Section 2: Coronary Heart Disease

Prevent and treat respiratory infections and rheumatic activity, avoid overexertion and the use of various drugs that suppress myocardial contractility, control all types of arrhythmias, and treat any complications that may affect cardiac function (such as pleural or abdominal effusions).
Section 2: Coronary Heart Disease
Coronary atherosclerotic heart disease, abbreviated as CHD, refers to ischemic heart disease caused by narrowing or obstruction of the coronary artery lumen due to atherosclerosis or accompanying spasm, also known as ischemic heart disease.
Causes and Risk Factors
The exact causes are not yet fully determined; this disease is multifactorial, resulting from the combined effects of multiple factors at different stages. The main risk factors include:

1. Dyslipidemia
   Abnormal lipid metabolism is the most important risk factor for atherosclerosis. Elevated total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL), or very-low-density lipoprotein (VLDL), along with reduced high-density lipoprotein (HDL), are all considered risk factors. In clinical practice, elevated TC and LDL are of particular concern.
2. Hypertension
   Hypertension is closely related to this disease. Approximately 60%–70% of patients with coronary atherosclerosis have hypertension, and hypertensive patients are 3–4 times more likely to develop this disease than those with normal blood pressure. Both systolic and diastolic hypertension are closely associated with the disease.
3. Smoking
   Compared with non-smokers, smokers have a 2–6 times higher incidence and mortality rate of this disease, and the risk increases proportionally with the number of cigarettes smoked per day. Passive smoking is also a risk factor.
4. Diabetes and Impaired Glucose Tolerance
   Among diabetic patients, the incidence of this disease is several times higher than among non-diabetics, and the disease progresses rapidly. Impaired glucose tolerance is also very common in patients with this disease.
5. Age and Gender
   Men aged 45 or older and women aged 55 or older, or women who experience early menopause without estrogen supplementation, have an increased risk of developing the disease; in recent years, there has been a trend toward younger onset. Compared with men, women have a lower incidence, but the incidence increases after menopause. Age and gender are immutable risk factors.
6. Family History
   If there is a family member under the age of 50 who has developed this disease, the risk for close relatives is five times higher than for families without such a history. Familial hyperlipidemia caused by autosomal dominant inheritance is a factor that makes these family members more susceptible to the disease. In addition, in recent years, more than 200 susceptibility or mutation genes associated with human atherosclerosis risk factors have been cloned.
7. Other Risk Factors
   ① Obesity. ② Sedentary lifestyle with intense mental work and frequent feelings of work pressure. ③ Western dietary habits—regular consumption of high-calorie foods rich in animal fats, cholesterol, sugar, and salt. ④ A-type personality characterized by impatience, competitiveness, strong drive, and difficulty balancing work and rest.
   In recent years, it has been proposed that when obesity coexists with dyslipidemia, hypertension, diabetes, and impaired glucose tolerance, it is referred to as “metabolic syndrome,” which is an important risk factor for this disease. Newly discovered risk factors also include: ① Elevated homocysteine levels in the blood. ② Increased insulin resistance. ③ Elevated fibrinogen and certain coagulation factors in the blood. ④ Viral and chlamydial infections.
   II. Classification
   In 1979, the World Health Organization classified coronary heart disease into five types: ① Silent or asymptomatic coronary heart disease. ② Angina pectoris. ③ Myocardial infarction. ④ Ischemic cardiomyopathy. ⑤ Sudden death. In recent years, based on differences in clinical characteristics and treatment principles, it has been divided into two major categories: ① Chronic coronary artery disease (CAD), also known as chronic myocardial ischemia syndrome (CIS). ② Acute coronary syndrome (ACS). The former includes stable angina, ischemic cardiomyopathy, and silent coronary heart disease, while the latter includes unstable angina (UA), non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction.
   III. Angina Pectoris
   Angina pectoris is a clinical syndrome caused by temporary, acute myocardial ischemia and hypoxia due to insufficient coronary blood supply. It is characterized by sudden, oppressive chest pain behind the sternum, accompanied by a feeling of tightness and discomfort, which may radiate to the left shoulder and upper limb. There are certain triggers, but symptoms can be quickly relieved by rest or nitroglycerin.
   (---) Causes and Pathogenesis
   Atherosclerosis of the coronary arteries leads to narrowing or occlusion of the arterial lumen, reducing the vessel's ability to dilate and decreasing blood flow, which can only meet the myocardium's oxygen demand under normal circumstances. When there is excessive exertion, emotional excitement, or sudden coronary spasm, as well as shock or tachycardia, the coronary blood flow suddenly decreases, failing to meet the myocardium's metabolic needs and leading to temporary, acute myocardial ischemia and hypoxia.
   The pathogenesis of unstable angina is due to rupture of the fibrous cap covering the atherosclerotic plaque, causing platelets to adhere and form a thrombus that blocks the coronary artery. The direct cause of pain may be that, during ischemia and hypoxia, excessive accumulation of acidic metabolic products such as lactic acid, pyruvic acid, and phosphoric acid, or peptide substances similar to kinins, stimulates the afferent nerve endings of the autonomic nerves within the myocardium, transmitting signals to the brain and causing pain.
   (2) Clinical Manifestations
8. Symptoms
   The main clinical manifestation of angina is episodic chest pain, characterized by: (1) Location: Episodic chest pain, usually located behind the middle and upper part of the sternum, possibly radiating to the left shoulder and upper limb. Atypical cases may present with pain in the upper abdomen, left or right anterior chest, neck, or below the xiphoid process; the nature of the pain may be burning or distending.
   (2) Nature
   It is a dull, oppressive, constricting, and gripping pain, often accompanied by a feeling of suffocation or impending death.
   (3) Triggers
   Physical activity, mental stress, overeating, cold stimulation, fatigue, smoking, shock, etc.
   (4) Duration
   The duration is brief, usually 1–5 minutes, rarely exceeding 15 minutes.
   (5) Relief
   Symptoms generally subside after stopping the activity that triggered them, or can be quickly relieved by taking nitroglycerin.
9. Physical Signs
   Generally, no abnormal signs are observed in daily life. During an attack, tachycardia, elevated blood pressure, anxious expression, cold skin or sweating are common, and sometimes a fourth or third heart sound—a gallop rhythm—may appear.
   (3) Laboratory and Other Examinations
   ① Blood glucose and lipid tests can assess risk factors for coronary heart disease; patients with obvious chest pain should undergo serum cardiac injury marker testing, including cardiac troponin I or T, creatine kinase (CK), and CK-MB; complete blood count should check for anemia, and thyroid function tests should be performed when necessary.
   ② Electrocardiogram, exercise stress test, dynamic electrocardiogram, echocardiography, and coronary angiography are also recommended.
   (4) Diagnosis
   Diagnosis: Patients with typical angina symptoms are relatively easy to diagnose. If objective evidence of myocardial ischemia can be obtained, the diagnosis becomes clear. Currently, the electrocardiogram remains the most commonly used and valuable non-invasive diagnostic tool for detecting myocardial ischemia. Combining the electrocardiogram with a stress test or continuous 24-hour dynamic electrocardiogram can help diagnose patients with atypical symptoms. Those with the means can also opt for radionuclide scanning or coronary angiography.
   (5) Treatment
   Treatment primarily focuses on preventing the occurrence and progression of new atherosclerosis and treating existing atherosclerotic lesions. The treatment principle is to improve coronary blood supply and reduce myocardial oxygen consumption to alleviate symptoms, improve quality of life, prevent myocardial infarction and death, and prolong survival.
10. General Treatment
    ① Stop activity and rest quietly.
    ② Adjust diet and reduce mental burden. ③ Administer oxygen and use sedatives as needed.
11. Pharmacological Treatment
    The goal is to terminate angina attacks and prevent recurrence.
    ① Anti-ischemic drugs: Including nitrates, beta-blockers, and calcium channel blockers.
    ② Antiplatelet therapy. ③ Anticoagulant therapy.
    ④ Lipid-lowering therapy.
12. Revascularization Therapy
    Whether to adopt conservative medical treatment or revascularization therapy (including percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG)) should be determined comprehensively based on the anatomical characteristics of the coronary lesions, the patient's clinical features, and the surgical experience of local medical centers.
    IV. Myocardial Infarction (MI)
    Acute myocardial infarction is caused by acute occlusion of the coronary artery, leading to localized necrosis of part of the myocardium due to severe, persistent ischemia. Clinically, it presents with sudden, severe, and persistent chest pain, acute circulatory dysfunction, systemic reactions from necrotic myocardium, as well as a series of characteristic electrocardiographic and serum enzyme changes reflecting acute myocardial ischemia, injury, and necrosis. This disease was previously common in Europe and America. According to data from China's cardiovascular disease reports, the incidence of MI is steadily increasing, and the overall mortality rate is also rising.
    (---) Causes and Pathogenesis
13. Basic Cause of Myocardial Infarction
    Severe narrowing of the coronary artery lumen due to atherosclerosis.
14. Factors Increasing Myocardial Oxygen Consumption
    Overwork, mental stimulation, overeating, straining during defecation, tachycardia, massive hemorrhage, hypotension, etc.
15. Direct Causes of Coronary Occlusion and Myocardial Necrosis
    Thrombus formation within the coronary artery; bleeding and rupture of atherosclerotic plaques leading to platelet aggregation and thrombus formation; coronary spasm causing occlusion of the coronary artery.
16. Severe Arrhythmias, Heart Failure, and Shock Following Myocardial Infarction, Further Reducing Coronary Perfusion and Expanding the Area of Necrosis
    (2) Pathology and Pathophysiology
17. Coronary Artery Lesions
    In the vast majority of MI patients, thrombi are found within the coronary arteries on top of atherosclerotic plaques, causing occlusion of the lumen. However, among those whose lumen is occluded due to coronary spasm, some may not have severe atherosclerotic lesions. In addition, the occurrence of infarction is not necessarily proportional to the number of coronary vessels affected by atherosclerosis and the degree of lumen narrowing they cause.
    (1) Occlusion of the Left Anterior Descending Artery
    Causes necrosis of the anterior wall, apex, inferior wall, anterior interventricular septum, and anterior papillary muscle of the mitral valve in the left ventricle.
    (2) Occlusion of the Right Coronary Artery
    Causes necrosis of the diaphragmatic surface, posterior interventricular septum, and right ventricle, and may also involve the sinoatrial node and atrioventricular node.
    (3) Occlusion of the Left Circumflex Artery
    Causes necrosis of the lateral wall, diaphragmatic surface, and left atrium of the left ventricle. May also involve the atrioventricular node.
    (4) Occlusion of the Left Main Coronary Artery
    Causes extensive necrosis in the left ventricle.
18. Myocardial Lesions
    After coronary occlusion, within 20–30 minutes, the corresponding myocardial area will undergo necrosis; within 1–2 hours, the vast majority of the myocardium will exhibit coagulative necrosis. Subsequently, the necrotic myocardium gradually dissolves, forming myositis foci, followed by granulation tissue formation.
19. Pathophysiology
    Primarily involves changes in ventricular systolic and diastolic function, as well as the resulting hemodynamic changes, the extent of which is related to the location and extent of the infarct.
    (3) Clinical Manifestations
    Closely related to the size and location of the infarct, as well as the status of collateral circulation in the coronary arteries.
20. Prodromal Symptoms
    About one-half to one-third of patients experience prodromal symptoms, manifested as prolonged fatigue, chest tightness, palpitations, irritability, and angina. Among these, the most common is the transformation of previously stable angina into unstable angina; or, for those who never had angina before, sudden onset of angina with frequent, severe, and prolonged attacks, accompanied by decreased efficacy of nitroglycerin, abnormal ST segment elevation or depression on the electrocardiogram, inverted or elevated T waves.
21. Major Symptoms and Physical Signs
    (1) Pain
    This is the earliest and most prominent symptom, often occurring in the early morning without obvious triggers. Its nature and location are similar to angina, but the intensity is much greater, often presenting as unbearable crushing and suffocating sensations, even accompanied by a sense of impending death, profuse sweating, and extreme restlessness. The duration is 1–2 hours, or up to 10 hours, sometimes fluctuating for several days. Nitroglycerin is ineffective, requiring narcotic analgesics to relieve the pain. The pain is mostly located behind the sternum and covers a wide area, often involving the entire anterior chest; about 10% of cases also involve the area below the xiphoid process and the upper abdomen, with radiation to the left and upward.
    (2) Systemic Symptoms
    Fever (body temperature usually around 38°C), generally appearing 24–48 hours after the infarction and lasting about a week. This is absorption fever, positively correlated with the area of infarction.
    (3) Gastrointestinal Symptoms
    Obvious nausea, vomiting, and upper abdominal distension; in severe cases, hiccups occur, particularly in cases of inferior wall myocardial infarction. These symptoms arise because necrotic tissue stimulates the vagus nerve and insufficient tissue perfusion.
    (4) Arrhythmias
    Very common, occurring within 3 days of onset, with an incidence rate exceeding 90%, making it one of the main causes of death in the acute phase. The most common is ventricular ectopic rhythm (including frequent ventricular premature beats, paroxysmal ventricular tachycardia, and ventricular fibrillation), which is most likely to occur within 24 hours of onset. Frequent (5 times/min), multi-source, paired occurrences, or ventricular premature beats where the R wave falls on the T wave may be precursors to ventricular fibrillation.

(5) Hypotension and Shock
Severe pain is often accompanied by a drop in blood pressure, though not necessarily shock. However, even after the pain subsides, systolic pressure may still remain below 80 mmHg.

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