Angina Pectoris – What happens

Anginal pain may be described as a cry of heart muscles for oxygen. The difference in demand and supply of oxygen to the heart muscles results in chest pain. This difference could be due to increased demand for oxygen as in high blood pressure or due to reduced supply of oxygen which commonly occurs due to decreased blood flow as a result of atherosclerosis. Atherosclerosis is initiated by deposition of lipid particles (“Fatty streak”) in the inner layer of the coronary artery. Later on accumulation of white blood cells, smooth muscle cells and cellular debris on the fatty streak leads to the formation of Plaque which further reduces the size of the lumen. Once the lumen of the artery is reduced substantially, coping with increased demand for blood (and hence oxygen) to the heart, as in case of exertion or emotional stress, becomes difficult leading to frequent attacks of angina.

In unstable angina the mechanism involves rupture of atherosclerotic plaque with subsequent clot formation (thrombosis) and vessel spasm (constriction) leading to reduced blood flow. In certain cases (such as in diabetes and elderly people) chest pain may not be present. Such episodes are therefore typically known as ‘silent ischemia’ and it can only be detected by exercise stress test.