heart failure without clinical or electrocardiographic evidence of previous ischemic heart disease (excluding other causes), the diagnosis of ischemic heart disease is speculative.
(v) Arrhythmia Arrhythmia is not the only symptom of ischemic heart disease. In this case, the diagnosis of ischemic heart disease is speculative unless coronary angiography is performed to prove coronary artery obstruction.
The names “pre-infarction angina” and “intermediate coronary syndrome” are not included in this report. This is because, according to our group’s opinion, the former diagnosis is a recall diagnosis, which can be confirmed in only a few cases, whereas all cases of the latter diagnosis can be classified as one of the ischemic heart disease classifications described in this report.
(1) This ECG presentation could also be called Ptimmaetal angina, but this condition has been reported by other authors before Prinzmetal’s report, so the name “variant angina” is used.
Pathogenesis, clinical manifestations, grading of severity, laboratory tests, diagnosis, differential diagnosis and treatment of angina pectoris
Angina pectoris is a group of symptoms that are caused by transient myocardial ischemia. Myocardial ischemia can be caused by myocardial oxygen demand exceeding the blood supply capacity of the diseased coronary artery (exertional angina); or by reduced coronary blood supply, (spontaneous angina); or both, i.e., angina due to the simultaneous presence of coronary artery tone changes or coronary spasm on top of fixed coronary stenosis (dynamic stenosis) (mixed angina).
The disease is mostly seen in men, and most patients are over 40 years old. Exertion, emotional excitement, satiety, cold, rainy weather, and acute circulatory failure are common triggers. In addition to coronary atherosclerosis, angina can also be caused by aortic stenosis or closure insufficiency, syphilitic aortitis, hypertrophic primary cardiomyopathy, congenital coronary artery malformation, rheumatic coronary arteritis, etc.
(I) Pathogenesis Mechanical stimulation of the heart does not cause pain, but myocardial ischemia and hypoxia cause pain. Angina pectoris occurs when there is a conflict between coronary artery blood supply and myocardial blood demand, and coronary artery blood flow cannot meet the myocardial metabolic needs, causing acute and temporary myocardial ischemia and hypoxia.
The amount of myocardial oxygen consumption is determined by myocardial tone, myocardial contraction strength and heart rate, so “heart rate × systolic blood pressure” (i.e., the product of two) is often used as an index to estimate myocardial oxygen consumption. Myocardial energy production requires a large oxygen supply. Myocardial cells take up 65% to 75% of the oxygen content of the blood, while other tissues in the body take up only 10% to 25%. Therefore, myocardial oxygen uptake in the blood is usually close to the maximum amount, and it is difficult to take in more oxygen from the blood when the oxygen supply needs to be increased again, and it can only be provided by increasing the blood flow in the coronary arteries. Under normal conditions, the coronary circulation has great reserve power, and its blood flow can vary significantly with the physiological condition of the body; during strenuous physical activity, the coronary arteries expand appropriately, and the blood flow can increase to 6-7 times of that at rest; during hypoxia, the coronary arteries also expand, and the blood flow can increase 4 or 5 times. When the coronary arteries are narrowed or partially occluded due to atherosclerosis, their dilatability is reduced, blood flow is decreased, and the amount of blood supply to the myocardium is relatively fixed. If the blood supply to the myocardium is reduced to the extent that it can still cope with the usual needs of the heart, it may be asymptomatic at rest. Once the cardiac load suddenly increases, such as exertion, excitement, left heart failure, etc., the myocardial tension increases (increased chamber volume, increased ventricular end-diastolic pressure), myocardial contractility increases (increased systolic pressure, increased rate of change of maximum pressure over time in the ventricular pressure curve) and heart rate increases, resulting in increased myocardial oxygen consumption, the myocardial demand for blood increases; or when the coronary artery spasm occurs (excessive smoking or neurological disorders such as alpha-adrenergic disorders). When coronary blood flow is further reduced due to spasm (excessive smoking or neurohumoral dysregulation such as alpha-adrenergic neuroexcitation, increased TXA2 or endothelin), or when a sudden decrease in circulating blood flow occurs (e.g., shock, extreme tachycardia, etc.), coronary blood flow is suddenly reduced. The contradiction between myocardial blood supply and demand deepens, and the myocardial blood supply is insufficient, thus causing angina pectoris. In patients with severe anemia, angina pectoris may be caused by insufficient oxygen supply to the myocardium, although the blood supply to the myocardium is not reduced.
In most cases, exertion-induced angina occurs at the same “heart rate x systolic blood pressure” level.
The direct factor of pain sensation may be the accumulation of excessive metabolites in the myocardium, such as lactic acid, pyruvic acid, phosphoric acid and other acidic substances, or peptides similar to kinins, which stimulate the afferent fiber endings of the autonomic nerves in the heart, and then transmit to the brain via 1-5 thoracic sympathetic ganglia and the corresponding spinal cord segments, resulting in pain sensation. This pain sensation is reflected in the skin area distributed by the spinal nerves at the same spinal cord segment as the autonomic nerve entry level, i.e., behind the sternum and the anterior medial side of both arms and the little finger, especially on the left side, but mostly not in the heart area. It is thought that abnormal pulling or constriction of the nerve-rich coronary vessels in the ischemic area can directly produce pain impulses.
(B) Clinical manifestations
1, symptoms Angina pectoris with episodic chest pain as the main clinical manifestation, the pain is characterized by.
(1) Location: mainly in the upper middle part of the sternal body after it can spread to the precordial area, palm-sized range, or even across the anterior chest, the boundaries are not very clear. It often radiates to the left shoulder, the medial side of the left arm up to the ring finger and little finger, or to the neck, pharynx or jaw, teeth, or the posterior back.
(2) Nature: Chest pain is often compressive, stuffy or constricting, and may also have a burning sensation, but not sharp, unlike pinprick or knife-like pain, occasionally accompanied by a fear of dying. During an attack, the patient often unconsciously stops the original activity until the symptoms are relieved.
(3) Triggers: The attack is often triggered by physical exertion or emotional excitement (such as anger, anxiety, overexcitement, etc.), and can also be triggered by satiety, cold, smoking, tachycardia, shock, defecation, etc. The pain occurs at the time of exertion or excitement and not after a day or a bout of exertion. Typical angina often occurs under similar conditions, but sometimes the same exertion causes angina only in the morning but not in the afternoon, suggesting an association with a lower pain threshold in the morning.
(4) Duration The pain is often progressively worse after it appears and gradually disappears within 3-5 min, usually relieved after stopping the activity that originally induced the symptoms. Sublingual nitroglycerin can also provide relief within a few minutes. The attack may occur once in a few days or weeks, or several times in a day.
2. Signs Normally, there are no abnormal signs. During an angina attack, increased heart rate, increased blood pressure, anxious expression, cold skin or sweating are common, and sometimes the fourth or third heart sound gallop rhythm appears. There may be a temporary apical systolic murmur, which is caused by mitral valve incompetence due to ischemia of the papillary muscles, and the second heart sound may have a reverse split or an alternating pulse.
(C) Laboratory and other tests
1.Electrocardiogram is the most common test to detect myocardial ischemia and diagnose angina pectoris.
(1) ECG at rest: about half of the patients are in the normal range, but there may also be changes of old myocardial infarction or non-specific ST segment and T wave abnormalities, and sometimes arrhythmias such as atrioventricular or bundle branch block or ventricular and atrial precontraction.
(2) ECG during angina attack: The majority of patients may present with temporary myocardial ischemia-induced sT-segment shift. The subendocardial myocardium is prone to ischemia; therefore, ST-segment depression of 0 or 1 mV (1 mm) or more is common and recovers after the attack is relieved. Sometimes there is T-wave inversion, and in patients who usually have persistent T-wave inversion, it can become upright during the attack (so-called “pseudo-normalization” or. “Although T-wave changes are less characteristic of myocardial ischemia than the ST segment, they can also help in the diagnosis if they are significantly different from the usual ECG. In variant angina (see below), ST-segment elevation in the relevant leads is commonly seen on the ECG as a “monophasic curve” during the attack, and ST-T returns to normal after the angina subsides.
(3) ECG load test: The most commonly used test is the exercise load test, which increases the burden on the heart to stimulate myocardial ischemia. The exercise is mainly graded pedal or pedal car, the intensity of which can be gradually escalated in stages, the former is more commonly used, so that the subject to face the rotation of the plate on the ground pedal. Exercise can be terminated until the patient has angina or significant fatigue, shortness of breath and other symptoms, called extreme exercise. Currently, it is commonly used in China to achieve 85% to 90% of the maximum heart rate expected to be achieved by age, called submaximal exercise. During the exercise period, 1-2 bipolar chest leads with negative pole placed on the sternal stalk and positive pole placed on the V5 site are used as the main focus. The ECG is monitored and recorded during the exercise oscillometric waveform, immediately after the exercise, and repeatedly recorded at 2, 4, 6 and 8 minutes. Blood pressure should be measured intermittently before, during and after exercise as much as possible. ECG changes were mainly based on ST-segment horizontal or downward-sloping depression t≥0,1mV (0,08 seconds from the J point) as a positive criterion. Exercise should be stopped immediately when gait instability, ventricular tachycardia (more than 3 successive pre-term contractions) or blood pressure drop occurs during exercise. Exercise test is prohibited in the acute phase of myocardial infarction, unstable angina, obvious heart failure, severe arrhythmia or acute disease.
(4) Continuous ECG monitoring: continuous recording of 24-hour ECG in 1-2 bipolar chest leads (dynamic ECG), from which ECG ST-T changes and various arrhythmias can be detected, and the time of appearance can be contrasted with the patient’s activity and symptoms. When there is no ischemic ST-T change in the ECG and there is no angina at that time, it is called asymptomatic myocardial ischemia.
2.Radionuclide examination
(1) 201Tl-myocardial imaging or also as a loading test: 201Tl is quickly taken up by normal myocardium with coronary blood flow. The perfusion defect shown by thallium imaging at rest is mainly seen at the site of scarring after myocardial infarction. In myocardium with inadequate coronary artery supply, significant perfusion deficits are seen only after exercise, and myocardial nuclear imaging at rest can be normalized, called “redistribution”. Patients who cannot exercise can be tested with dipyridamole, which is administered intravenously to dilate normal or more normal coronary arteries, causing “redistribution”.