What Is Variant Angina?

Variant angina pectoris is a type of spontaneous angina pectoris. In 1959, Prinzmetal et al. Named ischemic angina pectoris caused by coronary artery spasm as "variant angina pectoris", and pointed out that the onset of angina pectoris was not related to activity. The pain occurred at rest, the ST segment of the ECG was elevated during the episode, and the ST segment after the episode Decreased without pathological Q waves. More myocardial infarction and death occurred within six months. Variant angina pectoris can cause acute myocardial infarction and severe arrhythmias, and even ventricular fibrillation and sudden death.

Basic Information

English name

variant angina pectoris; Prinzme-tal angina

Visiting department

Cardiology

Common causes

Coronary spasm

Common symptoms

The onset of angina has nothing to do with the activity, and the pain occurs at rest

Causes of variant angina pectoris

Mainly due to coronary spasm.

Causes: Variant angina pectoris often occurs in people who smoke, especially young men who smoke heavily in the short term.

The use of illicit drugs such as cocaine and amphetamines is an important cause of coronary spasm.

Emotional tension and excessive mental stress are also an important cause of coronary spasm. Severe coronary spasm may be one of the important pathogenesis of Tako-tsubo cardiomyopathy.

In addition, endocrine diseases that cause neurohumoral abnormalities such as catecholamine secretion are also rare causes of coronary spasm, such as pheochromocytoma and hyperthyroidism.

Kounis also proposed the concept of "allergic angina pectoris syndrome" and found that patients with allergic reactions may develop symptoms of angina pectoris, because mast cells release a large amount of vasoconstrictor substances and platelet aggregation substances, such as histamine, leukotriene, and thrombosis Alkanes and other substances can not only rupture the original atherosclerotic plaque and cause thrombosis, but also cause normal vasoconstriction and coronary spasm.

In addition, the common predisposing factors of variant angina pectoris include abstinence, cold irritation, and the use of drugs that constrict blood vessels.

Clinical manifestations of variant angina pectoris

It was pointed out that the onset of angina had nothing to do with the activity. The pain occurred during the quiet period, the ST segment of the electrocardiogram was elevated during the episode, and the ST segment decreased after the episode without pathological Q waves. More myocardial infarction and death occurred within six months. Variant angina pectoris can cause acute myocardial infarction and severe arrhythmias, and even ventricular fibrillation and sudden death.

Diagnosis of variant angina pectoris

Patients with resting angina pectoris who are accompanied by transient ST-segment elevation and have no obvious fixed lesions on coronary angiography can be diagnosed as typical variant angina pectoris. However, for most patients, it is difficult to capture typical transient ECG changes (ST segment elevation or depression). During coronary angiography, transient stenosis or occlusion of blood vessels ("normal coronary arteries" or atherosclerotic stenosis) occurs. If the stenosis or occlusion disappears quickly after the application of coronary expansion drugs, or disappears on its own, it can also be excluded If the catheter is locally stimulated, coronary spasm can be considered. The challenge test is of great value in the diagnosis of coronary spasm, but there are certain risks, especially in the early years, the ergometrine challenge test may cause multiple blood vessels to contract at the same time, leading to severe arrhythmia, shock, and even death. In recent years, Japanese scholars have mostly used acetylcholine as a challenge test, which has a short half-life, fast metabolism, and relative safety. However, in current clinical practice, the routine use of challenge tests to diagnose coronary spasms is not recommended.

Treatment of variant angina pectoris

Treatment principles:

In the clinical management of coronary spasm, it is very important to first inquire about the medical history and physical examination in detail, and use necessary auxiliary examinations to actively search for systemic factors and diseases that may cause and induce coronary spasm. For the primary systemic condition, combined endocrine diseases, treatment of chronic inflammation and allergic states are the prerequisites for coronary spasm treatment. On this basis, apply reasonable drug treatment.

First, since prolonged coronary spasm can secondary to thrombosis, in the acute phase, antithrombotic therapy should be given in accordance with the conventional ACS treatment, and then aspirin can be taken for a long time.

Statins can not only regulate lipids, but also stabilize plaque and improve damaged endothelial function. They should be taken for a long time.

The application of calcium antagonists is that patients with variant angina pectoris are different from other ACS patients, and calcium antagonists should be selected in accordance with the patient's heart rate, blood pressure and heart function. Diltiazem is preferred, especially for repeated episodes of the acute phase, which can be applied intravenously. For patients with chronic arrhythmia, dihydropyridine calcium antagonists, such as nifedipine sustained-release agents, can also be selected.

It can also be combined with intravenous or oral nitrate drugs. Since most patients with variant angina pectoris develop at night or in the early morning, when applying the drug, one should consider adding calcium antagonists and nitrate drugs once before going to bed, based on the principle of time biology.

Because -blockers are used to block the vasodilator effect of -receptors, while the vasoconstriction effect of -receptors is relatively enhanced, which may induce and exacerbate arterial spasm, -blockers are generally not recommended. Drugs, unless combined with more severe muscle bridges or fixed stenosis.

For patients with variant angina pectoris without severe fixed stenosis, most patients do not need PCI or CABG treatment after strict smoking cessation, active treatment of systemic conditions and diseases that induce spasms, and intensive drug treatment, unless imaging examination suggests local presence Clear unstable plaques (such as dissections, ulcers, etc.). Moreover, even after receiving revascularization treatment, because the neurohumoral abnormal basis of coronary spasm may still exist, patients still need to adhere to the above medication. For variant angina pectoris associated with arrhythmia, the treatment of coronary spasm is the main treatment, and conventional implanted devices, including pacemakers and ICDs, are not recommended.