Angina pectoris is a private 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, provoked by physical activity or emotional stress, sometimes by inhalation of cold air. Pain due to compensatory mechanisms of expansion of the coronary arteries of the heart often stops on its own at rest after 3-5 minutes. Sometimes short-acting nitrates in sublingual tablets or sprays are required to relieve pain.
Pattern of an attack
Angina pectoris develops due to circulatory failure in the heart muscle at the time of increased functional load. It is with the increased consumption of the energy substrate and oxygen in the coronary arteries affected by atherosclerosis that a significant increase in blood flow is impossible. This creates conditions for energy starvation of myocardial regions, which are called ischemic zones. In response to thisanginal burning pain or the equivalent of exertional angina develops - shortness of breath at rest and a feeling of episodic dissatisfaction with the breath, its depth and breathing efficiency.
After the start of compensatory mechanisms, which involve the expansion of the coronary arteries, an angina attack stops, as the flow of nutrients and oxygen to the ischemic area of the myocardium increases. The functional activity of cells at this moment is restored, anginal pain stops.
Types of angina
CH 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 angina at rest, unstable and progressive forms of it, as well as vasospastic anginal pain.
In unstable angina, anginal pain occurs both during exercise and at rest. It is practically not stopped by taking short-acting nitrates, although the intensity of pain may 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 task of the doctor. Thanks to the assessment of the patient's complaints and the use of instrumental methods of diagnosis, the objectification of the condition is achieved,correct diagnosis. Each patient should understand that sometimes the current form of angina due to a blurry clinic is not immediately determined. However, inpatient therapy usually involves prescribing drugs to treat the more severe of the possible illnesses.
Etiology
The direct cause of exertional angina is coronary stenosing atherosclerosis. Its influence is realized as follows: during life, a cholesterol plaque is gradually deposited in the muscular-elastic arteries of the body from the inside of the artery. Due to this, the lumen of the artery narrows, and its throughput decreases significantly. Because of this, with an increase in the energy needs of the myocardium, for example, during exercise, the body is unable to quickly supply the myocardium with nutrients and oxygen.
The result is exertional angina, which develops when the artery narrows by 30-50%. As etiological factors, all phenomena that provoke and aggravate the development of coronary atherosclerosis should be indicated. Namely:
- hereditary disorders of fat and cholesterol metabolism;
- hereditary endothelial dysfunction;
- malnutrition (frequent consumption of thermally processed animal fats);
- metabolic syndrome, acquired hypertriglyceridemia and dyslipidemia, hyperuricemia, diabetes mellitus;
- arterial hypertension;
- smoking-induced endothelial dysfunction.
Gradationfactors
At the top of the list are the most significant factors, the influence of which is the most detrimental. This means that patients with higher risk factors feel the effects of angina and coronary heart disease at a much earlier age. Below are the phenomena that less actively cause the development and aggravation of atherosclerosis of the coronary arteries. They also cause the development of the disease, but not as quickly 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 exercise. Narrowed coronary arteries by 30% or more can no longer satisfy the increased need of functionally active myocardium for 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 need for oxygen in cardiomyocytes under conditions of physical exertion or stress and the delivery of oxygen 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 cellular acidosis develops.
These changes lead to diastolic and systolic dysfunction of the heart and electrophysiological disturbances. Electrocardiographic changes in the T wave and ST segment are recorded. emergenceAnginal pain in angina pectoris is explained by the release of adenosine from ischemic cardiomyocytes, which stimulates the A1 receptors of the endings of the nerve fibers of the heart muscle.
Symptoms
A characteristic sign of angina pectoris is anginal pain. The nature of the pain is burning, squeezing, cutting or pressing. Some patients may feel discomfort behind the sternum, tightness, heaviness in the chest. 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 an anginal attack is 3-5 minutes. Pain disappears after the cessation of physical activity or after taking nitroglycerin. If pain persists for more than 25-30 minutes and is not relieved by short-acting nitrates, medical attention should be sought.
In clinical practice, there is a painless form of ischemia. This condition is due to the short duration and weak severity of the pathological process. Painless ischemia is typical for patients with diabetes mellitus, elderly people with diseases of the spinal cord. The equivalent of pain in this group of patients is shortness of breath, palpitations, weakness. The diagnosis of exertional angina is certain in the presence of typical anginal pain, the presence of the above risk factors, and evidence of the effectiveness of short-acting nitrates.
Clinical forms of angina pectoris
Distinguish between stable and unstable clinical forms of angina pectoris. In the first case, the prescription of the appearance of retrosternal pain is 1 month or more. Thenattacks are stereotypical, 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 of seizures, 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 light physical activity, and may later occur at rest. Such changes in the dynamics of well-being indicate unstable angina (UA) - a form of acute coronary syndrome, characterized by the development of persistent myocardial ischemia. There are the following forms of NS: first-time progressive, early post-infarction angina and spontaneous.
Stable angina
Physical stress 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 atherosclerosis of the coronary arteries can endure, functional classes of angina pectoris are distinguished:
- Class I. Non-intense everyday physical activity does not provoke angina attacks, pain occurs only with excessive rapid or prolonged exercise.
- Class II. Slight limitation of physical activity. The patient notes the appearance of anginal pain or discomfort behind the sternum with a short walk on a flat area in comparison with peers. Walking more than 200m becomes difficult.
- Class III. Pronounced limitation of physical activity. Pain in the patient causes the slightest activity (for example, dressing).
- Class IV. Complete limitation of physical activity up to self-service, frequent angina attacks occur at rest.
Clinical diagnosis of angina pectoris is based on studies of the patient's functional activity. 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 ergometric test, allow you to visually evaluate the effectiveness of treatment and make changes when episodes of ischemia occur on the ECG.
Progressive angina
Progressive angina pectoris is a form of heart failure 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 the pain in the heart is often disturbing, is worse relieved by nitroglycerin, or occurs against the 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, whose symptoms are similar to the usual anginal attack with an increased frequency of pain episodes, often requires treatment in a cardiac hospital. Therapy is associated with the appointment of anticoagulants, increasing the dosebeta-blockers, antihypertensives, statins.
Diagnosis
In a disease such as exertional angina, the severity is related to the definition of the functional class. And the first stage of diagnosis is the collection of complaints and anamnesis: based on the typical characteristics of retrosternal pain, the onset of pain during physical or psycho-emotional stress, and the relief of an attack by rest and nitroglycerin, one can suspect the presence of heart failure. Later, the following laboratory and instrumental studies are used to detect coronary artery disease and concomitant lesions of the cardiovascular system:
- complete blood count, biochemical study, lipid profile;
- electrocardiogram at rest, during exercise, during rest, Holter monitoring;
- functional stress tests (bike test or treadmill test);
- chest X-ray, echocardiography;
- coronary angiography.
Order of diagnostic measures
Certainly, for a doctor, the most important factor for diagnosing angina pectoris is the symptoms. What needs to be done to objectify ischemia and make a diagnosis, the specialist decides depending on the availability of instrumental studies. The most useful method is planned coronary angiography, preparation for which sometimes takes more than a month. During this time, it is necessary to stabilize the course of angina pectoris, perform daily monitoring of ECG and ABPM, ECHO-KG, biochemical studies, fibrogastroscopy of the stomach.
The latter study may be contraindicated in severe angina pectoris, disability, decompensated congestive heart failure and atrial fibrillation. EGD is necessary to exclude an ulcer, which will prevent the administration of anticoagulants required after stenting. Some of the newer coronary artery stents are already drug-eluting, but EGD is still needed to rule out tumors, ulcers, and erosions.
