I. Occult coronary artery disease: The patient has coronary A atherosclerosis, but the lesion is mild or not mild but has good collateral circulation or the patient has a high pain threshold and therefore no pain symptoms, and the manifestation of myocardial ischemia such as ECG or radionuclide myocardial imaging may appear before resting or only when the heart load is increased. 24h ambulatory ECG often records no change in myocardial ischemia, but the patient is asymptomatic at this time. This is called asymptomatic myocardial ischemia. This condition can be seen in patients with this type of disease as well as in patients with angina pectoris. Yang Ming, Department of Traditional Chinese Medicine, Henan Provincial People’s Hospital
This type can be considered as early coronary heart disease, but not necessarily early coronary A atherosclerosis, which may suddenly turn into angina pectoris or infarction, or gradually evolve into myocardial fibrosis with heart enlargement, heart failure, arrhythmia and sudden death. Diagnosis of such patients can provide them with the opportunity for earlier treatment.
[Diagnosis and differential diagnosis] ECG, cardiac vector, ambulatory ECG and active plate or radionuclide examination (ECT). Differentiation: ① Cardiac neurosis: This disease is mostly caused by central nervous system dysfunction, which affects autonomic function and causes abnormal cardiovascular function. Among the types with increased excitability of adrenergic β receptors, patients mostly show mental stress and increased heart rate, their myocardial oxygen consumption ↑, the ECG appears ST depression and T inversion and other changes but the disease is mostly in middle-aged and young women, and can be differentiated by the insulin test. ② various organic heart disease, especially myocarditis, cardiomyopathy, pericardial disease, dielectric disorders, endocrinopathies and drug effects can appear in the electrocardiogram ST and T changes.
Angina pectoris: angina pectoris is a clinical syndrome caused by insufficient coronary A blood supply and acute, temporary ischemia and hypoxia of the myocardium. Features: paroxysmal anterior chest crushing pain sensation, may be accompanied by other symptoms, pain is mainly located in the posterior sternum, can be radiated to the precordial area and upper limbs, often occurs when exertion or emotional excitement, lasts for several minutes, disappears after rest or nitrate preparations.
The disease is mostly seen in men, and most patients are over 40 years old. Exertion, emotional excitement, diet, cold, rainy weather, acute circulatory failure, etc. are common triggers.
When the coronary A blood flow cannot meet the needs of myocardial metabolism, causing acute, temporary ischemia and hypoxia of the myocardium, angina is produced. The 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, the myocardium normally receives the maximum amount of oxygen in the blood, and it is difficult to take up more oxygen from the blood when the demand increases again, and only relies on increasing the blood flow in the coronary A to provide. Under normal conditions, the coronary A circulation has a large reserve capacity and its blood flow can vary significantly with the physiological conditions of the body. During strenuous activity, the coronary A dilates appropriately and blood flow can increase up to 6-7 times that at rest, and during hypoxia, the coronary A also dilates and can increase blood flow 4-5 times. When atherosclerosis causes coronary A stenosis or partial branch occlusion, its dilatability is reduced, blood flow is decreased, and the blood supply to the myocardium is relatively fixed. If the blood supply to the myocardium is reduced or can still cope with the usual needs of the heart, it can be asymptomatic at rest. Once the heart load suddenly increases, such as exertion, excitement, left heart failure, etc. The demand for blood from the myocardium increases; or when the coronary A spasm (such as excessive smoking or neurohumoral regulation disorder), the coronary blood flow further decreases, or in the case of a sudden decrease in the amount of circulating blood (such as shock, extreme tachycardia), the myocardial blood supply is insufficient and causes angina pectoris.
The typical angina attack is a sudden onset of crushing, boring or suffocating pain behind the upper or middle part of the sternal body, and may involve most of the precordial region, radiating to the left shoulder, the anterior medial side of the left upper limb, reaching the ring finger and little finger, occasionally accompanied by a fear of dying. It often causes the patient to stop activities immediately, and in severe cases, sweating. The pain lasts from 1 to 5 minutes, rarely more than 15 minutes, and disappears within 1-2 minutes (rarely more than 5 minutes) with rest or nitroglycerin. It often occurs with physical exertion, emotional stress, cold, full stomach, or smoking. The pain may be located in the lower part of the sternum, the left precordial region or the upper abdomen radiating to the neck, jaw, left scapula or the right anterior chest.
Typology: ① Exertional angina: It is induced by exercise or other conditions that increase myocardial oxygen demand (a, stable exertional angina; b, primary exertional angina; c, worsening exertional angina).
②Spontaneous angina: angina attack is not significantly related to myocardial oxygen demand, compared with exertional angina, the pain duration is generally longer and more severe, and it is not easily relieved by nitroglycerin (a, prone angina; b, variant angina; c, intermediate syndrome, d, post-infarction angina).
(iii) Mixed angina: a mixture of the above two.
After the 1990s, the angina pectoris typing was simplified to: ① stable type; ② unstable type; ③ variant type.
Differential diagnosis: 1. Cardiac neurosis; with symptoms of neurasthenia; 2. Acute heart attack; 3. Intercostal pain, involving 1-2 intercostal areas, is persistent rather than episodic, exacerbated by coughing, deep exhalation, turning the body, and localized pulling pain by raising the arm.
3. Myocardial infarction: It is the occlusion of coronary A and interruption of blood flow, causing local necrosis of part of the myocardium due to severe and persistent ischemia. Clinically, there is severe and more persistent retrosternal pain, fever, white blood cell ↑, accelerated blood sedimentation, increased cardiac enzyme activity and progressive electrocardiographic changes, arrhythmia, shock or heart failure may occur.
The incidence of this disease is rare in China in the past, but gradually increased in recent years, urban > rural areas, the incidence rate of 0.2-0.6‰, male > female, domestic data male to female ratio of 1.9:1 to 5:1. 87% to 96.5% of the disease age above 40 years old, female than male 10 years later. The peak age of disease for men is 51-60 years old; for women 61-75 years old. The gap between men and women decreases with age. 60-89% of patients have hypertension before the onset of the disease, and half of them have angina pectoris, smoking, obesity, diabetes, and lack of activity are more prone to the disease. The disease is more frequent in spring and winter, related to the cold climate and temperature changes, most of the onset of the disease without obvious causes, often in quiet or sleep, with the most frequent onset in the morning 6h to 12h noon, some of them occur in strenuous labor, nervousness or after a full meal, in addition to shock, bleeding and tachycardia, forceful defecation can also be induced.
Pathogenesis】In the coronary A atherosclerosis based on complications of atheromatous plaque rupture, hemorrhage, intravascular thrombosis, subintimal hemorrhage or A persistent spasm, so that the lumen quickly occurred lasting and complete occlusion, such as the artery and other coronary A collateral circulation was not fully established, can lead to the A supply of myocardium severe and persistent ischemia, more than 1 h will cause myocardial necrosis.
Pathology】In the acute stage, myocardium shows large focal coagulation necrosis, myocardial interstitial congestion, edema with a large amount of inflammatory cell infiltration, and later the necrotic myocardial fibers are gradually dissolved and absorbed, followed by granulation tissue formation. After 1-2 weeks, the necrotic tissue starts to absorb and gradually fibrosis, and after 6-8 weeks, it enters the chronic phase to form a scar and heal, which is called old myocardial infarction.
Clinical manifestations] There are three phases: acute, subacute and chronic. Clinical manifestations mainly appear in the acute phase, and some have aura symptoms.
1. Aura: sudden or more intense angina pectoris than before, long duration, no obvious trigger, poor efficacy of nitroglycerin, attack with nausea, vomiting, sweating, bradycardia, acute cardiac insufficiency, severe arrhythmia or large fluctuations in blood pressure, etc. In this case, the electrocardiogram ST momentarily significantly elevated or depressed, T-wave inversion or elevation, more attention should be paid!
2. Symptoms: ① Pain is the same as before, but often occurs in quiet or during sleep, with heavy degree and wide range, for several hours or days. Containing nitroglycerin much can not be relieved, the patient is irritable, sweating, fear of a sense of near death. About 1/6 to 1/3 of patients in China have pain of atypical nature and location, such as located in the upper abdomen, often misdiagnosed as an acute abdomen such as gastric ulcer, perforation or acute pancreatitis. If the pain is located in the lower jaw or neck, it is often misdiagnosed as osteoarthritis. Some patients have no pain, mostly diabetic or elderly, and show shock or acute heart failure at the beginning, and a few have no pain throughout, but only afterwards are found to have had a heart attack.
(ii) Systemic symptoms: mainly fever, bradycardia, white blood cell ↑, blood sedimentation ↑, caused by the absorption of necrotic material.
(iii) Gastrointestinal symptoms: 1/3 had nausea, vomiting, epigastric distention and pain, and in severe cases, eruption.
④Cardiac arrhythmias: 75% to 95% have ventricular arrhythmias, especially within 24h.
⑤ hypotension and shock.
⑥Heart failure: mainly acute left heart failure.
3. Signs: mild to moderate enlargement of the turbinate, fast or slow heart rate, diminished apical 1st heart sound, gallop rhythm may appear, and a few have pericardial friction sounds.
Laboratory and special tests
Leukocyte ↑, ESR ↑, cardiac enzyme spectrum ↑, ECG, cardiac vector; ECT; coronary angiography, etc.
Differential diagnosis】Angina pectoris, acute abdomen.
Complications】①Papillary muscle dysfunction or rupture, mainly mitral valve papillary muscle contraction weakness or rupture due to ischemia, necrosis, resulting in incomplete closure, easily causing heart failure.
(ii) Heart rupture: often occurs within a week, resulting in sudden death due to the production of blood accumulation or blockage.
③Ventricular wall expansion tumor: formed when the ventricular wall at the infarct site expands outward under the influence of intraventricular pressure.
④Embolism: caused by the broken and dislodged thrombus of the ventricular appendage.
⑤ Post-myocardial infarction syndrome: it appears after several weeks and months and can recur, manifesting as: pericarditis, pleurisy, and pneumonia with fever, chest pain, shortness of breath, and cough. It may be caused by an allergic reaction of the organism to the necrotic substance.
4. Ischemic cardiomyopathy: It is caused by long-term deficiency of myocardial blood supply due to coronary A atherosclerosis, nutritional disorders and atrophy of myocardial tissue, or repeated local necrosis and healing to fibrous tissue proliferation, also called myocardial fibrosis or myocardial sclerosis. Its clinical characteristics: heart stiffness, gradual enlargement, occurrence of arrhythmia-type and heart failure-type coronary heart disease.
Pathophysiology】The heart is enlarged, more obvious in heart failure, and the myocardium is diffusely fibrotic with hypertrophy and atrophy of cardiomyocytes. The lesion mainly involves the left ventricular muscle and papillary muscle, but also the pacing and conduction system. The patient’s coronary arteries are often extensively and severely atherosclerotic, with marked luminal narrowing but no occlusion, and fibrous tissue is also focally, scattered or irregularly distributed in the myocardium. This condition is often caused by scar formation after infarction or multiple small focal myocardial infarction, which results in a decrease in cardiomyocytes and an increase in fibrous connective tissue, and then the coronary A has occlusive lesions.
Clinical manifestations】1. heart enlargement; 2. heart failure; 3. arrhythmia
Diagnosis and differential diagnosis】The above history and signs, combined with electrocardiogram, can be diagnosed. Differentiation: Cardiomyopathy, myocarditis, hypertension, heart disease, etc.
5. Sudden death: refers to the natural occurrence, unexpected sudden death. The World Health Organization defines sudden death as death within 6h after the onset of the disease. All kinds of heart disease can cause sudden death, but more than half of sudden death in heart disease is caused by coronary heart disease. Sudden death as a type of coronary heart disease is gradually gaining attention. 80s: the annual incidence of sudden death from coronary heart disease in the north is 22.5/100,000 population.
Sudden death coronary heart disease is most common in winter, and it occurs suddenly at home, at work, or in public places, with cardiac arrest and death. Surviving patients have non-isotropic and mild aura symptoms, such as fatigue, chest pain, or mood changes, which do not attract the attention of patients and physicians. In fact, some patients are “healthy” and die during the night in their sleep, only to be discovered the next morning. In some cases, the patient has a precursor symptom of a heart attack. Pathological examination shows that the patient has coronary A atherosclerotic changes, but in most patients no thrombus is seen in the coronary, no occlusion of the A-lumen is seen, and no pathological process of acute heart attack is seen. Since this type of patient may survive, the World Health Organization considers it more appropriate to call it “primary cardiac arrest coronary artery disease”.