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Tension angina: causes
Last reviewed: 06.07.2025
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Angina pectoris develops when the work of the myocardium and, as a result, its need for oxygen exceed the ability of the coronary arteries to provide adequate blood flow and deliver a sufficient amount of oxygenated blood (which occurs when the arteries are narrowed). The cause of narrowing is most often atherosclerosis, but spasm of the coronary artery or (rarely) its embolism are possible. Acute coronary thrombosis leads to the development of angina pectoris if the obstruction of blood flow is partial or transient, but this condition usually leads to the development of myocardial infarction.
Since myocardial oxygen demand is determined primarily by heart rate, systolic wall stress, and contractility, coronary artery stenosis usually results in angina, which occurs during exercise and is relieved at rest.
In addition to physical exertion, the work of the heart may increase in diseases such as arterial hypertension, aortic stenosis, aortic regurgitation or hypertrophic cardiomyopathy. In such cases, angina may occur regardless of the presence of atherosclerosis. In these diseases, a relative decrease in the blood supply to the myocardium is also possible due to an increase in its mass (resulting in a limitation of diastolic filling).
Decreased oxygen delivery, such as in severe anemia or hypoxia, can trigger or worsen angina.
In stable angina, the effects of exercise on myocardial oxygen demand and ischemia are usually relatively predictable. However, the narrowing of the arteries caused by atherosclerosis is not a completely constant value, since the vessel diameter changes due to normal fluctuations in arterial tone (which occurs in all people). As a result, most patients have attacks of angina in the morning, when arterial tone is relatively high. Endothelial dysfunction may also contribute to changes in arterial tone; for example, endothelium damaged by the atherosclerotic process, under the influence of stress or the release of catecholamines, more often responds to stimulation by vasoconstriction rather than by dilation (the normal response).
As myocardial ischemia occurs, the pH of the blood in the coronary sinus decreases, cellular potassium is lost, lactate accumulates, ECG data changes, and ventricular function deteriorates. During an attack of angina, left ventricular (LV) pressure often increases, which can lead to pulmonary congestion and shortness of breath.
The exact mechanism of development of discomfort during ischemia is unclear, but it is assumed that metabolites appearing during hypoxia have a stimulating effect on nerve endings.
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