What is vasospastic angina. Features of an attack of vasospastic angina pectoris, methods of diagnosis and treatment Spastic angina pectoris

Angina pectoris is one of the clinical forms of coronary artery disease, which is manifested by bouts of pain and other symptoms. The disease is due to the fact that the blood flow to the myocardium decreases, and he himself begins to require more oxygen. The disease is divided into several types, one of which is vasospastic angina, which in turn refers to an unstable form of the disease. We will discuss this type of disease in this article.

To begin with, it is worth noting that he has two more names - variant angina and Prinzmetal's angina. The last name reveals to us the name of an American cardiologist who first described this type of disease in 1959. However, the word "vasospastic" most accurately conveys the essence of this disease.

Vasospastic type angina pectoris most often occurs in people aged 30 to 50, although the form itself affects only five percent of the disease. The difference between this form is that during its development, a spasm of the heart vessels occurs, although processes associated with the coronary arteries usually occur. But still there is evidence that with this form in the coronary arteries in which spasm occurs, there is a minimal lesion of atherosclerosis.

Causes of the disease

As we have already said, the coronary artery gives in to spasm. Because of this abnormal local contraction smooth muscle there is a narrowing of the lumen, as a result of which blood enters the heart muscle in a smaller amount than necessary. There are factors that provoke an attack of angina pectoris:

• emotional stress;
• hypothermia;
• hyperventilation;
• diabetes;
• smoking and excessive drinking and so on.

There are so-called age-related causes of angina pectoris.

1. Age. There is a certain age threshold at which the risk of the disease increases. It should be noted that fifteen years ago, the primary signs of angina pectoris appeared after reaching the age of 50. Today there is a decrease in this number, cardiovascular diseases increasingly common in younger people. Now, it is even difficult to say that the threshold has dropped to forty years, since there are cases when even twenty-year-olds have not only symptoms of angina pectoris, but also myocardial infarction.
2. Heredity. It is noticed that there is a connection between the occurrence of the disease among the next of kin. Therefore, if among those there are persons with diseases of the cardiovascular system, then you need to be on the alert and carefully monitor yourself.

Symptoms of the disease

Consider the differences between variant angina and the classic form of the same disease. First, we note that these differences mainly relate to the main symptom of the disease - pain.

1. The pain develops at rest. It is not provoked by emotions or physical stress. Under these conditions, the pain may disappear or weaken.
2. It is noticed that the pain increases and decreases for approximately the same duration. Classical angina implies that the pain disappears more quickly if the patient maintains complete rest.
3. In variant angina, the pain is often more severe and prolonged, it may last for more than twenty minutes, although it is possible that it will last only a few minutes and be mild.

1. Pain attacks usually occur at the same time of the night or day.
2. Pain is cyclical. It always has a climax observed after a few minutes. Pain can also increase with interruptions, which are noted sometimes during an attack.
3. There are usually no changes on the working electrocardiogram, but the ST segment may be shifted down, as in the classical form of the disease. A stress test usually does not cause pain.

During an attack, blood pressure and pulse usually remain unchanged. Otherwise, the symptoms of vasospastic angina are the same as in stable angina. The pain is cutting, pressing or burning in nature and is localized mainly in the region of the heart.

The attack may be accompanied by other signs:

• nausea;
• high blood pressure;
• profuse sweat;
• headache;
• pallor;
• heart rhythm disturbances;
• fainting.

It is worth noting that pain, like discomfort, can be felt in different areas, from the lower jaw to the epigastric region. In addition, shortness of breath, defined as the equivalent of pain, may occur. It appears at the moment when it is difficult to exhale or inhale. Shortness of breath is associated with a violation of the contractile activity of the heart, which occurs due to a lack of oxygen. Shortness of breath can occur both with a painless course of angina pectoris, and together with pain, as an accompanying factor.

Violations heart rate with variant angina pectoris is unstable. This means that someone may experience a feeling of an accelerated heartbeat, and someone, on the contrary, a feeling of cardiac arrest.

Any of these symptoms require emergency care and see a doctor as soon as possible. To make an accurate diagnosis to identify the causes, it is necessary to conduct a qualitative diagnosis of the patient's condition.

Diagnostic methods

So far, there are no reliable methods for diagnosing variant angina pectoris, however clinical picture similar to resting angina. But it is worth noting that most often there is no atherosclerotic plaque. An accurate diagnosis is based on the exclusion of unstable and stable angina pectoris. A number of methods are used for examination.

1. ECG. If it is possible to record during an attack, ST segment elevation will be noted. Most often, this is observed in several leads at once. In addition, you can see the return of this segment to the field of how it turned out to stop the pain syndrome.
2. Daily ECG monitoring. It helps to detect episodes of elevation in the same segment.

1. ECG during a test with a load of the physical plane. This method provokes angina pectoris in the active phase, which is characterized by the rise of the ST segment in thirty percent of cases.
2. provocative tests. These include: hyperventilation test, cold test, pharmacological tests using acetylcholine and dopamine. A cold test helps to identify an attack and changes on the ECG. To do this, you need to prepare water, the temperature of which is four degrees above zero. There you should lower your hand to the middle of the forearm for five minutes. If there are manifestations of ischemic changes on the ECG within ten minutes or during the dive, then the sample is considered positive.
3. coronary angiography. With it, you can determine the local transient spasm of the coronary artery.

Coronary angiography provides very important information. If there are no atherosclerotic lesions of the coronary artery, which are detected by angiography, then intravenous provocative tests with methacholine, methylergonovine and acetylcholine can be used.

The same tests are used to examine individuals who have episodes of transient ST segment elevation. They will help to identify local vasospasm of the coronary artery. However, this method can only be used for individuals with non-obstructive lesions. If there are significant obstructive lesions of the coronary artery, such tests are prohibited.

It should be remembered that drug provocative tests pose a threat in relation to the development of long multi-vessel intense episodes of coronary spasm. This means that they can only be performed if nitroglycerin is immediately administered in order to eliminate the spasm.

After conducting the necessary studies, the doctor can make a diagnosis and prescribe treatment. The sooner it begins to act, the better for the person.

How to treat

The treatment of vasospastic angina includes a number of certain measures, the observance of which is very important for the future condition of the patient.

1. The first thing to do in relation to each patient is to identify diseases that aggravate the course of angina pectoris, as well as its clinical manifestations. Each of the detected diseases must be treated.
2. Despite the fact that variant angina is practically independent of atherosclerosis, it is still important to eliminate factors that increase the risk of atherosclerosis.
3. Avoid complications such as heart attack and death. It turns out that it is necessary to improve the prognosis of the disease, to facilitate its course.
4. It is important to reduce the frequency of seizures and their intensity, which will help improve the patient's quality of life.

All these goals can be achieved in three ways. The first is not drug treatment which includes lifestyle adjustments. Now it should be aimed at maintaining the cardiovascular system in an acceptable state through moderate physical activity, proper nutrition and the rejection of bad habits.

However, this method does not mean that you can, without consulting a doctor, adjust your lifestyle yourself. It is the doctor who will be able to choose such a degree of physical activity and such a diet that will have the maximum effect and positively affect human health. Everything is selected individually and only after passing a full examination, which is also important for the second direction.

The next direction is drug treatment, which is selected, again, directly by the attending physician. Usually drugs are used that aim to improve the prognosis. There are several groups of such funds.

1. Antiplatelet drugs. Their action is aimed at protecting against the formation of blood clots at the most early stages. These drugs include Clopidogrel or Acetylsalicylic acid. If the last remedy is taken for a long time, then the risk of developing a heart attack can be reduced by thirty percent. This is especially true for those who have previously suffered a heart attack.
2. Beta blockers. This group is responsible for not allowing stress hormones to act on the heart. In addition, they reduce myocardial oxygen demand, thereby balancing the imbalance in volume and oxygen demand, which is delivered through the coronary arteries that have become a victim of the narrowing process.
3. calcium antagonists. These drugs also reduce myocardial oxygen demand. These include Verapamil, Diltiazem and other medicines. However, it must be remembered that drugs in this group should not be taken in case of disorders that are associated with atrioventricular patency and with sick sinus syndrome.

1. Nitrates. Thanks to them, the veins have the opportunity to expand, so the load on the heart, produced by a joint decrease in oxygen demand from the myocardium, becomes lower. Nitrates include nitroglycerin and dinitrate.

If these methods are ineffective or for other reasons significant for the doctor, a decision on surgical intervention may be made. Let's consider two well-known methods.

1. coronary angioplasty. This method, which has an invasive basis, is focused on restoring the blood supply to myocardial tissues. In order to be sure of the appropriateness of using this method, you need to understand the severity of the disease well. You also need to be sure that drug therapy cannot bring the desired results, and the coronary artery or several arteries really have a significant lesion. Thanks to coronary angioplasty, angina attacks are eliminated, and myocardial contractility improves. However, the risk that re-narrowing of the artery will begin to develop occurs in forty cases in which six months have passed after the procedure.
2. Aorto-coronary bypass. This method assumes that the blood supply to the myocardium will not be restored in the very area of ​​vasoconstriction, but somewhat lower. Another, additional path is formed along which the blood flow will be carried out. This surgical intervention is performed in the third and fifth classes of angina pectoris and in the event that the lumen of the coronary arteries is reduced by more than seventy percent. After such an operation, about a quarter of patients experienced a recurrence of angina pectoris within eight to ten years, so the question may subsequently arise of repeating this operation.

Do not despair if variant angina is revealed. Of course, this disease has its complications. However, consequences such as myocardial infarction and death are not so common. Nothing serious will happen if you consult a doctor in time and start treatment.

In addition, preventive measures aimed at normalizing physical activity, observing the regime of work and rest, giving up bad habits and maintaining proper nutrition are very important. Under these conditions, angina pectoris will not only not want to worsen, but it will even be afraid to develop in a person who is serious about his health.

MD V.P. Lupanov
Institute clinical cardiology them. A.L. Myasnikova RKNPK Ministry of Health of the Russian Federation, Moscow

stable angina. When an atherosclerotic plaque narrows the diameter of the main coronary artery by 70% or more, the reduced blood flow may still be sufficient to provide a low myocardial oxygen demand at rest, but not enough to increase this demand under the influence of physical or psycho-emotional stress. This results in an increase in heart rate, blood pressure(BP) and increased myocardial contractility; All these factors increase myocardial oxygen demand. One factor that can potentially exacerbate inadequate oxygen delivery in stable angina is inadequate vasoconstriction due to endothelial dysfunction. Normally, an increase in myocardial oxygen demand during exercise is balanced by an increase in blood flow, since the accumulation of local metabolites causes vasodilation. With endothelial dysfunction, vasodilation is impaired and paradoxical vasoconstriction is possible. In some patients with stable angina, fluctuations in arterial tone play a minimal role in reducing oxygen delivery to the myocardium, and the level of physical activity that causes angina is almost constant. These patients have "fixed threshold angina". In other cases, the degree of dynamic obstruction caused by vasoconstriction or vasospasm plays a more significant role, and in this group of patients "variable threshold angina" may be observed.

For example, there are days when the patient can exercise without chest discomfort, but on other days the same level of myocardial oxygen demand causes symptoms - this difference reflects fluctuations in vascular tone in places with fixed stenosis.

Clinical manifestations of myocardial ischemia. During ischemia, cardiomyocytes switch from aerobic to anaerobic metabolism. Reduced ATP production disrupts the interaction between contractile proteins and leads to a transient decrease in both systolic contractility and left ventricular (LV) diastolic relaxation. In addition, there is a local accumulation of products of anaerobic metabolism (for example, lactate, serotonin, adenosine). These substances activate peripheral pain receptors in the C7–Th4 segments of the spinal cord and cause angina pectoris. During the pain syndrome, generalized sympathetic and parasympathetic stimulation can cause tachycardia, sweating, and nausea. Since ischemia leads to impaired diastolic relaxation of the myocardium, LV stiffness increases and intraventricular diastolic pressure increases. High blood pressure is transmitted to the pulmonary vasculature and can cause dyspnea and pulmonary edema. In addition, transient disorders of ion transport in the cardiomyocyte and local accumulation of metabolites can cause dangerous ventricular arrhythmias. After the resolution of an acute ischemic episode (that is, after the balance between oxygen supply and demand is restored), the symptoms of angina completely disappear, and in the case of short-term ischemia, there is no persistent damage to the myocardium. Stable angina pectoris is usually divided into classes of severity (Table 2).

Vasospastic angina. A number of patients develop episodes of local spasm of the coronary arteries in the absence of obvious atherosclerotic lesions; this syndrome is called "variant" angina or Prinzmetal's angina. In this case, oxygen delivery to the myocardium is reduced due to intense vasospasm, which causes angina pectoris. The mechanism of development of such a pronounced spasm is completely unknown. Many of these patients are thought to have initial atherosclerosis manifesting only as endothelial dysfunction, as patients with this condition have an abnormal response to many endothelium-dependent vasodilators (eg, acetylcholine and serotonin).

Vasospastic angina often develops at rest, since the cause of ischemia is a pronounced transient decrease in oxygen delivery, and not myocardial demand for it.

"Silent" (painless, asymptomatic) ischemia. Episodes of myocardial ischemia sometimes develop in the absence of subjective discomfort or pain (such cases are called "silent ischemia"). These asymptomatic episodes may occur in patients who otherwise experience typical angina symptoms, but sometimes "silent" ischemia may be the only manifestation of CAD. "Silent" ischemia can be detected using instrumental methods (outpatient Holter ECG monitoring or stress test). Silent ischemic episodes occur in 40% of patients with stable angina and in 2.5–10% of middle-aged men who do not present complaints. Given the importance of the symptom of angina pectoris as a physiological alarm signal, the asymptomatic nature of ischemia becomes a negative factor. The reason why some episodes of ischemia are "silent" and others are symptomatic is not fully understood. The severity of ischemia cannot fully explain these differences, as some patients can even tolerate myocardial infarction without symptoms.

Syndrome X. This term refers to patients with typical symptoms of angina pectoris who do not have evidence of significant stenosing coronary artery disease on coronary angiography. Some of these patients show evidence of ischemia during exercise testing. The pathogenesis of ischemia in this situation may be associated with inadequate vasodilation of the resistive coronary arteries. It is believed that resistive vessels (which are too small to be seen on coronary angiography) in these patients may not dilate adequately during periods of increased myocardial oxygen demand. The prognosis of patients with "X" syndrome is better than that of patients with overt atherosclerotic lesions.

Treatment of chronic ischemic heart disease

The goal of CHD treatment is to improve the patient's quality of life by reducing the frequency of anginal attacks, preventing acute myocardial infarction and improving survival. Modern strategy for the treatment of myocardial ischemia is to restore the balance between the need and delivery of oxygen to the myocardium. In patients with chronic coronary artery disease with various symptoms (pain, arrhythmias, heart failure), treatment is carried out with antianginal (AA), antiarrhythmic and other drugs in order to achieve the disappearance of existing symptoms or their significant reduction in the shortest possible period.

In other words, purely symptomatic tasks are set first, and the tasks of the strategic plan are solved within the framework of a secondary prevention program, the goals of which are: preventing premature death, inhibiting the progression and achieving partial regression of coronary artery atherosclerosis, preventing clinical complications and exacerbations of the disease, reducing the number and duration of hospitalizations (especially urgent ones).

Antianginal therapy

Table 3 lists the drugs used for AA therapy. These include: nitrates, b-blockers, calcium antagonists and metabolic agents.

Relief of an acute attack of angina pectoris. With the development of an attack of angina pectoris, the patient should stop physical activity. Sublingual nitroglycerin (NGT) is the drug of choice. NTG acts in 1-2 minutes and stops ischemia mainly due to the relaxation of the smooth muscles of the vascular wall, while dilatation of the veins occurs. Venous dilation reduces venous return to the heart, so that the result is a decrease in LV volume and a decrease in myocardial oxygen consumption. Another effect of IGT is coronary vasodilation with a corresponding effect on coronary blood flow. This effect is of particular importance mainly in cases of vasospastic angina. All patients with coronary artery disease should always carry NTG (sublingual tablets or aerosol (spray) in cans) with them and know how to behave when symptoms characteristic of coronary pain occur. So, in the event of retrosternal pain (anginal pain for more than 2-3 minutes), it is necessary to stop activity, take NTG. If NTG is ineffective within 5 minutes - re-take two tablets of NTG. Further persistence of pain requires contacting the ambulance service "03". Patients with angina when the nature of the pain changes, you should consult a doctor to correct the treatment.

Organic nitrates are the main class of AA drugs and come in a variety of forms. NTG sublingual tablets or spray are intended for the relief of acute attacks due to their rapid onset of action. In addition, if the drug is taken immediately before the expected exercise, which usually causes angina pectoris, fast-acting nitrates may be useful in the prevention of anginal attacks. Prevention of angina pectoris is achieved with various forms of nitrates, including oral isosorbide di- or mononitrate tablets or (less commonly) a once-daily transdermal nitroglycerin patch.

Long-term therapy with nitrates is limited by the development of tolerance to them (i.e., a decrease in the effectiveness of the drug with prolonged, frequent use), which appears in some patients, and withdrawal syndrome - with a sharp cessation of taking drugs (symptoms of exacerbation of coronary artery disease).

The undesirable effect of developing tolerance can be prevented by creating a nitrate-free interval of several hours, usually while the patient is asleep. This is achieved by intermittent administration of short-acting nitrates or special forms of retarded mononitrates. A drug Olicard 40 retard is a retarded form of isosorbide-5-mononitrate, presented as a microsphere coated with a dosing membrane, with a gradual release active substance. After ingestion of the drug Olikard 40 retard, the level of the active substance - isosorbide-5-mononitrate - in the blood plasma decreases below the minimum effective concentration (100 ng / ml) after 19 hours. The phase following this with a low content of nitrate in the blood - the nitrate-free period - ensures the restoration of vascular activity and tone. The characteristic dynamics of the level of the active substance in the blood plasma when using Olikard prevents the emergence of tolerance.

Nitrates, apparently, do not affect the survival of patients with coronary artery disease. They can only be prevented by creating a nitrate-free interval of several hours, usually while the patient is asleep. Nitrates, apparently, do not affect the survival of patients with coronary artery disease. They are used only to relieve symptoms, during periods of deterioration and with increased stress. The use of nitrates in patients after myocardial infarction has a beneficial effect: it reduces myocardial ischemia, leads to the prevention of left ventricular remodeling, helps maintain collateral circulation, causes an antithrombotic effect, and contributes to electrical stabilization of the myocardium. Side effects of nitrates: headache, dizziness and palpitations caused by reflex sinus tachycardia. The latter can be leveled by a combination of nitrates with b-blockers, and a headache - by the simultaneous administration of a tablet of validol or analgesics. When treating with nitrates: 1) the practitioner is faced with a choice among a variety of nitropreparations that differ in chemical structure, form of release, production technology and, as a result, pharmacokinetic and pharmacodynamic features; 2) the results of the studies indicate the low efficiency of depot-nitroglycerin preparations, which is due to low and unstable plasma trinitrate concentrations, often not exceeding the subtherapeutic level and insufficient to achieve a pronounced effect; 3) the main trend in therapy is the orientation towards retard forms of drugs that are convenient for the patient, because

allow you to reduce the frequency of administration, while maintaining a stable clinical effect, for example, the retard form of isosorbide-5-mononitrate, Olikard 40 retard, taken 1 time per day; 4) reduction in the use of patches, discs and ointments with nitroglycerin.

b-blockers have an AA effect based on a decrease in myocardial oxygen demand. They interact with b-adrenergic receptors, which are of 2 types: b2-adrenergic receptors are localized on peripheral blood vessels and in the bronchi, and b1-adrenergic receptors are found almost exclusively in the myocardium. Stimulation of b1-adrenergic receptors with catecholamines or drugs (sympathomimetics) leads to an acceleration of heart rate and an increase in myocardial contractility. Therefore, adrenoreceptor blockers reduce the force of ventricular contractions and slow down the rhythm, thus reducing myocardial oxygen demand and stopping ischemia. b-blockers are generally well tolerated but have side effects. For example, they can provoke bronchospasm in patients with concomitant asthma due to antagonism with bronchial b2-adrenergic receptors. Although selective b1-blockers are theoretically less likely to cause bronchospasm in such patients, the full selectivity of these drugs for b1-receptors is not observed, and in general, the use of all b-blockers in patients with obstructive pulmonary disease, heart failure should be avoided. Bisoprolol and nebivolol have the highest degree of selectivity. Relative contraindications to β-blockers are bradycardia and heart block, as further impairment of conduction should be avoided. β-blockers sometimes cause weakness and sexual dysfunction and may impair glycemic control in diabetic patients. The drugs could theoretically impair myocardial perfusion by blocking the vasodilating b2-adrenergic receptors of the coronary arteries. However, this effect is usually offset by self-regulation and vasodilation of the coronary arteries in response to the accumulation of local metabolites. The optimal heart rate in a patient receiving b-blockers should be 55-60 beats / min. at rest. However, physicians still underuse this class of drugs, especially in outpatient practice, due to fear of side effects and the need to monitor the patient and ECG when prescribing them. The most commonly used drugs include b1-selective: atenolol, metoprolol, betaxolol, acebutolol, nebivolol and non-selective ones - propranolol, pindolol, nadolol, penbutalol, carvedilol.

Carvedilol is a new multifunctional neurohumoral antagonist that has a combined non-selective b-, a1-blocking and antioxidant effect. It blocks both b1- and b2-adrenergic receptors without its own sympathomimetic activity. Due to the blockade of a1-adrenergic receptors located in the smooth muscle cells of the vascular wall, carvedilol causes pronounced vasodilation. Thus, carvedilol combines b-blocking and vasodilatory activity, which is mainly associated with its AA and anti-ischemic effect. In an open non-comparative study conducted at the Institute of Cardiology studied the clinical efficacy of 2-month monotherapy carvedilol (25 mg/day) in 15 patients with stable angina I-II FC. A significant decrease in the frequency of angina attacks (by 91%), an increase in tolerance to physical activity(threshold power by 33%, total work by 81%). Carvedilol can also be successfully used in the treatment of moderate arterial hypertension associated with IHD. When comparing carvedilol (mean daily dose 20.5 mg) and atenolol (average daily dose of 25.9 mg) both drugs, given twice a day, were shown to be equally effective in the treatment of patients with stable exertional angina.

b-blockers should be preferred in patients with coronary heart disease in: 1) there is a clear relationship between physical activity and the development of an angina attack; 2) concomitant arterial hypertension; 3) supraventricular or ventricular arrhythmias; 4) myocardial infarction; 5) a pronounced state of anxiety.

Calcium antagonists (calcium channel blockers, /CCC/). CCBs are antagonists of type L voltage-gated calcium channels. However, the effects various drugs this class are different. Dihydropyridines (eg, nifedipine) are potent vasodilators. They stop myocardial ischemia by: 1) reducing myocardial oxygen demand (vasodilation reduces LV filling and size; arterial vasodilation reduces arterial resistance) and 2) increasing oxygen delivery to the myocardium by dilating the coronary arteries. The latter mechanism leads to the fact that CCBs are also powerful drugs for the treatment of coronary artery spasm. Verapamil and diltiazem are also vasodilators, but not as strong as the drugs of the dihydropyridine group. However, these agents have additional positive AA effects: they reduce the force of ventricular contractions (inotropy) and slow the heart rate.

Accordingly, verapamil and diltiazem reduce myocardial oxygen demand through these mechanisms. Recent studies have discussed the safety of short-acting dihydropyridine CCBs (nifedipine) in patients with CAD. In meta-analyses of randomized trials, treatment with these drugs was associated with an increased incidence of myocardial infarction and mortality. However, these data are not supported by recent studies, although the negative effects caused by CCBs may be associated with a rapid hemodynamic response and fluctuations in blood pressure. Therefore, at present, mainly long-acting CCBs (amlodipine, felodipine) are recommended for the treatment of stable angina pectoris; they are used as second-line drugs if symptoms are not relieved by b-blockers and nitrates. CCB should be preferred for concomitant: 1) obstructive pulmonary diseases; 2) sinus bradycardia and severe disorders of atrioventricular conduction; 3) variant angina (Prinzmetal). The undoubted advantages of drugs from the BPC group is a wide range of pharmacological effects, pathophysiologically aimed at eliminating the manifestations of coronary insufficiency. These include: the actual AA effect, hypotensive effect, antiarrhythmic effect, especially in relation to supraventricular arrhythmias. BCC therapy also has a beneficial effect on the course of atherosclerosis; their inhibitory effect on the atherosclerotic process was shown. The beneficial effects of calcium antagonists in relation to the regression of LV hypertrophy and their nephroprotective effect, which should be taken into account in the treatment of patients with coronary artery disease, also deserve attention.

AA drugs can be used as monotherapy or in various combinations. Combination therapy of AA drugs in patients with stable angina II–IV FC is carried out according to the following indications: impossibility of selection of effective monotherapy; the need to enhance the effect of ongoing monotherapy (for example, during a period of increased physical activity of the patient); correction of adverse hemodynamic changes (for example, tachycardia caused by BCC of the dihydropyridine group or nitrates); with a combination of angina pectoris with hypertension or cardiac arrhythmias that are not compensated in cases of monotherapy; in case of intolerance to patients of conventional doses of AA drugs in monotherapy (in this case, to achieve the desired AA effect, small doses of drugs can be combined).

However, β-blockers should be combined with caution with verapamil and diltiazem, since the summation of their negative effects can lead to excessive bradycardia and the appearance of congestive heart failure. The combined use of nitrates and calcium antagonists may not lead to the expected increase in the severity of the effectiveness of treatment.

In addition to the main AA drugs, other drugs (drugs of metabolic action, potassium channel activators, ACE inhibitors, antiplatelet agents) are sometimes prescribed.

metabolic agents. This term is understood as therapeutic approaches to the treatment of patients with coronary artery disease, designed not to increase blood flow to the ischemic myocardium, but to increase the resistance of cardiomyocytes to transient ischemia. Currently, trimetazidine has a reliably proven metabolic effect. Trimetazidine at a dose of 20 mg 3 times a day and modified-release trimetazidine 35 mg 2 times a day have a cardioprotective effect on cardiomyocytes, improve the efficiency of oxygen utilization by tissues. Trimetazidine is an anti-ischemic drug, the first in a class of metabolic drugs known as 3-ketoacyl CoA thiolase (3-CAT) inhibitors. Trimetazidine optimizes myocardial energy metabolism due to partial suppression of fatty acid b-oxidation caused by selective inhibition of long-chain 3-CAT. As a result, there is a shift towards glucose oxidation, which leads to: a balance of anaerobic glycolysis and glucose oxidation; reduction of intracellular acidosis and an excess of calcium; maintaining the production of ATP. Trimetazidine also increases the exchange of phospholipids, which provides membrane protection. At the same time, the specific metabolic mechanism of action is not accompanied by hemodynamic side effects. Trimetazidine reduces the severity clinical manifestations angina pectoris and increases exercise tolerance, improves LV contractility in patients with coronary artery disease. Trimetazidine provides full complementary efficacy in combination therapy with b-blockers, calcium antagonists, long-acting nitrates.

When conducting AA therapy, one should strive to almost completely eliminate anginal pain and return the patient to normal activity. However, therapeutic tactics do not give the desired effect in all patients. In some patients with exacerbation of coronary artery disease, there is sometimes an aggravation of the severity of the condition.

In these cases, it is necessary to consult cardiac surgeons in order to be able to provide the patient with cardiac surgery.

Secondary prevention

The goal of secondary prevention is to stop disease progression and prevent clinical complications. Moreover, numerous studies have shown that long-term complex prevention can achieve partial regression of coronary atherosclerosis with an expansion of the diameter of the affected arteries. Secondary prevention consists of drug and non-drug components.

Medical component of secondary prevention

The main recommendations for pharmacotherapy aimed at preventing recurrence of coronary artery disease and its progression include: 1) taking acetylsalicylic acid 75–325 mg/day; in the presence of contraindications - clopidogrel at a dose of 75 mg / day; 2) b-blockers (in the absence of contraindications); 3) lipid-lowering therapy and/or diet to achieve an LDL-cholesterol level of less than 100 mg/dl; 4) angiotensin-converting enzyme inhibitors (ACE inhibitors) - in the presence of heart failure, left ventricular failure (ejection fraction less than 40%), arterial hypertension, diabetes.

Acetylsalicylic acid and other antiplatelet agents. Antiplatelet therapy with acetylsalicylic acid is a standard addition to the CHD treatment regimen. Acetylsalicylic acid inhibits platelet aggregation (and therefore reduces the subsequent release of procoagulants and vasoconstrictors from them) and has a proven reduction in the risk of myocardial infarction in patients with stable angina pectoris. In the absence of contraindications (allergies, stomach pathology), acetylsalicylic acid is prescribed to patients with confirmed coronary heart disease for life, especially after myocardial infarction. Those who suffer from coronary artery disease should always have an acetylsalicylic acid tablet and NTG with them. If there is pain behind the sternum that does not go away at rest or after taking NTG under the tongue, acetylsalicylic acid must be chewed and swallowed. To reduce the risk of complications from the gastrointestinal tract (bleeding) associated with long-term use of acetylsalicylic acid, two main approaches are proposed: the appointment of low doses of acetylsalicylic acid (75-100 mg) and the use of special dosage forms of the drug (buffered and enteric-soluble forms ).

You can also use gastroprotective agents (ranitidine, etc.).

Ticlopidine is a thienopyridine derivative that inhibits platelet aggregation induced by adenosine diphosphate (ADP) and other factors (thrombin, collagen, thromboxane A2, and platelet activating factor). In addition, ticlopidine reduces blood viscosity by reducing plasma fibrinogen concentration. In patients with stable angina, ticlopidine limits platelet aggregation, but unlike acetylsalicylic acid, its administration does not appear to improve prognosis. The drug has side effects: gastrointestinal disorders, skin rashes, pathological reactions from the liver. The most serious side effect is severe neutropenia, occurring in approximately 1% of patients. Usually it quickly regresses after discontinuation of the drug. Rare side effects (less than 1:1000) include episodes of thrombocytopenic purpura. Taking ticlopidine should be accompanied by monitoring of blood counts. After angioplasty (PTCA) and stenting of the coronary arteries, in cases of contraindications for treatment with acetylsalicylic acid, ticlopidine can be prescribed for 2 days at 250 mg 3 times a day, and then 250 mg 2 times a day for 6 months. The combination of ticlopidine with acetylsalicylic acid has an advantage over acetylsalicylic acid monotherapy.

Clopidogrel is a thienopyridine derivative, similar in chemical structure to ticlopidine, but superior to the latter in its antithrombotic effect. The drug prevents ADP-induced platelet activation by selective irreversible blockade of the interaction between platelet ADP receptors and ADP, as well as by inhibiting the ability of glycoprotein IIb-IIIa receptors to fix fibrinogen. Clopidogrel can be considered as an alternative drug to ticlopidine after PTCA and coronary stenting. Clopidogrel is given 72 hours before PTCA, initially at a loading dose of 300 mg followed by a maintenance dose of 75 mg daily. A small number of cases of thrombocytopenic purpura have been reported in patients taking clopidogrel, so it is necessary to monitor blood counts for the timely detection of this complication.

b-blockers. In addition to the positive properties of b-blockers in the treatment of stable angina, numerous studies have demonstrated their ability to reduce the incidence of recurrent heart attacks and mortality in acute myocardial infarction.

Moreover, β-blockers have been shown to reduce the likelihood of primary myocardial infarction in hypertensive patients. Therefore, b-blockers are considered first-line drugs in the secondary prevention of coronary artery disease. It has been established that long-term use of b-blockers in patients with coronary artery disease reduces mortality by an average of 25%. In this case, the following doses of drugs are effective: bisoprolol 5-10 mg once, propranolol 20-80 mg 2 times a day, metoprolol 50-200 mg 2 times a day and carvedilol 25-50 mg 2 times a day. The duration of the appointment of b-blockers after myocardial infarction should be long (several years), although the exact duration of treatment is unknown. It has only been shown that early interruption of therapy can significantly worsen the result of treatment.

lipid-lowering drugs. Despite controlling the symptoms of angina pectoris, none of the classes of AA drugs can slow or reverse the atherosclerotic process that underlies chronic CAD. However, there is evidence that this goal is achieved by medically lowering LDL cholesterol. Studies have shown a marked reduction in coronary events and mortality in patients who were able to significantly reduce blood LDL cholesterol levels with the help of diet and pharmacotherapy (statins).

Non-pharmacological methods of prevention. The main risk factors for coronary artery disease: smoking, blood pressure і140/90 mm Hg, HDL cholesterol<40 мг/дл у мужчин и <45 мг/дл у женщин), наличие ИБС у ближайших родственников (у мужчин <55 лет, у женщин <65 лет). Дополнительными факторами, требующими коррекции при гиполипидемической терапии, являются ожирение, гиподинамия, характер питания, повышенные уровни липопротеина (а), гомоцистеина, протромботических факторов, уровень С–реактивного белка, признаки бессимптомного атеросклероза, нарушение толерантности к глюкозе.

Taking into account the mechanism of action, the following are used in atherogenic hyperlipidemias: main classes of lipid-lowering drugs: 1) inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase ("statins"), which include: lovastatin, simvastatin, pravastatin, fluvastatin, atorvastatin, rosuvastatin; 2) fibrates, or fibric acid derivatives (gemfibrozil, fenofibrate, bezafibrate, ciprofibrate, etc.); 3) nicotinic acid and its derivatives; 4) omega 3-polyunsaturated fatty acids from fish oil, which are recommended as a means of secondary prevention (class I) in patients with myocardial infarction.

In recent years, statins have discovered many new therapeutic properties that are not related to their lipid-lowering effect, although in some cases the same effect can be achieved by both lipid and non-lipid mechanisms of action. The pleiotropic effects of statins can be divided into 4 groups according to their effect on: 1) endothelial function of the arteries; 2) atherogenesis (antiproliferative, anti-inflammatory effect); 3) some clinical cardiac syndromes not associated with atherosclerosis (hypotensive, antiarrhythmic); 4) various types of non-cardiac pathology (dissolution of cholesterol stones, prevention of osteoporosis, etc.).

ACE inhibitors (ACE inhibitors) play an important role in the secondary prevention of CHD and its complications. By inhibiting excessive production of angiotensin, a powerful vasoconstrictor and atherogenic factor, as well as by protecting bradykinin, which has vasoprotective properties, from decay, ACE inhibitors normalize blood pressure, prevent remodeling of resistive arteries and arterioles, cause regression of the hypertrophied left ventricle of the heart, and restore normal endothelial function. They are of particular importance in patients with heart failure and patients with post-infarction cardiosclerosis. With their help, it is possible to significantly increase the contractile function of the myocardium and prevent pathological remodeling of the left ventricle. Indications for the appointment of ACE inhibitors are: 1) hypertension, as well as renovascular and some other forms of secondary hypertension; 2) chronic heart failure caused by LV systolic dysfunction, regardless of etiology, functional class and the presence or absence of clinical manifestations; 3) secondary prevention in patients with myocardial infarction; 4) treatment of diabetic nephropathy and some other parenchymal diseases. According to numerous prospective studies, it has been established that long-term use of ACE inhibitors in patients with myocardial infarction can reduce mortality by 25%.

Non-drug component of secondary prevention

Fight against risk factors. The key point aimed at achieving the goals of secondary prevention in coronary artery disease is the impact on the risk factors underlying atherosclerotic lesions of the coronary arteries. Influence on risk factors implies: mandatory smoking cessation, careful control of blood pressure and normalization of its level, systematic exercise and training loads for 30-40 minutes 2-3 times a week, taking lipid-lowering drugs (statins), careful control of glycemia in diabetes mellitus diet, and weight control.

Depending on the functional class for patients with coronary artery disease, one can choose the types and intensity of ordinary physical activity (walking, climbing stairs, carrying heavy loads, sexual activity), housework and work in the garden.

In this way, In the initial therapy of patients with angina pectoris, all elements of the following checklist should be included: BUT. Acetylsalicylic acid and antianginal therapy. AT. b-blockers and blood pressure control. C. Smoking and cholesterol (smoking cessation, lowering cholesterol). D. Diet and diabetes mellitus (following a diet and normalizing glucose levels). E. Educational program in the treatment and prevention of cardiovascular diseases, physical activity.

Dynamic monitoring of patients with chronic forms of coronary artery disease. The principles of differentiated and stepwise treatment of chronic coronary artery disease were developed by local scientists and still have not lost their significance. . The appointment of AA therapy, depending on the form of chronic coronary artery disease, the severity of angina pectoris (functional class) and its clinical course, the patient's condition, comorbidities, myocardial infarction, taking into account the side effects of drugs and other factors, is considered reasonable and allows the doctor to choose adequate treatment and increase its efficiency. However, in outpatient settings, there are frequent cases when drugs are chosen incorrectly (the most effective and “expensive” ones are excluded) or their single and daily doses are reduced; irrational combinations of AA drugs are used; insufficient duration of treatment is prescribed (for example, short courses); insufficient control over the condition of patients is carried out.

In the post-hospital period, the attending physician should schedule follow-up examinations. Patients with adequately treated stable angina may be advised to reevaluate their condition every 4 to 12 months. If the patient is in a stable condition and is able to come to the doctor's office, then during the first year of observation, it is recommended to conduct an assessment of the condition every 4–6 months; after the first year - it is recommended to evaluate the condition annually (in these cases, the annual visit may be replaced by a phone call or other form of contact between the patient and the doctor). Some patients are incapable of a real assessment of their condition, so they should be called and examined more often. During the period of outpatient management of patients with coronary artery disease with stable angina, it is necessary to assess: whether the patient's level of physical activity has decreased since the last visit; whether there is an increase in the frequency and severity of angina pectoris (if symptoms worsen or the patient has reduced physical activity to avoid angina attacks, then his condition should be assessed using ECG registration, the method of dosed physical activity, echocardiography and prescribe treatment in accordance with the data obtained).

It is also necessary to find out how well the patient tolerates the treatment; how successful is the elimination of risk factors and improvement of his knowledge about coronary artery disease; whether new comorbidities have arisen or the severity of known comorbidities has increased. In the absence of angina pectoris or the presence of stable angina pectoris I-II at the follow-up examination, patients are advised to continue drug therapy. Often, after discharge from the hospital, doctors unreasonably reduce the dose of AA drugs, transfer patients to other, more "affordable" and cheaper drugs - thus, patients do not receive the desired effect from the treatment. Therapy on an outpatient basis should be carried out according to the same principles as in the hospital, especially since the physical activity of patients after discharge from the hospital, as a rule, increases. In addition, social factors such as uncertainty about the future, lack of funds, lack of necessary medicines, chronic stress and the resulting depressive states affect the health of patients in the most unfavorable way.

With the progression of symptoms, the appearance of angina pectoris III–IV FC or unstable angina on the background of maximum drug therapy, or the appearance of new symptoms (ventricular arrhythmias, heart failure), patients should be referred to cardiological hospitals for coronary angiography and invasive treatment of coronary artery disease (coronary angioplasty, stenting or CABG).

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From this article you will learn: what is vasospastic angina, how it differs from other forms of angina, how dangerous the disease is. Causes of pathology, symptoms, methods of diagnosis and treatment. Disease prognosis.

Vasospathic angina (or, another name, Prinzmetal's angina pectoris) is called spontaneously occurring attacks of ischemia (oxygen starvation) of the heart muscle, accompanied by prolonged and severe pain behind the sternum (heart, angio pain). The main reason is a sudden spasm of the coronary vessels.

Typical manifestations of angina pectoris (new onset, unstable, tension) are attacks of ischemia and heart pain associated with physical and emotional stress, which usually disappear at rest. Prinzmetal's angina is distinguished as a special form of unstable, it is characterized by:

• longer, severe attacks that occur against the background of absolute rest (during a night's rest);
• attacks appear at the same time (a few hours after falling asleep or early in the morning).

For the development of ischemia of the heart muscle, narrowing (stenosis) of the vascular bed of large coronary arteries by more than 70% is required. With Prinzmetal's angina, such a spasm develops suddenly, for various reasons (atherosclerosis, smoking, hypertension, allergies), the inner layer of blood vessels becomes overly sensitive to various substances that can cause severe narrowing (vasoconstrictors, thromboxane).

It provokes the production of vasoconstrictors, an increase in the activity of the sympathetic or parasympathetic autonomic system (sections of the nervous system that regulates automatic processes - breathing, digestion). The narrowing often occurs in the area of ​​the vessel affected by atherosclerosis, which at the usual time (between attacks) cannot be the cause of ischemia (unexpressed stenosis that does not affect the blood supply to the heart muscle, in 50%).

Prinzmetal's angina is a rare (2% of the total) and rather dangerous forms of the disease. If severe attacks are repeated frequently, the disease quickly (within 1.5-2 months) leads to extensive myocardial infarction (acute ischemia of the heart muscle), life-threatening arrhythmias and can cause cardiac arrest (in 25%). Infrequent attacks lead to fatal complications in combination with obstructive coronary artery disease (lumen blockage by cholesterol plaques or blood clots).

It is impossible to cure Prinzmetal's angina pectoris, methods of prevention and drug therapy can significantly improve the condition of patients with uncomplicated forms (without vascular obstruction). Surgical treatment (stenting, shunting) is used if the disease occurs in combination with severe vascular stenosis.

Patients with vasospastic angina pectoris are observed and treated by a cardiologist, and cardiac surgeons operate.

Characteristic features of vasospastic angina

Attacks can be single or cyclically repeated at certain intervals (from 2 to 15 minutes), sometimes the disease occurs in combination with angina pectoris.

Causes of pathology

The main reason for the development of an attack in vasospastic angina is the narrowing of the coronary arteries (coronary) to a critical state (the diameter of the vascular lumen decreases by more than 70%) due to an increase in the sensitivity of the vascular walls to serotonin, thromboxane, histamine, aggiotensin or adrenaline (vasoconstrictor substances).

An attack can provoke:

• spontaneous increase in the activity of the autonomic nervous system;
• hypothermia (hypothermia);
• hyperventilation of the lungs (increased, rapid breathing);
• emotional stress;

In 90%, an attack of angina pectoris develops for no apparent or obvious reasons, against the background of complete well-being.

Factors against which the disease most often develops:

1. Tobacco smoking (80% of patients are heavy smokers).
2. Atherosclerotic vascular disease.
3. Peptic ulcer, cholecystitis.
4. Arterial hypertension.
5. Allergic reaction.
6. Vegetative-vascular dystonia.
7. Physical inactivity.
8. Obesity.
9. Nervous stress.

Increased blood viscosity plays a certain role.

Symptoms

Before the onset of complications (myocardial infarction), the symptoms of vasospastic angina worsen the quality of life and affect the ability to work only at the time of the attack (from 15 to 30 minutes), then the patient's condition is fully restored.

An attack or a series of attacks usually develop suddenly, during a night's sleep, less often - under the influence of moderate physical activity, at the same time of the day and are accompanied by:

• sharp and intense, pressing, burning, cutting pains behind the sternum;
• increased sweating;
• characteristic pallor of the skin;
• rhythm disturbances (tachycardia);
• fluctuations in blood pressure (increase or decrease);
• nausea;
• dizziness;
• headache;
• loss of consciousness.

Frequent and prolonged attacks of Prinzmetal's angina are quickly complicated by various life-threatening arrhythmias and heart pathologies:

• atrioventricular blockade (violation of the conduction of the excitation impulse from the atria to the ventricles);
• paroxysmal ventricular extrasystole and tachycardia (violation of impulse conduction in the ventricles);
• atrial flutter (violation of conduction in the atria);
• extensive (damage to more than 50% of the myocardium) infarction (acute oxygen starvation and massive cell death);
• aneurysm of the heart (pathological protrusion of the thinned walls of the organ, threatening to rupture).

Complicated Prinzmetal's angina (vasospastic) causes death in 25% of cases.

Diagnostics

The most reliable and informative methods for diagnosing vasospastic angina:

1. ECG during an attack and 24-hour Holter ECG monitoring. These methods allow you to see the characteristic short-term changes in heart rhythm, conduction disturbances, fix myocardial ischemia.
2. Tests with the introduction of chemicals that provoke vascular spasm (acetylcholine, ergometrine), the results of which are positive for vasospastic angina.
3. Tests with exercise (hyperventilation of the lungs, bicycle ergometry, physical exercises) with a negative result (with Prinzmetal's angina attacks in 90% are not associated with physical exertion, they develop at rest).

With the help of coronary angiography (angiography of the coronary vessels), the degree of concomitant atherosclerosis is determined in order to assess the prognosis and prescribe adequate treatment.

Treatment Methods

It is completely impossible to cure vasospastic angina, mainly due to the fact that the causes of critical vascular spasm in 90% are unknown.

At the time of an acute attack, emergency hospitalization is recommended - it is necessary to eliminate the consequences of myocardial ischemia and prevent the development of a heart attack. The only way to provide first aid at home is a nitroglycerin tablet under the tongue (2 times with an interval of 20 minutes until the medical team arrives).

Preventive methods and drug treatment can significantly improve the general condition of patients with uncomplicated forms (rare attacks, the absence of severe atherosclerotic stenosis of the coronary arteries).

Vasospastic angina is treated with surgical methods in cases where attacks develop against the background of a pronounced narrowing of the coronary arteries due to concomitant diseases (atherosclerosis).

Medical treatment

Purpose of treatment:

• prevention of repeated attacks of angina pectoris;
• elimination of violations of the blood supply to the heart and the consequences of ischemia;
• improvement of metabolism and contractility of the heart muscle.

Drugs for vasospatic angina

Surgical methods

As surgical methods of treatment use:

• coronary artery bypass grafting - the creation of an additional vascular bed bypassing the stenosis;
• stenting - expansion of a section of a stenotic vessel by installing a special frame that retains its shape (stent);
• balloon angioplasty - expansion of a vessel section using a catheter with an inflating balloon at the end.

The purpose of the methods is to improve the blood supply to the heart muscle and prevent the development of deadly ischemia (heart attack).

Prevention measures

Prevention is aimed at eliminating risk factors that could affect the development of the disease:

1. It is necessary to get rid of the bad habit - smoking.
2. Normalize nutrition and get rid of obesity.
3. Control and treat atherosclerosis and arterial hypertension.
4. Eliminate the cause of nervous stress.

Forecast

Prinzmetal's angina is a rare and severe form of the disease, it is diagnosed in only 2% of patients.

The prognosis for vasospastic angina depends entirely on the form of the disease, uncomplicated by atherosclerosis of the coronary arteries, rarely recurring attacks are less dangerous (lethal outcome - 0.2% per year) than severe and prolonged ones. With this form of the disease, the probability of developing a massive myocardial infarction and death reaches 10–25% within a year.

Since it is completely impossible to cure the disease, angina pectoris can suddenly recur (recur) - patients are registered with a cardiologist throughout their lives.

Article last updated: April, 2019

Vasospastic angina- this is pain in the chest of a certain nature, which occurs as a result of a spasm of the arteries that feed the heart muscle. If we go into the description of the symptoms in more detail, then we are talking about pressing or baking pain behind the sternum, which often radiates to the neck and left arm. However, sometimes pain can appear in not quite typical places, for example: in the right half of the chest or even in the upper abdomen.

Why does pain appear

Pain in this case is a signal that the oxygen demand of the heart exceeds the capacity of the arteries.

This situation can occur in two cases:

1. There is a mechanical obstruction in the form of an atherosclerotic plaque that closes the lumen of the artery
2. Suddenly there was a spasm of the artery.

If we are talking about the first option, then this condition is called "angina pectoris", if the second - "vasospastic angina". Another synonym for vasospasm is "Prinzmetal's angina", although this is not quite the same thing, since the latter is characterized by changes in the ECG, and with vasospastic angina, the ECG may remain normal.

Why does spasm and vasospastic angina occur?

If coronary angiography is performed on a patient suffering from vasospastic angina pectoris, then it will not reveal significant narrowing of the arteries and significant atherosclerotic plaques. It is believed that vasospasm occurs out of the blue. However, for some reason, the muscle fibers of the arteries still contract, which leads to a narrowing of the lumen of the vessels.

It should be noted that the narrowing of the arteries is a normal response to physical activity: a decrease in the lumen of the vessels increases the rate of blood flow. In addition, the difference in diameters in different arteries allows you to correctly redistribute the blood flow between individual parts of the heart. But for some reason that is not yet clear to us, this reaction sometimes goes beyond the bounds of reason and the artery narrows to such an extent that the lumen of the vessel can be almost completely closed.

It is assumed that vasospasm is associated with a violation of the nervous regulation of muscle fibers, which is a consequence of the deposition of cholesterol in the walls of blood vessels. At the same time, the severity of atherosclerosis may be so insignificant that it may not be possible to detect it by any modern research methods.

How is vasospastic angina treated?

Treatment does not differ significantly from that of coronary heart disease. Commonly prescribed drugs are blood thinners, drugs that control heart rate, drugs to lower cholesterol levels. Additionally, medications can be used to treat concomitant diseases.

At the time of the attack itself, nitroglycerin can be used, but what can really effectively prevent arterial spasm is drugs from the group of calcium antagonists (Diltiazem or Verapamil).

Considering that there are no plaques in the arteries in this type of angina, it seems that the benefit of coronary angiography is not significant, but it is not. Apart from vasospasm in one artery, no one is forbidden to have a few more plaques in others.

In conclusion, it is worth mentioning another variety of vasospastic angina, which is called syndrome X. It manifests itself with the same pain in the chest as ordinary angina pectoris, but its mechanism is the spasm of the smallest, distal (terminal) arteries. Until now, the mechanism of this phenomenon remains unclear, and there is no specific treatment.

Angina pectoris is one of the serious cardiac pathologies. A similar condition is formed as a result of other diseases of the main muscular organ (defect, coronary heart disease - IHD, anemia, etc.). It should be noted that there are several, and one of them is precisely vasospastic angina (according to ICD-10). What it is, what clinical picture the disease has and how to deal with pathology, we analyze below.

What is vasospastic angina?

Vasospastic angina is a type of rest angina. That is, the patient, even at rest, feels the characteristic signs of oxygen starvation of the heart muscle. As a rule, they develop suddenly (sometimes even at night in a dream) for no particular reason (physical activity, stress, etc.).

During an attack of this type, a spasm of the muscles of the walls of blood vessels occurs, which leads to a sharp decrease in the diameter of the coronary artery (it is this that feeds the human heart). As a result, the rate of blood flow to the myocardial zone decreases sharply or the blood supply to this area stops altogether.

Important: spasm of the walls of blood vessels occurs as an anginal attack, which provokes severe pain behind the sternum in the patient. This type of heart attack is diagnosed quite rarely (only 2% of all patients in the cardiology department). More often, females in the age category of 35 - 50 years are ill.

Symptoms

Vasospastic angina symptoms are quite characteristic. That is why an experienced cardiologist or even an ambulance paramedic can immediately make a preliminary diagnosis and provide first aid to the patient. In general, the clinical picture looks like this:

1. Cyclicity of heart attacks. They occur at equal time intervals. That is, the patient can feel attacks either once a day, or once an hour, etc. At these moments, the patient also notes a slight soreness in the chest.
2. Pain. Most often, an attack of this type of angina pectoris develops in the early morning. At these moments, the patient experiences a sharp pressing pain in the region of the heart, which first increases and then subsides. After 5-20 minutes, the pain subsides. As a rule, the pain during such attacks is the most intense.
3. The development of seizures without reference to physical activity or any other provoking factors. That is, vasospastic angina occurs at rest. This is the wording chosen by cardiologists to describe the symptoms of this type of angina pectoris.

Causes of pathology

Having found out what it is - vasospastic angina pectoris, it is important to understand the reasons why this cardiac pathology occurs. As a rule, provoking factors are:

• frequent emotional experiences of a negative nature (stress);
• adherence to bad habits (alcoholism and smoking);
• diabetes mellitus type 1 and 2;
• hyperventilation;
• frequent hypothermia;
• cardiac pathologies in the patient's history;
• heredity;
• age.

It is interesting: compared with the last century, the vasospastic type of angina has become much younger. If in the 90s such a diagnosis was made in patients from the 50+ age group, today it is not uncommon for it to be detected in younger patients (20+).

Diagnostics

It is necessary to diagnose this type of cardiac pathology very carefully in order to choose the right treatment. An experienced cardiologist prescribes and conducts the following diagnostic methods:

Treatment of angina pectoris

Any cardiac pathologies and attacks are treated only in a hospital. A cardiologist takes care of a patient. Treatment is based on taking medications of the following groups:

1. Fast action nitrates. Used mainly at the time of the attack. These drugs include "Nitroglycerin" (tablets) or "Nitromint" (spray).
2. calcium antagonists. Help relieve spasm of the heart vessels and coronary arteries. Such drugs include Verapamil, Nifedipine, etc. The dosage is prescribed only by the attending physician, depending on the age and primary condition of the patient.
3. Antiplatelet agents. Prevent the formation of thrombosis. The most common prescription is just aspirin.
4. Alpha blockers. It is used in very rare cases, if previously prescribed drug therapy does not give the expected effect.

Important: alternative methods and methods of treatment are not used for angina pectoris as an urgent therapy. Perhaps their use only as a preventive measure.

Complications

It is important to understand that any type of angina pectoris significantly inhibits the work of the human heart against the background of its periodic defective blood supply. As a result, if such a pathology is not treated, sooner or later the patient will die (10% of cases) or form (20% of cases).

Prevention

Preventive measures aimed at preventing angina pectoris can be primary and secondary. Primary prevention includes:

• A healthy lifestyle, including moderate physical cardio exercise, the rejection of bad habits, a healthy diet.
• Stay in a healthy psycho-emotional state.
• Uniform distribution of rest and work regimes.
• Control of existing chronic diseases.

Secondary prevention is carried out after the first and is aimed at preventing relapses. Here, as a preventive measure, the patient is shown:

1. Taking prescribed medications.
2. Hiking outdoors.
3. Constant monitoring of the state of heart health.
4. Taking a nitroglycerin tablet before sports and other moderate physical activity.

It is important to realize that the diagnosis is not a sentence, and the overall prognosis can be favorable. Most patients who follow the recommendations of the attending physician successfully live a full life for more than a dozen years.

Self-confidence and respect for your heart, plus the competent work of a cardiologist, work wonders.