Variant angina pectoris (Prinzmetal's angina)

Angina pectoris occurs due to increased myocardial oxygen demand ("secondary angina"). In this case, the affected coronary arteries are unable to provide an adequate increase in coronary blood flow. Spontaneous angina occurs at rest, without an increase in heart rate and blood pressure. The cause of spontaneous angina is a primary decrease in coronary blood flow due to spasm of the coronary artery. Therefore, it is often called "vasospastic" angina. Other synonyms for spontaneous angina: "variant angina", "a special form of angina".

The diagnosis of spontaneous angina is much more difficult to establish than the diagnosis of angina of effort. The most important sign is missing - the connection with physical exertion. All that remains is to take into account the nature, localization and duration of attacks, the presence of other clinical manifestations or risk factors for coronary heart disease. The relieving and prophylactic effect of nitrates and calcium antagonists is of great diagnostic importance.

For the diagnosis of spontaneous angina, ECG recording during an attack is very important. The classic sign of spontaneous angina is a transient ST segment elevation on the ECG. Recording any transient ECG changes during an angina attack at rest also increases the reliability of the diagnosis of spontaneous angina. In the absence of ECG changes during attacks, the diagnosis of spontaneous angina remains presumptive or even doubtful.

The classic variant of spontaneous angina is Prinzmetal's angina (variant angina). In patients with angina described by Prinzmetal (1959), attacks of angina occurred at rest, they did not have angina of effort. They had "isolated" spontaneous angina. Attacks of Prinzmetal's angina usually occur at night or early in the morning, at the same time (from 1 a.m. to 8 a.m.), attacks are usually longer than with angina of effort (often from 5 to 15 minutes). During attacks, the ECG records an increase in the ST segment.

During an attack of angina pectoris, a sharply expressed elevation of the ST segment is observed in leads II, III, aVF. In leads I, aVL, V1-V4, reciprocal depression of the ST segment is noted.

According to strict criteria, variant angina includes only cases of angina at rest accompanied by ST segment elevation. In addition to ST segment elevation, some patients experience significant rhythm disturbances, enlarged R waves, and transient Q waves during an attack.

Variant angina is angina that occurs as a result of arterial spasm (Prinzmetal's angina).

Causes of variant angina

Prinzmetal was the first to suggest that spontaneous angina is caused by coronary artery spasm, and this was confirmed in subsequent studies. The development of coronary artery spasm is visualized by coronary angiography. The cause of spasms is localized endothelial dysfunction with increased sensitivity to vasoconstrictor effects. 70-90% of patients with spontaneous angina are men. It has been noted that there are many heavy smokers among patients with spontaneous angina.

Numerous subsequent studies have also shown that patients with isolated ("pure") spontaneous angina are very rare and account for less than 5% of all patients with angina. You can work for more than 10 years and not meet a single patient with Prinzmetal's angina. Only in Japan was a very high incidence of spontaneous angina recorded - up to 20-30%. However, at present, the incidence of spontaneous angina has decreased even in Japan - to 9% of all cases of angina.

Much more often (in 50-75% of cases) patients with attacks of spontaneous angina have concomitant angina of effort (the so-called "mixed angina"), and coronary angiography reveals hemodynamically significant stenoses of the coronary arteries within approximately 1 cm of the spasm site in 75% of patients. Even in patients with coronary arteries unchanged during coronary angiography, non-stenotic atherosclerosis is revealed in the spasm area using intracoronary ultrasound.

Most patients have significant proximal stenosis of at least one major coronary artery. Spasm usually occurs within 1 cm of the obstruction (often associated with ventricular arrhythmia).

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Symptoms of variant angina

Symptoms of variant angina include chest discomfort that occurs mainly at rest and very rarely and inconstantly during exertion (unless there is also significant coronary artery obstruction). Attacks tend to occur regularly at the same time.

Diagnosis of variant angina

A presumptive diagnosis is made if ST segment elevation occurs during an attack. Between angina attacks, ECG data may be normal or have persistent changes. Confirmation of the diagnosis is possible by conducting a provocative test with ergonovine or acetylcholine, which can provoke coronary artery spasm with confirmation) a pronounced ST segment elevation or reversible spasm during cardiac catheterization. Most often, the test is performed in the catheterization laboratory, less often - in the cardiology department.

The basis for diagnosing spontaneous angina is recording an ECG during an attack - ST segment elevation is observed in 70-90%. In 10-30% of patients, ST segment elevation is not observed on the ECG during attacks, but ST segment depression or "pseudonormalization" of the negative T wave is recorded. The probability of recording spontaneous angina significantly increases with daily ECG monitoring. Spontaneous angina can be diagnosed using provocative tests. The most effective way to provoke a spasm is intravenous administration of ergonovine. However, this test is dangerous.

Intracoronary administration of ergonovine or acetylcholine is also used. In some patients, coronary artery spasm occurs during a hyperventilation test. It should be noted that there are patients with induction of spasm to intracoronary administration of ergonovine or acetylcholine, but without ST segment elevation, and vice versa, ST segment elevation in response to ergonovine without coronary artery spasm. In the latter case, it is assumed that the cause of ST elevation is constriction of small distal coronary arteries.

Spontaneous angina is characterized by transient changes in disease activity - periods of exacerbation and remission. In approximately 30% of patients, during the intensification of spastic reactions, spontaneous angina and ST segment elevation are observed during physical exertion (especially if the stress test is performed in the morning).

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Prognosis and treatment of variant angina

The average 5-year survival rate is 89 to 97%, but the risk of mortality is higher in patients with both types of angina and atherosclerotic artery obstruction.

In 40-50% of patients with spontaneous angina, remission is observed within approximately 1.5 months from the onset of attacks of spontaneous angina. Against the background of taking calcium antagonists, remission is observed in 70-90% of patients (with an observation period of 1 to 5 years). In many patients, attacks of spontaneous angina do not recur (and are not provoked by intravenous administration of ergonovine) even after discontinuation of calcium antagonists.

Usually, sublingual nitroglycerin rapidly reduces the symptoms of variant angina. Calcium channel blockers can effectively prevent an attack. Theoretically, the use of beta-blockers may increase spasm by causing alpha-adrenergic vasoconstriction, but this effect has not been proven clinically. The most commonly prescribed drugs for oral administration are:

• prolonged-release diltiazem at a dose of 120 to 540 mg once a day;
• prolonged verapamil from 120 to 480 mg once a day (the dose should be reduced in patients with renal or hepatic insufficiency);
• amlodipine 15-20 mg once a day (the dose should be reduced in the elderly and patients with liver failure).

In refractory cases, amiodarone may be given. Although these drugs reduce symptoms, they probably do not change the prognosis.