Angina pectoris is a particular clinical form of coronary heart disease , reversible myocardial damage, characterized by episodes of compressive, pressing or burning pain in the chest, often behind the sternum or in the projection of the heart. The pain attack is short-term and lasts 3-5 minutes, is provoked by physical exertion or emotional stress, sometimes by inhaling cold air. The pain due to the compensatory mechanisms of the expansion of the coronary arteries of the heart is often stopped independently at rest after 3-5 minutes. Sometimes, pain relief requires the use of short-acting nitrates in sublingual tablets or sprays.
Patterns of attack
Angina pectoris develops due to circulatory failure in the heart muscle at the time of increased functional load. It is with increased expenditure of energy substrate and oxygen in coronary arteries affected by atherosclerosis that a significant increase in blood flow is impossible. This creates the conditions for energy starvation of the myocardial areas, which are called zones of ischemia. In response to this, anginal burning pain or equivalents of angina pectoris develops - shortness of breath at rest and a feeling of episodic dissatisfaction with the inspiration, its depth and effectiveness of breathing.
After the start of compensatory mechanisms, which involve the expansion of the coronary arteries, the attack of angina pectoris stops, as the influx of nutrients and oxygen to the ischemic myocardium increases. The functional activity of the cells at this moment is restored, anginal pain ceases.
Types of Angina Pectoris
HF is a form of angina pectoris in which anginal pain develops precisely at the time of physical or emotional stress and stops either after they stop, or after taking nitroglycerin. This is the clear line that separates the angina pectoris, its unstable and progressive forms, as well as vasospastic anginal pains.
With unstable angina pectoris, anginal pain occurs both during exercise and at rest. It practically does not stop with the use of short-acting nitrates, although the intensity of the pain can decrease. If such pain bothers you for more than 30 minutes after taking nitrates 2 times, then the condition should be interpreted as a heart attack and seek medical help.
It is important that with angina pectoris, the classification and isolation of the form of the disease is the doctor’s task. Thanks to the assessment of patient complaints and the use of instrumental diagnostic methods, objectification of the condition is achieved, the correct diagnosis is made. Each patient should understand that sometimes the current form of angina pectoris due to a lubricated clinic is not immediately determined. However, inpatient therapy usually involves the appointment of drugs to treat the more severe of possible diseases.
Etiology
The immediate cause of angina pectoris is coronary stenosing atherosclerosis. Its influence is realized as follows: a cholesterol plaque during life gradually deposits in the muscular-elastic arteries of the body from the inside of the artery. Due to this, the lumen of the artery narrows, its throughput significantly decreases. Because of this, with an increase in the energy requirements of the myocardium, for example, during physical exertion, the body cannot quickly supply the myocardium with nutrients and oxygen.
The result is angina pectoris, which develops with narrowing of the artery by 30-50%. As etiological factors, all the phenomena that provoke and exacerbate the development of coronary atherosclerosis should be indicated. Namely:
- hereditary disorders of the metabolism of fats and cholesterol;
- hereditary endothelial dysfunction;
- eating disorders (frequent use of heat-treated animal fats);
- metabolic syndrome, acquired hypertriglyceridemia and dyslipidemia, hyperuricemia, diabetes mellitus;
- arterial hypertension;
- smoking-induced endothelial dysfunction.
Gradation factors
At the top of the list are the most significant factors, the influence of which is most harmful. This means that patients with higher risk factors experience the effects of angina pectoris and coronary heart disease at a much younger age. Below are the phenomena that are less active in causing the development and aggravation of atherosclerosis of the coronary arteries. They also cause the development of the disease, but not as fast as in the case of hereditary disorders of lipid and cholesterol metabolism, endothelial dysfunction.
The occurrence of an attack of angina pectoris depends on the degree of damage to the arteries of the heart by atherosclerosis. Vasoconstriction up to 30% does not affect the blood supply to the heart during physical exertion. Narrowed coronary arteries by 30% or more can no longer satisfy the increased demand for functionally active myocardium in oxygen, which contributes to the development of ischemia and the appearance of anginal pain.
Pathogenesis
With an attack of angina pectoris, the balance between the demand of cardiomyocytes in oxygen under conditions of physical activity or stress and oxygen delivery by the bloodstream is disturbed. As a result, reversible myocardial ischemia develops. Such episodes entail changes in the metabolism of heart cells: ionic balance is disturbed, ATP synthesis decreases, and cell acidosis develops.
These changes lead to diastolic and systolic dysfunction of the heart and electrophysiological disorders. Electrocardiographic changes in the T wave and ST segment are recorded. The occurrence of anginal pain in angina pectoris is explained by the release of adenosine from ischemic cardiomyocytes, which stimulates the A1 receptors of the terminal nerve fibers of the heart muscle.
Symptoms
A characteristic sign of angina pectoris is anginal pain. The nature of the pain is burning, constricting, cutting, or pressing. Some patients may feel discomfort behind the sternum, tightness, heaviness in the chest. A typical localization of pain is behind the sternum, although they can radiate to the left shoulder, to the neck and lower jaw, less often to the interscapular region and under the left shoulder blade. The duration of a sore throat is 3-5 minutes. Pain disappears after the cessation of physical activity or after taking nitroglycerin. If the pain lasts more than 25-30 minutes and does not stop with short-acting nitrates, seek medical help.
In clinical practice, a painless form of ischemia occurs. This condition is due to the short duration and weak severity of the pathological process. Painless ischemia is typical for patients with diabetes mellitus, the elderly with spinal cord diseases. The equivalent of pain in this group of patients is shortness of breath, palpitations, weakness. The diagnosis of angina pectoris is undeniable in the presence of typical anginal pain, the presence of the above risk factors, and in the presence of data on the effectiveness of taking short-acting nitrates.
Clinical forms of angina pectoris
There are stable and unstable clinical forms of angina pectoris. In the first case, the prescription of chest pain is 1 month or more. Then the attacks are stereotypical, the pain always has the same character, localization, irradiation, duration, occurs with the same (stereotypical) physical activity and stops at rest or after taking nitroglycerin. Outside attacks, the patient feels well.
With an increase in the degree of stenosis of the coronary artery and a decrease in its lumen, anginal pains appear more often, become longer, are provoked by mild physical activity, and can later occur at rest. Such changes in the dynamics of well-being indicate unstable angina pectoris (NS), a form of acute coronary syndrome characterized by the development of persistent myocardial ischemia. The following forms of NS exist: the first progressive, early post-infarction angina pectoris and spontaneous.
Stable angina
Exercise or psycho-emotional stress in patients with severe atherosclerosis can cause an attack of anginal pain. And depending on the intensity of the load that a patient with coronary heart disease and coronary artery atherosclerosis can carry, the functional classes of angina pectoris are distinguished:
- Class I. Non-intense daily physical activity does not provoke angina attacks, pain occurs only with excessive fast or prolonged exercise.
- Class II Slight restriction of physical activity. The patient notes the appearance of anginal pain or discomfort behind the sternum with a short walk on flat terrain in comparison with peers. Walking over 200 m becomes difficult.
- Class III Severe restriction of physical activity. A pain attack in a patient causes the slightest activity (for example, dressing).
- Class IV A complete limitation of physical activity up to self-care, frequent angina attacks occur at rest.
The clinical diagnosis of angina pectoris is based on studies of the functional activity of the patient. This is a measure of the objectification of the severity of the disease. At the same time, periodic functional tests, for example, a treadmill test or a bicycle ergometry test, allow you to visually evaluate the effectiveness of treatment and make corrections in the event of episodes of ischemia on the ECG.
Progressive angina pectoris
Progressive angina pectoris is a form of heart failure that is characterized by an increase in typical anginal attacks, an increase in their duration, and a decrease in the threshold of occurrence. If the patient feels that pain in the heart is often disturbed, worse when they stop with nitroglycerin or arise against a background of a much lower load, then such a diagnosis is likely. This requires a visit to the doctor, re-registration and interpretation of the ECG in comparison with the previous ones.
Progressive angina pectoris, the symptoms of which are similar to a usual anginal attack with an increased incidence of pain episodes, often requires treatment in a cardiology hospital. Therapy is associated with the appointment of anticoagulants, an increase in the dose of beta-blockers, antihypertensive drugs, and statins.
Diagnostics
In a disease such as angina pectoris, the severity is associated with the definition of a functional class. And the first stage of diagnosis is the collection of complaints and anamnesis: on the basis of a typical characteristic of chest pain, the occurrence of pain during physical or psycho-emotional stress, and relief of the attack by rest and nitroglycerin, the presence of HF can be suspected. Later, to detect coronary heart disease and concomitant lesions of the cardiovascular system, the following laboratory and instrumental studies are used:
- general blood test, biochemical examination, lipid profile;
- electrocardiogram at rest, during exertion, during rest, Holter monitoring;
- functional stress tests (bicycle ergometry test or treadmill test);
- chest x-ray, echocardiography;
- coronary angiography.
The order of diagnostic measures
Of course, for the doctor, the most important factor for diagnosing angina pectoris is symptoms. What should be done to objectify ischemia and diagnosis, the specialist decides depending on the availability of instrumental studies. The most useful method is planned coronary angiography, the preparation for which sometimes takes more than a month. During this time, the course of angina pectoris should be stabilized, daily monitoring of ECG and SMAD, ECHO-KG, biochemical studies, gastric fibrogastroscopy should be performed.
The latest study may be contraindicated in severe angina pectoris, disability, decompensated congestive heart failure, and atrial fibrillation. FGDS is necessary to exclude an ulcer, which will not allow you to take the anticoagulants necessary after stenting. Some new stents of coronary arteries already have a drug coating, however, FGDS is still necessary to exclude tumors, ulcers, and erosion.