Variable angina (angina of the Prinzmetal type)

Stenocardia of stress arises from an increase in myocardial oxygen demand ("secondary angina"). In this case, the affected coronary arteries are not able to provide an adequate increase in coronary blood flow. Spontaneous angina occurs in a state of rest, without increasing heart rate and blood pressure. The cause of spontaneous angina is the 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 are: "variant angina", "special form of angina".

The diagnosis of spontaneous angina is much harder to establish than the diagnosis of angina pectoris. There is no the most important sign - the connection with physical activity. It remains only to account for the nature, location and duration of seizures, the presence of other clinical manifestations or risk factors for IHD. Very important diagnostic value is the stopping and preventive effect of nitrates and calcium antagonists.

For the diagnosis of spontaneous angina, it is very important to record the ECG during an attack. The classic sign of spontaneous angina is the transient rise of the ST segment on the ECG. The registration of any transient ECG changes during an angina at rest also increases the reliability of the diagnosis of spontaneous angina. In the absence of ECG changes during seizures, the diagnosis of spontaneous angina remains suspect or even questionable.

The classical variant of spontaneous angina is angina of the Prinzmetal type (variant angina). In patients with angina pectoris described by Princemetal (1959), angina attacks occurred at rest, they did not have angina pectoris. They had an "isolated" spontaneous angina. Attacks with angina prinzmetal occur, usually at night or early in the morning, at the same time (from 1 am to 8 am), usually seizures are more prolonged than with angina pectoris (often from 5 to 15 min). On the ECG during the seizures, the rise of the ST segment is recorded.

During an attack of angina, there is a pronounced elevation of the ST segment in the leads II, III, aVF. In the leads I, aVL, V1-V4, there is a reciprocal depression of the ST segment.

According to strict criteria, only cases of stenocardia at rest, accompanied by ST segment elevation, are included in variant angina pectoris. In addition to the elevation of the ST segment, in some patients, at the time of an attack, marked rhythm disturbances, an increase in the R wave, and the appearance of transient Q teeth are noted.

Variant angina pectoris is angina due to spasm of the artery (Prinzmetal angina).

Causes of variant angina pectoris

Prinzmetal first suggested that the cause of spontaneous angina is a spasm of the coronary artery, and in subsequent studies it was confirmed. The development of coronary artery spasm is visualized in coronary angiography. The cause of spasms is localized dysfunction of the endothelium with an increase in sensitivity to vasoconstrictor effects. 70-90% of patients with spontaneous angina are men. It is noticed that among patients with spontaneous angina there are a lot of malignant smokers.

In numerous subsequent studies, it was also found that patients with isolated ("clean") spontaneous angina are very rare and account for less than 5% of all patients with angina pectoris. You can work for more than 10 years and not meet a single patient with stenocardia such as Prinzmetal. Only in Japan was recorded a very high incidence of spontaneous angina pectoris - up to 20-30%. However, at present, the incidence of spontaneous angina has decreased even in Japan - up to 9% of all cases of angina pectoris.

Much more often (in 50-75% of cases) in patients with spontaneous angina attacks there is concomitant angina of tension (the so-called "mixed angina"), and in coronary angiography in 75% of patients hemodynamically significant coronary artery stenoses are detected within 1 cm from the spasm site . Even in patients with coronary arteries unchanged during coronary angiography with the help of intracoronary ultrasound in the spasm area, non-stenosing atherosclerosis is detected.

Most patients show significant proximal narrowing of at least one major coronary artery. Spasm usually occurs within 1 cm of the site of obstruction (often accompanied by ventricular arrhythmia).

[1], [2], [3], [4], [5], [6], [7]

Symptoms of variant angina pectoris

Symptoms of variant angina include chest discomfort, arising mainly at rest, very rarely and not consistently during exercise (except when there is also severe obstruction of the coronary artery). Attacks tend to appear regularly at the same time.

Diagnosis of variant angina pectoris

A presumptive diagnosis is made if ST segment elevation occurs during an attack . Between attacks of angina pectoris, ECG data can be normal or have persistent changes. Confirmation of the diagnosis is possible by conducting a provocative test with ergonovin or acetylcholine, which can provoke a spasm of the coronary artery with confirmation of a marked rise in the ST segment or reversible spasm during cardiac catheterization. The test is most often performed in a catheterization laboratory, less often in a cardiology unit.

The basis for the diagnosis of spontaneous angina is the registration of the ECG during an attack - 70-90% of the ST segment is marked up. In 10-30% of patients during ECG seizures, there is no ST segment elevation, and depression of ST segment or "pseudonormalization" of negative T wave is recorded. The probability of recording spontaneous angina is significantly increased with daily monitoring of ECG. Spontaneous angina can be diagnosed with provocative samples. For the provocation of spasm, the most effective intravenous administration of ergonovin. However, this test is dangerous.

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

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

[8], [9], [10],

Prognosis and treatment of variant angina pectoris

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

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

Usually taking nitroglycerin under the tongue quickly reduces the manifestations of variant angina. Calcium channel blockers can effectively prevent an attack. Theoretically, the use of b-adrenoblockers may increase spasm, causing a-adrenergic vasoconstriction, but this effect has not been clinically proven. The most commonly prescribed drugs for oral administration are:

• Prolonged diltiazem in a dose of 120 to 540 mg once a day;
• Prolonged verapamil 120 to 480 mg once a day (dose should be reduced in patients with renal or hepatic insufficiency);
• Amlodipine 15-20 mg once a day (dose must be reduced in the elderly and patients with hepatic insufficiency).

In refractory cases, you can appoint amiodarone. Despite the fact that these drugs reduce the symptoms, they probably do not change the prognosis.