What is Prinzmetal's angina? Clinical tests and tasks During an attack of variant angina, it is inappropriate to use

This is a type of angina that develops at rest as a result of spasm of the coronary arteries and occurs with severe, prolonged attacks. Anginal pain with Prinzmetal's angina usually occurs at night or in the morning, is intense, accompanied by tachycardia, impaired heart rate, profuse sweat, hypotension, fainting. Diagnosis of Prinzmetal's angina is based on ECG registration, daily ECG monitoring, stress tests, and coronary angiography. Drug therapy for Prinzmetal's angina includes taking antiplatelet agents, nitrates (during an attack and prophylactically), and calcium antagonists.

ICD-10

I20.1 Angina with documented spasm

General information

Prinzmetal's angina (vasospastic, variant, spontaneous angina) – clinical form resting angina pectoris, which occurs as a result of coronary vasospasm in the absence of an increase in the metabolic needs of the heart muscle before the onset of an attack. Vasospastic angina got its name from the American cardiologist M. Prinzmetal, who first described this form of the disease in 1959.

An attack of Prinzmetal's angina lasts from 5 to 15 minutes, sometimes up to half an hour, is tolerated by the patient much more severely than an attack of ordinary angina, and is difficult to stop. Attacks can be repeated in series, several times in a row at intervals of 2-15 minutes; in other cases, attacks are single, sporadic, occurring once a day, week, month. Outside of attacks, patients feel practically healthy.

Complications

Main clinical features Prinzmetal's angina is characterized by more severe and prolonged anginal attacks that occur at rest and occur with severe autonomic disturbances and life-threatening rhythm and conduction disorders. Against the background of an attack of Prinzmetal's angina, an extensive transmural myocardial infarction may develop, resulting in a cardiac aneurysm or sudden stop hearts.

Diagnostics

The main objective diagnostic criterion for Prinzmetal's angina is the ECG recorded during the attack. The classic sign of Prinzmetal's angina is S-T segment elevation, characteristic of transmural myocardial ischemia. Unlike myocardial infarction, in which the elevation of the corresponding segment lasts for about a month, with Prinzmetal’s angina these changes are recorded briefly, usually within 5–20 minutes, while the anginal pain lasts.

Less specific electrocardiographic signs of Prinzmetal's angina may include widening and increasing the amplitude of the R wave, sharpening or inversion of the U wave, and disturbances in heart rhythm and conduction. Subsequent Holter ECG monitoring can detect transient episodes of ischemia that occur without significant changes in heart rate, which confirms the fact of vasoconstriction.

If Prinzmetal's angina is suspected, to induce vasospasm, provocative tests with hyperventilation, administration of ergometrine, acetylcholine, ischemic test, and cold test are performed. Load studies (bicycle ergometry, treadmill test) reveal a relatively high tolerance to physical activity. Coronary angiography reveals the absence of functionally significant (more than 50%) stenosis of the coronary arteries in half of the patients with Prinzmetal's angina.

Treatment of Prinzmetal's angina

Patients must be hospitalized. The goal of treatment is to eliminate vasospasm and myocardial ischemia, reduce the likelihood of arrhythmias, acute myocardial infarction and sudden coronary death. To relieve attacks of Prinzmetal's angina, sublingual nitroglycerin is prescribed; in the future, it is recommended to take long-acting nitrates.

At the same time (or instead of nitrates), calcium antagonists (nifedipine, verapamil, diltiazem), which dilate the coronary and collateral arteries, are prescribed. For obstructive diseases of the coronary arteries, b-blockers are added to therapy. Patients with Prinzmetal's angina are also advised to take small doses of antiplatelet agents (acetylsalicylic acid).

It should be remembered that if treatment is abruptly stopped large doses nitrates and calcium antagonists, withdrawal syndrome may develop, expressed in an increase in the frequency anginal attacks up to 50% or more, the development of acute myocardial infarction. When Prinzmetal's angina is combined with severe atherosclerosis coronary vessels Maybe surgery- coronary artery bypass surgery, angioplasty and stenting of coronary arteries.

Prognosis and prevention

The risk of complications from Prinzmetal's angina is directly related to the degree of coronary obstruction, duration, frequency and severity of attacks. In the absence of obstructive lesions of the coronary arteries, the risk of sudden coronary death is extremely low and is about 0.5% per year. In the case of prolonged, frequently recurring and severe attacks of Prinzmetal angina, the likelihood fatal outcome increases to 20-25%.

Since Prinzmetal's angina is considered as one of the variants of progressive coronary insufficiency (unstable angina), all patients should be monitored by a cardiologist. Preventive actions include the fight against hyperlipidemia, smoking cessation, normalization of ANS tone.

Vasospastic angina is also known under other names: variant, spontaneous, Prinzmetal's angina. This type of pathology is rare, but due to some complications it can be fatal. In most cases, drug treatment is sufficient, but some concomitant diseases may require surgical intervention.

general characteristics

Vasospastic angina is a spasm of the blood vessels supplying the heart. This condition often occurs against the background of atherosclerosis - in 75% of cases the patient has atherosclerotic plaques.

An attack of spontaneous angina is characterized by pronounced ischemia of the heart muscle, that is, its insufficient blood supply. Against this background, disturbances in the electrical function of the heart are possible.

At variant angina artery spasm is observed. This pathology destroys endothelial cells, and platelets accumulate in the affected area. Against this background, a special lipid, thromboxane, is produced above normal, increasing smooth muscle contractions.

Causes

Possible reasons there is a lot of coronary artery spasm. To the most probable factors the occurrence of pathology include:

stressful situations, causing strong emotional shocks;
metabolic problems (usually diabetes);
bad habits: cigarettes, alcohol, narcotic drugs(cocaine, amphetamine);
hyperventilation;
autoimmune pathologies;
effects on the body of low temperature.

Elderly patients are at risk of developing vasospastic angina. Previously, it most often affected people over 50 years of age, but today the problem has become younger, so the disease often occurs after 30 years of age. The cause of the pathology can also be heredity, therefore, when diagnosing, it is important to take into account cases of heart disease in relatives.

Symptoms of variant angina resemble other pathologies of the cardiovascular system. A distinctive feature of the disease is the nature of the pain. They can be pressing, cutting or intensely burning. There are other features:

occurs at rest in the absence of physical or emotional stress;
exposure to physical or emotional stress can increase pain or reduce its intensity;
painful sensations appear at regular intervals;
pain intensity is higher than with other types of angina;
the attack can last up to 20 minutes;
attacks occur at approximately the same time;
The pain is cyclical - its intensity gradually increases and then subsides.

In addition to pain of a special nature, there are other signs of vasospastic tachycardia. It may manifest itself:

sharp increase blood pressure;
nausea (rare);
pain in the head;
pallor skin;
profuse sweat (very profuse);
shortness of breath.

In some cases, the patient may even lose consciousness. The manifestation of any of these signs means you need to see a doctor.

If the attack is accompanied by arrhythmia, then this condition can be life-threatening. It is with this complication that loss of consciousness occurs and there is a risk of death.

Spontaneous angina is characterized by a protracted nature. In most cases, spasm appears at night or in the early morning hours. Attacks may recur for weeks or even months.

When a patient complains of symptoms of vasospastic angina, the specialist begins the diagnosis by collecting an anamnesis. It is necessary to evaluate the signs of pathology: the nature of the pain, the duration of the attacks, the time of their appearance and duration, provoking factors.

The patient must be questioned about cardiovascular diseases in the family, cases of sudden death. Further diagnosis is performed through clinical and instrumental studies, as well as some samples:

Blood and urine tests (general, biochemistry). Such studies make it possible to identify concomitant pathologies and check sugar and cholesterol levels.
Electrocardiogram. To make an accurate diagnosis, it is necessary to carry out Holter monitoring, that is, measure indicators throughout the day.
Test with ergometrine. The drug is administered intravenously as a bolus. If the patient begins an angina attack and the ST interval rises above the isoline by more than 1 mm, then the test is considered positive. The entire course of the study is monitored by an ECG and parallel measurement of blood pressure.
Cold test. The patient's hand is immersed in cold water for a maximum of 5 minutes. During this procedure, as well as 5 minutes after it, an electrocardiogram is used to monitor the condition. The test is considered positive when pain in the heart appears. On the cardiogram this is expressed by an increase in the ST interval.
Hyperventilation test. In this case, the patient needs to breathe deeply and often for a certain time. This technique allows you to reduce the level of hydrogen ions in the blood, which provokes a spasm of smooth muscle cells. Thanks to these features, it is possible to detect areas of the heart with impaired contractility. Such data is obtained thanks to the control ultrasound examination.
Echocardiography. This study is used to identify factors that disrupt the functioning of the heart, as well as to assess the functionality of the ventricles.
Coronary angiography. This study allows us to identify atherosclerotic vascular stenosis.

An accurate diagnosis can be made based on the patient's complaints and the results of Holter monitoring.

Carrying out tests as part of diagnostic measures is dangerous for the patient’s life, therefore control of the equipment and specialist is necessary. All manipulations must be carried out in intensive care unit so that, if necessary, the necessary measures can be taken without delay.

Drug treatment of vasospastic angina

In most cases, drug therapy is used. It includes taking the following medications:

Nitroglycerine. It is a short-acting nitrate. It is usually taken in tablet form, less often as a spray. Patients with this disease must always have nitroglycerin with them. The same drug is used in the case of a test with ergometrine if the patient experiences a spasm. Taking Nitroglycerin helps prevent an attack of the disease, therefore it is recommended to take it before physical activity.
Blockers calcium channels. More often from this pharmacological group choose Nifedipine or Verapamil. These drugs relax the smooth muscles of the coronary arteries by reducing the calcium cells in them. The dosage should be selected by the doctor, taking into account individual characteristics the course of the pathology.
Antiplatelet agents. Usually used acetylsalicylic acid. Taking this medication is necessary to prevent blood clots.
α-blockers. Drugs in this group are used in rare cases when the classic set of drugs has not brought the desired result. Usually they resort to Prazosin.
Lipid-lowering drugs (statins). They can reduce cholesterol concentrations and improve endothelial function.
If the pathology occurs against the background of diabetes mellitus, then the use of angiotensin-converting enzyme inhibitors is indicated.

The doctor selects the treatment regimen individually. Appropriate therapy can be prescribed only after a complete examination of the patient and identification of the necessary indicators. It is important to identify concomitant pathologies, especially those affecting the cardiovascular system, and their correct treatment.

The effectiveness of therapy largely depends on eliminating the factors that provoke the disease.

Surgery

Drug treatment may not be effective. In this case, surgery will be required. The patient may undergo coronary angioplasty or coronary artery bypass surgery. In the first case, the operation allows you to restore the flow of blood into the myocardium, in the second, it creates an additional path for this.

In case of dangerous ventricular taryarrhythmia or ineffectiveness conservative therapy the patient may need to have a pacemaker or cardioverter-defibrillator implanted.

Forecast

The prognosis for vasospastic angina is usually favorable. The five-year survival rate is 90-95%.

The prognosis is less favorable if the pathology is complicated by dangerous ventricular tachyarrhythmia. One of the serious complications of variant angina is myocardial infarction. It is observed in 20% of patients. It is necessary to take it as a preventive measure.

Spontaneous remission is possible, that is, the disappearance of symptoms of the disease without treatment. Sometimes this period lasts for several years.

In predicting the consequences of the disease important role the timeliness of its detection plays a role. Complications that can lead to death usually occur in the first year of development of the pathology. The sooner it is diagnosed, the faster and more effectively appropriate treatment will be provided.

Prevention

As primary prevention, that is, in the absence of variant angina, the following rules are important:

conducting healthy image life;
rejection of bad habits;
moderate physical activity;
alternation physical activity with rest;
good sleep;
timely detection and treatment of pathologies of the cardiovascular system;
maintaining normal level sugar and cholesterol.

If vasospastic angina has already manifested itself and is diagnosed, then it is appropriate secondary prevention. It includes:

constant use of prescribed medications and strict adherence to dosage;
treatment of concomitant pathologies;
medical check-up with a cardiologist;
dosed physical activity;
absence of severe stress;
rejection of bad habits;

The diet of a patient with variant angina should include a sufficient amount of fruits, vegetables, vegetable oils, oily fish. Animal fats should be avoided.

Video about vasospastic angina

Watch the program dedicated to recognizing the symptoms, diagnosing and treating this pathology:

Vasospastic angina is a rare pathology. Clinical picture it is similar to the signs of other cardiovascular diseases, so it can only be identified through differentiated diagnostics. Treatment is mostly conservative, but surgery, including implantation of an electronic device, may be necessary.

Angina pectoris, which is characterized by pain at rest with transient ST segment elevation (according to ECG readings), called variant. This type of angina is caused by transient spasm of the coronary arteries, so it usually occurs unrelated to physical activity. Variant angina was described by Prinzmetal in 1959.

The prevalence is unknown, but the disease appears to be quite rare.

Pathogenesis

Tone coronary vessels depends on the balance of vasodilator and vasoconstrictor factors. An increase in the activity of vasoconstrictor agents contributes to the development of spasm of the coronary arteries. Severe spasm causes ischemia, which is characterized by ST segment elevation on the ECG.

Clinical picture of variant angina.

Variant angina is characterized by the appearance of typical chest pain, often at night or in the early morning hours; the duration of the attack can be more than 15 minutes. At the height of pain, ventricular arrhythmias or AV blockade may occur. Taking nitroglycerin in most cases stops attacks of variant angina. Variant angina can occur with stable angina pectoris in 50% of patients. Its appearance is often noted in patients in acute period myocardial infarction.

A characteristic feature A variant of angina is migraine, which occurs in 25% of patients. In 25% of patients, variant angina is combined with Raynaud's phenomenon. Syncope due to ventricular arrhythmias or AV block may be diagnostic signs variant angina. The disease can occur in waves - after several attacks, a long break is possible, and then resumption of attacks of variant angina.

Diagnostics.

If it is possible to record an ECG during a painful attack, then a rise in the ST segment (usually in several leads) is recorded, returning to the baseline after relief of the pain syndrome. Daily monitoring An ECG may also detect episodes of ST segment elevation. An ECG during an exercise test provokes angina pectoris with ST segment elevation in 30% of patients in the active phase of the disease.

To diagnose variant angina, a cold test is sometimes used (place the hand up to the middle of the forearm in water with a temperature of 4 degrees Celsius for 3-5 minutes; the test is considered positive when ischemic changes appear on the ECG during immersion or over the next 10 minutes).

In some cases, MRI is performed in vascular mode during stress tests, the data can reveal abnormalities in the speed of coronary blood flow in the anterior interventricular branch of the left coronary artery. Today, MRIs are performed in many clinics that are equipped with modern diagnostic devices.

Treatment of variant angina.

Nitroglycerin is used to relieve an attack of variant angina. In case of exacerbation of the disease (increasing frequency of attacks), it is possible to use long-acting nitrates. Slow calcium channel blockers may also be recommended. Marked positive effect use of alpha-blockers, amiodarone, guanethidine, clonidine for variant angina. Beta blockers can prolong an attack of variant angina, so they are not indicated for this category of patients. For patients with variant angina, as with other forms of coronary heart disease, the use of acetylsalicylic acid is indicated for the prevention of myocardial infarction.

If coronary angiography reveals severe atheroscrotic narrowing of the arteries, coronary bypass surgery or balloon dilatation is recommended. However, there is evidence that the rates of operative mortality and postoperative myocardial infarction in patients with variant angina are higher than in patients without variant angina.

Forecast.

Quite often, spontaneous disappearance of attacks occurs, which sometimes lasts for years. A number of patients experience myocardial infarction within 3 months. To a large extent, the prognosis of patients with variant angina is influenced by the severity of atherosclerosis of the coronary arteries.

Some patients with coronary artery disease experience episodes of local spasm of the coronary arteries in the absence of obvious atherosclerotic lesions. This pain syndrome called variant angina, or Prinzmetal's angina. With this form of angina, anginal attacks are accompanied by transient elevations of the ST segment on the ECG. In this case, oxygen delivery to the myocardium is reduced due to intense vasospasm of large, often subepicardial, arteries. It is believed that many of these patients have initial atherosclerosis, manifested only by endothelial dysfunction.

Variant angina often develops at rest; the cause of ischemia in this case is a pronounced transient decrease in oxygen delivery, and not the increased myocardial need for it due to the load.

Criteria for clinical and ECG diagnosis of vasospastic

angina:

anginal attacks are accompanied by a transient rise (rather than a decrease) in the ST segment on the ECG;

anginal attacks can sometimes appear during physical exercise, which is usually well tolerated at other times, the so-called variable threshold for the occurrence of angina pectoris. These attacks develop after physical exercise performed in the morning, but not in the afternoon and evening;

anginal attacks can be prevented and treated with calcium antagonists (CA) and nitrates, the effect of β-blockers (BB) is less pronounced; in some patients with angiospastic angina, BBs can cause a proischemic effect.

3. Painless (silent) myocardial ischemia (bbim)

A significant proportion of episodes of myocardial ischemia may occur without symptoms of angina or its equivalents, up to the development of silent MI. Within the framework of stable

Noy IHD is divided into 2 types of BBIM: type I – completely BBIM; Type II – combination

BBIM and painful episodes of myocardial ischemia. Episodes of BBIM are usually diagnosed during tests with physical activity and during daily monitoring (CM) of the ECG, as well as during routine ECG registrations. In the diagnosis and assessment of the severity of BBIM, stress tests and SM ECG

complement each other. The treadmill test, bicycle ergometer (VEM) test, transesophageal atrial electrical stimulation (TEES) can detect BBIM and characterize its relationship with blood pressure, heart rate, and exercise function. Simultaneous myocardial perfusion scintigraphy and stress echocardiography help to assess the resulting hypoperfusion and impaired myocardial contractile function. SM ECG records the total number

and duration of BBIM episodes, as well as cases of BBIM at night and not associated with physical activity.

BBIM is an unfavorable prognostic sign. The damaging effect of ischemia on the myocardium is determined not by the presence of pain, but by the severity and duration of the disturbance in its perfusion.

EXAMPLES OF FORMULATION OF DIAGNOSIS

1. IHD: exertional angina, first occurring (date). Atherosclerosis of the coronary arteries. H0.

2. IHD: angina pectoris, FC IV and (or) rest. Atherosclerosis of the coronary arteries. Ventricular extrasystole. H0.

3. IHD: silent myocardial ischemia, FC II. Atherosclerotic cardiosclerosis. Atherosclerosis of the coronary arteries. Supraventricular extrasystole. HI. (Nyha FC I)

4. IHD: exertional angina, FC III. Post-infarction cardiosclerosis (date). Atherosclerosis of the coronary arteries, blockade of the left bundle branch. HIIB. (Nyha FC III)

5. IHD: microvascular angina, FC II. Atherosclerotic cardiosclerosis. Atherosclerosis of the coronary arteries. AV block Ist. HIIA. (Nyha FC II).

DEFINITION

Spontaneous (variant, vasospastic, Prinzmetal) angina was first described by M. Prinzmetal in 1959. This is a special form of resting angina, which occurs suddenly, without the action of provoking factors, characterized by coronary spasm, severe painful anginal attack and a significant transient rise in the RS-T segment by ECG. Variant angina is based on pronounced spasm of the coronary artery, leading to its short-term dynamic occlusion. Termination or sharp decrease coronary circulation leads to deep, often transmural, myocardial ischemia, decreased local contractility of the LV, asynergy of contractions and significant electrical instability of the myocardium, manifested by rhythm and conduction disturbances.

Morphological changes in coronary vessels in patients with stable angina very variable. In some cases, there is a more or less pronounced fixed stenosis of the proximal coronary artery, caused by an atherosclerotic plaque narrowing the lumen of the artery. In other cases, atherosclerotic narrowing of large coronary arteries according to coronary angiography may be minimal or even absent altogether. Coronary spasm occurs at the level of small intramural coronary vessels, morphological changes which are usually not recorded during coronary angiography.

CLINICAL PICTURE

Clinical manifestations of spontaneous (variant) Prinzmetal angina have some features that distinguish it from typical exertional angina. Intense painful attacks occur at rest, more often at night during sleep, or in the early morning hours (from 4 to 6 am). Painful attacks are usually not preceded by any obvious provoking factors, including those that are accompanied by an increase in myocardial oxygen demand (increase in heart rate, rise in blood pressure). The pain is localized behind the sternum, radiating to the left arm, shoulder, and shoulder blade. The duration of pain can vary (from 5-10 to 20-30 minutes). Bradycardia often occurs against the background of a painful attack. Tachycardia may appear at the height of an attack or at the end of it, but only as a consequence of reflex activation of the SAS in response to pain, awakening or taking nitroglycerin.

Pain may be accompanied by shortness of breath, weakness, sweating, dizziness, which indicates a decrease in LV contractility and severe autonomic disorders. Taking nitroglycerin does not always relieve pain and alleviate the patient's condition. Good effect obtained from the use of slow calcium channel blockers of the nifedipip group. Other common manifestations of variant angina are rhythm and conduction disturbances that occur during an anginal attack and are caused by severe electrical instability of the ischemic heart muscle and slow conduction.

During an attack of variant angina, a patient may develop transient intraventricular and atrioventricular blockades, frequent high-grade ventricular extrasystole, paroxysmal tachycardia or even ventricular fibrillation. Sudden formation of 2nd or 3rd degree AV block, arrest sinus node may be accompanied by syncope.

There are two clinical variants of the course of coronary artery disease in patients with Prinzmetal's angina. In half of the patients with fixed coronary artery stenosis, nocturnal attacks of spontaneous angina are combined with typical exertional angina caused by fixed coronary artery stenosis and increased myocardial oxygen demand. In these cases, attacks of angina pectoris occur during the daytime and are usually provoked by physical activity, psycho-emotional stress, and an increase in blood pressure, while attacks of variant angina caused by coronary artery spasm occur spontaneously at night or in the morning. Exercise tolerance in such patients can be significantly reduced due to the presence of coronary artery stenosis.

Cases where a patient suffering from exertional angina first experiences the described attacks of spontaneous angina pectoris deserve close attention, which usually indicates an exacerbation of coronary artery disease caused by the formation of a complicated atherosclerotic plaque (unstable angina).

In persons young, there is no hemodynamically significant narrowing of the coronary artery, so spontaneous vasospastic angina may be the only clinical manifestation IHD, but no exertional angina. Characterized by relatively good tolerance to physical activity. Physical findings in patients with vasospastic angina can be very varied. They often resemble those with stable angina pectoris. The prognosis for spontaneous angina is determined by the severity of coronary stenosis (Rovai D. et al., 1997). These patients are slightly more likely to develop myocardial infarction, arrhythmias and sudden death(Mayer S., Hillis L.D., 1998), especially with increased frequency of attacks (Malaya J1.T., Babajan V.D., 2005). With treatment, the prognosis is favorable.

LABORATORY AND INSTRUMENTAL DIAGNOSTICS

Electrocardiography

A typical ECG sign of spontaneous angina is an elevation of the RS-T segment above the isoline, indicating the presence of severe transmural myocardial ischemia caused by transient dynamic occlusion of the coronary artery. In rare cases, ischemic depression of the ST segment below the isoline is observed, which indicates the occurrence of subendocardial ischemia caused by incomplete occlusion of a large coronary artery or spasm of smaller intramural coronary vessels ( small arteries and arterioles) with the development of collaterals. After stopping an attack of vasospastic angina, the RS-T segment returns to the isoelectric line.

Here is our own observation. Patient T., 36 years old, was taken to the city cardiology center of Samara with a diagnosis of MI. In the department intensive care and resuscitation during thrombolytic therapy, nitrate infusion, and administration of P-blockers, anginal pain lasting up to 30 minutes recurred 4 times.

Figure 12. ECG of patient T., 46 years old. Diagnosis: IHD. Variant angina (M.L. Kachkovsky)

During each attack, the ECG showed a rise in the ST segment in leads V1-V6, reaching 9 mm (Figure 12). After the attack, the ECG returned to normal. Cardiospecific enzymes in the blood serum did not increase. Variant angina pectoris was diagnosed. Therapy with calcium antagonists gave a quick effect and stopped the recurrence of anginal pain.

Daily allowance ECG monitoring according to Holter

Long-term Holter ECG monitoring is important in the diagnosis of Prinzmetal's vasospastic angina. On the ECG, during attacks of angina, a sudden rise in the RS-T segment above the isoline is observed (transmural ischemia). These changes in the segment, as well as attacks of angina, develop at rest, more often at night, and are not accompanied by an increase in heart rate by more than 5 beats per minute. This fundamentally distinguishes vasospastic angina from exertional angina attacks caused by increased myocardial oxygen demand.

attacks of vasospastic angina and ECG signs of myocardial ischemia may disappear, despite an increase in heart rate caused by a reflex response to pain, awakening and/or taking nitroglycerin (the phenomenon of “passing through pain”). Continuous ECG recording reveals another important distinguishing feature: the displacement of the RS-T segment at the beginning of an attack occurs very quickly, spasmodically, and disappears just as quickly after the end of the spastic reaction.

Functional load tests

In a significant number of patients, tests with dosed physical activity are negative. This is due to the absence of a hemodynamically significant organic narrowing of the lumen of the coronary vessels, as well as the fact that physical activity and an increase in heart rate can rarely provoke an attack of variant angina, accompanied by pronounced spasm of the CL. Only in patients at the height of the load is it possible to provoke an attack of vasospastic angina and/or elevation of the RS-T segment. Characteristic is the constant fluctuation of tolerance to physical activity, rapid change degree of coronary reserve. Such changes are caused by changing CL tone and the degree of dynamic obstruction of the vessel lumen.

Functional tests

Cold test. The patient's hand up to the middle of the forearm is placed for 3-5 minutes in water cooled to a temperature of + 4°C. The ECG is recorded within 10 minutes after the end of the cold exposure. The test is characterized by low sensitivity, since ischemic changes in the RS-T segment are detected in approximately 15-20% of patients with vasospastic angina.

The test with ergometrine is considered the most adequate for identifying vasospastic reactions in patients with coronary artery disease in whom CL stenosis is not detected during coronary angiography. A test with ergometrine is dangerous for development severe complications(MI, sudden death, ventricular arrhythmias), therefore it is used in the diagnosis of coronary artery disease in specialized research institutions.

The basis of drug therapy is slow calcium channel blockers. Any drugs from the verapamnl, nifedipine or diltiazem group, including their combination, may be effective. It is preferable to use long-acting calcium antagonists (retarded forms). Attacks of nocturnal angina at rest are usually treated with nitroglycerin. In these cases, nitroglycerin acts as an arteriolar vasodilator, eliminating CL spasm. Long-acting nitrates are used to prevent attacks of Prinzmetal's vasospastic angina. In most cases, it is necessary to consider taking nitrates in the evening, and not in the morning and during the day, as with stable angina pectoris. A combination of retard forms of nitrates with one or even two slow calcium channel blockers is possible: nitrates + nifedipine + verapamil or nitrates + nifedipine + diltiazem.

Sometimes it is advisable to use α-adrenergic receptor blockers.

Unlike patients with stable angina, in patients with vasospastic angina, the use of b-blockers can sharply worsen the condition. To prevent ACS in this category of patients, it is advisable to use chimes, which has not only a powerful antiplatelet effect, but also pronounced vasodilatory properties. The drug is taken at a dose of 225 mg per day. Surgical treatment of patients with Prinzmetal's angina is ineffective. The coronary arteries, which are prone to spasms, are very sensitive to various mechanical manipulations. Therefore, in such patients any surgery can lead to the development of MI and life-threatening ventricular arrhythmias.

The prognosis is determined by two main factors: the degree of fixed coronary obstruction; the presence or absence of a complicated atherosclerotic plaque in the coronary artery, leading to destabilization of coronary artery disease and an increased risk of developing MI and sudden cardiac death. If a patient has severe, prolonged or new and recurring attacks of Prinzmetal's angina, which can be classified as unstable angina, the prognosis is quite serious: 20-25% of patients develop MI or sudden cardiac death within 3 months. With the stable nature of variant angina, rare and easily relieved painful attacks stop under the influence of treatment, sometimes for many years, and the prognosis is determined by the degree of coronary obstruction and the number of affected coronary arteries. The seven-year survival rate of patients is 97%.

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Causes and mechanisms of Prinzmetal's angina

Prinzmetal's angina is based on a sudden sharp transient spasm of a large branch of the coronary artery to a state of critical or total obstruction, which leads to a reduction or significant decrease in blood flow to the myocardium.

Main etiological factor Prinzmetal's angina is atherosclerosis, often still in its initial stage. Patients with Prinzmetal's angina are usually heavy smokers and often have various accompanying illnesses (arterial hypertension, cholecystitis, peptic ulcer, allergic reactions etc.), characterized by an imbalance in the state of vegetative nervous system and a tendency to vascular spasms.

Attacks of Prinzmetal's angina can be caused by local or general cooling, emotional stress, hyperventilation, accompanied respiratory alkalosis, however, more often occur without visible reasons. A characteristic sign of Prinzmetal's angina is the development of attacks at rest, in the absence of provoking factors, or during normal, well-tolerated physical activity.

Spasm vascular wall and a decrease in the lumen of the coronary artery may be due to an increase in the activity of the sympathetic and parasympathetic nervous system, as well as the vasoconstrictor effect of serotonin, histamine, and thromboxane. The important point is functional state endothelium of the coronary arteries: endothelial dysfunction and blood coagulation plays a significant role in the pathogenesis of coronary disease.

In 95% of patients with Prinzmetal's angina, hemodynamically significant stenosis does not develop in the coronary arteries. Vascular spasm usually occurs in the subepicardial (proximal) part of the arteries, in the area of its atherosclerotic changes, but can diffusely cover the entire artery with its smallest branches. With Prinzmetal's angina, spasm of morphologically unchanged coronary arteries is possible.

Symptoms of Prinzmetal's angina

Prinzmetal's angina attacks occur at rest, usually at night or in the early morning hours. It is possible that anginal pain may occur during everyday moderate physical activity, often at the same time of day.

Clinically, an attack of Prinzmetal's angina is characterized by the sudden appearance of pain in the heart, intense pressing, burning, cutting in nature. At the height of the attack, profuse sweating, tachycardia, arterial hypotension(sometimes, on the contrary, there is an increase in blood pressure), headache, nausea, pale skin, fainting. There may be disturbances in heart rhythm and conduction, most often such as atrial flutter, paroxysmal ventricular tachycardia, ventricular extrasystole; atrioventricular block, bundle branch block; in rare cases - ventricular fibrillation.

Thus, the main clinical features of Prinzmetal's angina are more severe and prolonged anginal attacks that occur at rest, occurring with severe autonomic disorders, life-threatening rhythm and conduction disorders.

Diagnosis of Prinzmetal's angina

If Prinzmetal's angina is suspected, provocative tests with hyperventilation, administration of ergometrine, acetylcholine, ischemic test, and cold test are performed to induce vasospasm. Load studies (bicycle ergometry, treadmill test) reveal a relatively high tolerance to physical activity. Coronary angiography reveals the absence of functionally significant (more than 50%) stenosis of the coronary arteries in half of the patients with Prinzmetal's angina.

Treatment of Prinzmetal's angina

If Prinzmetal's angina is suspected, patients should be hospitalized. The goal of treatment is to eliminate vasospasm and myocardial ischemia, reduce the likelihood of arrhythmias, acute myocardial infarction and sudden coronary death.

To relieve attacks of Prinzmetal's angina, sublingual nitroglycerin is prescribed; in the future, it is recommended to take long-acting nitrates. At the same time (or instead of nitrates), calcium antagonists (nifedipine, verapamil, diltiazem), which dilate the coronary and collateral arteries, are prescribed. For obstructive diseases of the coronary arteries, b-blockers are added to therapy. Patients with Prinzmetal's angina are also advised to take small doses of antiplatelet agents (acetylsalicylic acid).

It should be remembered that with an abrupt cessation of treatment with large doses of nitrates and calcium antagonists, a withdrawal syndrome may develop, expressed in an increase in the frequency of anginal attacks to 50% or more, and the development of acute myocardial infarction. When Prinzmetal's angina is combined with severe atherosclerosis of the coronary vessels, surgical treatment is possible - coronary artery bypass grafting, angioplasty and stenting of the coronary arteries.

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Causes

Prinzmetal's angina occurs due to obstruction of coronary blood flow as a result of spasm of the coronary artery that supplies blood to the heart. When performing coronary angiography, arterial spasm is clearly visualized. Coronary angiography is a study of the heart vessels using X-rays using a contrast agent.

It is not known exactly why arterial spasm occurs. Some experts believe that spasm occurs due to local dysfunction of the endothelium (the layer of cells lining the surface of blood vessels from the inside). Many people associate the occurrence of variant angina with the presence of coronary disease heart, decreased patency of the coronary artery, since spasm usually occurs in an area with impaired patency.

The main difference between spontaneous angina and other types is that it occurs as a result of vascular spasm, and not as a consequence of vessel narrowing (reduction of the lumen) due to atherosclerosis. Atherosclerosis is a disease in which inner surface fats are deposited in the vessels in the form of plaques. That is, a person who does not suffer from atherosclerosis may experience an attack of variant angina.

Up to 90% of cases of variant angina are registered in men. This rare disease. It was revealed that the majority of patients with this diagnosis are heavy smokers, often suffering from other diseases and conditions, for example:

Arterial hypertension.
Cholecystitis.
Peptic ulcer disease.
Allergies.
Severe stress.
Use of alcohol, drugs, some medicines leading to vasoconstriction.

These diseases, such as smoking and other bad habits, cause an imbalance in the autonomic nervous system and increase the likelihood of spasms.

Prinzmetal's angina is diagnosed in no more than 5% of patients who consult a doctor with complaints characteristic of angina. It is noted that in different countries this figure is significantly different. For example, in the UK these cases are rare, and in Japan, South Korea spasms of the heart arteries are observed in 40% of people suffering from angina pectoris.

Variant angina is rarely the only diagnosis, it often accompanies exertional angina.

Symptoms

Symptoms of spontaneous angina are:

Diagnostics

Spontaneous angina is much more difficult to diagnose than common species– angina pectoris. Seizures occur at rest. The main criterion for making a diagnosis in this case is the ECG readings. Coronary angiography helps to see the narrowing of the arteries and identify the location of the spasm.

Provocative tests are used for diagnosis. Their essence is that specialists deliberately cause artery spasm using medicines and monitor the work of the heart in this state using an ECG. Several patients died during the first such procedures. Therefore, today tests are carried out using coronary angiography, which helps to quickly see the spasm and, if necessary, relieve it by administering a certain drug.

Treatment

The basis of treatment is the elimination of factors that provoke attacks:

Alcohol.
Smoking.
Stress.
Anxiety.

During an attack, you need to take nitroglycerin. Further treatment is carried out under the supervision of a specialist on an inpatient basis. The following medications are commonly used:

Calcium channel blockers to prevent spasms.
Beta-blockers and nitrates and/or blockers are prescribed in the presence of coronary artery disease.
In some cases, surgical treatment is indicated.

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Features of the disease

Prinzmetal's angina is one of the forms of angina at rest, which occurs against the background of coronary vasospasm. The pathology got its name in honor of the cardiologist M. Prinzmetal, who was the first to describe this form in 1959. IN international classification diseases of the 10th revision, the disease was assigned code I20.

Prinzmetal's angina is also called unstable vasospathic, variant and spontaneous. The pathology is rare, as it occurs in approximately 3% of patients. Most often encountered by men aged 30-50 years. Sometimes variant angina is combined with exertional angina.

We will tell you further about what causes variant angina of the Prinzmetal type.

Elena Malysheva will tell you more about the features of Prinzmetal’s angina in her video:

Causes

Prinzmetal's angina occurs against the background of coronary artery spasm. The spasm lasts until a critical form of obstruction occurs, which leads to a deterioration in blood flow to the myocardium. Most common reason spasm - atherosclerosis, plaques of which narrow the lumen of blood vessels.

The following can also lead to spasm:

hypothermia of the body;
severe emotional stress;
hyperventilation;
excessive activity of the sympathetic and parasympathetic nervous system;
stenosis;

As statistics show, most of the sick (over 50%) are smokers with a long history, and also suffer from concomitant diseases, for example, hypertension, cholecystitis, ulcers, etc.

Read on to learn about the symptoms of variant (spontaneous, vasospastic) Prinzmetal angina.

Symptoms

A characteristic symptom of angina pectoris is painful attacks. Most often they appear at night or in the morning, and may not have a good reason for this. The pain comes from the side of the heart, has a pressing and cutting character, and can radiate to other parts of the body. The attack is characterized in the same way:

profuse sweating;
tachycardia;
hypotension;
pain in the head area;
pale skin;
fainting;

Sometimes the condition may be accompanied by disturbances in the rhythm of the heart muscle, atrioventricular block, and ventricular fibrillation.

Typically, attacks last no longer than 15 minutes. In very rare cases, the pain lasts up to half an hour and is very difficult to bear. During an attack, myocardial infarction may develop, so if it lasts for a long time, you must call an ambulance.

Diagnostics

At first diagnostic procedures The doctor collects a family and life history. Then he performs auscultation, which listens for murmurs, as well as a physical examination. These procedures are necessary to carry out differential diagnosis and making a primary diagnosis.

In the future, the patient is prescribed:
Urine and blood tests to detect concomitant diseases.
A biochemical blood test to evaluate cholesterol, protein and other elements that help determine the cause of the disease.
An ECG that determines the main symptom of Prinzmetal's angina is an increase in the S-T segment
ECG Holter monitoring, which detects transient ischemia.
Provocative test with hyperventilation to induce vasospasm.
Ischemic and cold tests.
Bicycle ergometry, which reveals the degree of physical tolerance. exercises.
Coronary angiography, which detects stenosis in half of patients.

The patient may also be prescribed an MRI if his locality there is a suitable research instrument. We will talk about the treatment of Prinzmetal syndrome further.

Treatment

Treatment is optimally carried out in a hospital, since this way the dynamics of the disease can be monitored. The basis of treatment is a combination of therapeutic and medicinal methods. In very rare cases, the patient requires surgery.

In a therapeutic way

The basis of the therapeutic technique is a complete revision life principles. The patient must give up bad habits, quit smoking and drinking. It is also important to adjust your diet:

Limit animal fat consumption to 30% of total calories.
Limit salt intake.
Limit your consumption of spices and herbs.
Take multivitamins.
Pay special attention to protein foods and vegetables.

Along with this, the patient should engage in physical therapy including cardio exercises.

By medicinal method

For long-term drug therapy, patients are prescribed:

nitrates;
calcium antagonists;
alpha-blockers;

To relieve angina attacks, the patient should take nitroglycerin (under the tongue) and nifedipine.

Operation

Surgery is indicated only in cases of significant narrowing of the artery and when angina develops in the area of stenosis. The following manipulations are used:

Angioplasty. During the operation, the vessel is expanded using a balloon, and in this state it is fixed with a metal awning.
Coronary artery bypass surgery. The operation involves suturing any of the patient’s vessels to the coronary artery to allow blood to bypass the narrowed area.

In very rare cases, the disease affects the heart to such an extent that it is no longer able to work on its own. Then the patient is indicated for surgical intervention.

Prevention of variant Prinzmetal angina

Preventive measures for Prinzmetal angina come down to general rules:

Diet with reduced content animal fat and salt, increased - vegetables and cereals.
Exclusion of alcohol and tobacco.
Compliance with the rest and work schedule.
Healthy sleep of at least 8 hours.
Avoiding stress.

Complications

Most common complication Prinzmetal's angina is a myocardial infarction in which some of the heart muscle cells die. Also, in the absence of adequate treatment, angina pectoris can lead to:

arrhythmias;
severe form of tachycardia;

The most terrible complication of the disease is sudden cardiac death, which can be reversible if medical attention is provided in time.

In conclusion, let's talk about the prognosis for vasospastic angina.

Forecast

It is difficult to predict the course of angina pectoris, since the condition depends on various factors: the severity of the attacks, the patient’s age and others.

If the heart is weakly affected, then the mortality rate is extremely low: only 0.5 per year.
With severe heart damage, the mortality rate is 25%.

You will find even more useful information on Prinzmetal’s angina and its other types in the following video: