Coronary artery spasm

Introduction Coronary artery spasm refers to a group of clinical syndromes in which the subepithelial conduction artery undergoes a transient contraction, causing partial or complete occlusion of the blood vessels, leading to myocardial ischemia. Coronary artery spasm is the basic cause of various cardiac ischemic diseases, including variant angina pectoris, unstable angina pectoris, acute myocardial infarction, and sudden death. Coronary spasm easily occurs in atherosclerotic coronary arteries, occasionally in the "normal" coronary arteries, and any one or more branches can be affected.

Cause

The mechanism of coronary artery spasm can be divided into two aspects: neural mechanism and body fluid mechanism. From the perspective of neural mechanisms, central nervous and autonomic nerve activities play an important role in the occurrence of coronary artery spasm. Coronary artery spasm can be induced when the state of psychological stress (such as excessive excitement, nervousness, anxiety, panic, etc.), or cold stimulation, strenuous exercise, excessive sympathetic excitation, and local hypersensitivity of the coronary artery. Coronary spasm can also be induced when using beta blockers or epinephrine. From the humoral mechanism, between thromboxane (TXA2) and prostaglandin (PGI2), endothelin (EDCF) and endothelium-derived relaxing factor (EDRF), local balance is an important factor in regulating blood vessel diameter. When coronary atherosclerosis, the number of platelets in the stenotic vessels increases, due to endothelial detachment, platelets adhere to aggregate, release TXA2 and serotonin, and the reduction of PGI2 synthesis in the atherosclerotic wall, there is a strong vasoconstriction. The increase in TXA2 and the decrease in PGI2 with vasodilating effect, the two lose balance and cause coronary spasm. At the same time, the EDRF synthesis of the diseased vessel wall is reduced, and the production of EDCF with obvious vasoconstriction is increased, and coronary artery spasm is also easily induced. Studies have shown that the effects of Ca, H+, and Mg, as well as smoking and drinking, can cause central nervous system and autonomic dysfunction, thereby inducing coronary spasm. Of course, a narrow coronary artery must be a semilunar or eccentric lesion with a contractile capacity on the contralateral wall. In the case of severe concentric lesions, the smooth muscle of the wall is atrophied, and the plaque stiffness is irreversible, and no sputum occurs. Thus, coronary artery spasm is the result of a combination of factors.

an examination

Related inspection

Electrocardiogram coronary angiography coronary CT examination of anti-acetylcholine receptor antibody

The main clinical manifestation of CAS is variant angina pectoris, that is, angina pectoris with resting state and transient ST-segment elevation of ECG. In recent years, it has been found that patients with typical angina pectoris are rare. Even in patients with typical angina who are in a quiet state, ST-segment elevation is not recorded on the dynamic electrocardiogram; however, chest tightness occurs at rest. In patients with chest pain, the CAS challenge test can induce similar symptoms of usual symptoms. Coronary angiography shows obvious CAS, indicating that CAS is the cause of angina at rest. The standard lead electrocardiogram has no ST-segment elevation, indicating that the clinical manifestations of CAS are mostly atypical variant angina. Whether or not CAS with ST-segment elevation may depend mainly on the degree of coronary artery spasm. Non-complete occlusion tendon is often characterized by ST-segment depression or T-wave changes. Only severe sputum causes ST-segment elevation when the vessel is nearly completely occluded. In addition, the collateral circulation and occlusion stenosis time established by long-term repeated sputum may also be the reason why the ST segment does not rise. Based on this, we divide CAS into two types, typical and atypical.

Differential diagnosis

Acute pericarditis

In particular, acute non-specific pericarditis can have more severe and persistent precordial pain, and ECG has ST segment and T wave changes. However, patients with pericarditis have fever and white blood cell counts at the same time as or before pain. Pain is often aggravated by deep breathing and coughing. Physical examination can find pericardial friction sounds. The condition is generally worse than myocardial infarction. Electrocardiogram except aVR, lead All of the ST segments have a downward back and no abnormal Q waves appear.

Acute pulmonary embolism

Large pulmonary embolism can often cause chest pain, shortness of breath and shock, but there is a sharp increase in right heart load. For example, the right ventricle increases sharply, the pulmonary valve area beats and the second heart sounds hyperthyroidism, and the systolic murmur in the tricuspid area. Fever and leukocytosis occur earlier. The electrocardiogram shows that the electric axis is right-biased, the S-wave or the original S-wave is deepened in the I lead, the Q-wave and the T-wave are inverted in the III lead, the high-R wave appears in the aVR lead, and the chest lead transition zone is shifted to the left, left T-wave inversion of the chest lead, etc., is different from the change of myocardial infarction and can be identified.

acute abdomen

Acute pancreatitis, perforation of peptic ulcer, acute cholecystitis, gallstones, etc., patients may have upper abdominal pain and shock, which may be confused with the pain of the upper abdomen in patients with acute myocardial infarction. However, careful medical history and physical examination are not difficult to identify, and electrocardiogram and serum myocardial enzyme assay can help to confirm the diagnosis.

Aortic dissection

It starts with severe chest pain and resembles an acute myocardial infarction. However, the pain reaches the peak at the beginning, often radiating to the back, ribs, abdomen, waist and lower limbs. The blood pressure and pulse of the upper limbs may be significantly different. A few have aortic regurgitation, and may have temporary paralysis or hemiplegia of the lower limbs. X-ray chest X-ray, CT, echocardiography to detect the liquid in the aortic wall sandwich can be identified.

The main clinical manifestation of CAS is variant angina pectoris, that is, angina pectoris with resting state and transient ST-segment elevation of ECG. In recent years, it has been found that patients with typical angina pectoris are rare. Even in patients with typical angina who are in a quiet state, ST-segment elevation is not recorded on the dynamic electrocardiogram; however, chest tightness occurs at rest. In patients with chest pain, the CAS challenge test can induce similar symptoms of usual symptoms. Coronary angiography shows obvious CAS, indicating that CAS is the cause of angina at rest. The standard lead electrocardiogram has no ST-segment elevation, indicating that the clinical manifestations of CAS are mostly atypical variant angina. Whether or not CAS with ST-segment elevation may depend mainly on the degree of coronary artery spasm. Non-complete occlusion tendon is often characterized by ST-segment depression or T-wave changes. Only severe sputum causes ST-segment elevation when the vessel is nearly completely occluded. In addition, the collateral circulation and occlusion stenosis time established by long-term repeated sputum may also be the reason why the ST segment does not rise. Based on this, we divide CAS into two types, typical and atypical.

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