Stenocardia tension: causes
Last reviewed: 23.04.2024
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Stenocardia of tension develops when the work of the myocardium and, as a consequence, its need for oxygen exceed the ability of the coronary arteries to provide adequate blood flow and to deliver a sufficient amount of oxygenated blood (what happens when the arteries narrow). The cause of narrowing often becomes atherosclerosis, but a spasm of the coronary artery or (rarely) its embolism is possible. Acute coronary thrombosis leads to the development of angina, if the obstruction to blood flow is partial or transitory, but this condition usually leads to the development of myocardial infarction.
Since myocardial oxygen demand is determined mainly by heart rate, cardiac wall tension in systole and contractility, the narrowing of the coronary artery usually leads to angina that occurs during exercise and decreases at rest.
In addition to physical exertion, heart work can be intensified with diseases such as hypertension, aortic stenosis, aortic regurgitation, or hypertrophic cardiomyopathy. In such cases, angina may appear regardless of the presence of atherosclerosis. With these diseases, it is also possible to reduce the blood supply to the myocardium by increasing its mass (resulting in a restriction of diastolic filling).
Reduction of oxygen delivery, for example, in severe anemia or hypoxia, can provoke or aggravate the course of angina pectoris.
With stable angina, the effect of exercise on myocardial oxygen demand and ischemia is usually relatively predictable. However, the narrowing of the arteries caused by atherosclerosis is not entirely constant, because the diameter of the vessel changes due to the usual oscillation of the artery tone (which occurs in all people). As a consequence, in most patients, angina attacks occur in the morning, when the arterial tone is relatively high. Endothelial dysfunction can also contribute to changes in arterial tone; Thus, the endothelium, damaged by the atherosclerotic process, under the influence of tension or ejection of catecholamines, reacts more often to irritation by vasoconstriction rather than by dilatation (normal response).
As myocardial ischemia occurs, the blood pH in the coronary sinus decreases, cell potassium loss occurs, lactate accumulation, changes in ECG data appear, ventricular function deteriorates. When angina attacks often increase pressure in the left ventricle (LV), which can lead to stagnation in the lungs and dyspnea.
The exact mechanism of development of discomfort in ischemia is unclear, but it is suggested that metabolites that appear during hypoxia have a stimulating effect on nerve endings.
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