Angina and heart attacks usually have a common denominator. A disease process in an artery or a group of arteries that supply the heart’s own muscle (the myocardium) interferes with the supply of blood to that muscle. Muscles thus deprived of oxygen soon become flooded with metabolites – the breakdown ‘afterbum’ products of muscular activity. These in conjunction with lack of oxygen give cramp-like pain in any muscle group. When this cramp-like pain arises in the heart muscle we call it angina, from a Greek word meaning ‘to throttle’. The angina victim does actually feel that he is being throttled – choked, you might say – by what is going on in his heart.
Heart attacks, or coronary thrombosis attacks, stem from a further progression of artery disease. The pain of angina, basically caused by a reduction in the bore of the artery, sometimes signals an alteration in the structure of the artery wall. Doctors call this process atheroma, and the patches of changed structure in the blood vessel wall are sometimes referred to as atheromatous plaques or patches. These alterations of the vessel wall are microscopic to start with. Gradually over the years they grow until they are visible to the naked eye. A constant and sustained higher than normal blood pressure helps them to progress. We know that constant and sustained stress and tension tend to produce a constant and sustained rise in blood pressure, and so the first major relationship between tension and disease is manifest.
But there is another bodily change brought about by stress. Strangely, perhaps, this is an entirely natural one. Stress is (in Nature) the body mobilizing itself for a natural situation. For instance there will be a biological advantage for the fighter, or the man who flees, if his wounds stop bleeding quickly. Wounds stop bleeding quickly if the blood clots easily, is rapidly coaguable in other words; stress alters blood so that it is rapidly coaguable.
An unfortunate situation is thus built into the system. Stress and tension are the 20th-century equivalent of ‘fight and flight’. Only rarely are wounds inflicted and blood actually flows. But the stress-induced blood stickiness still occurs. And if arteries are also providing a suitable niche for blood to ‘stick’ in (the atheroma patch), then clotting (a coronary thrombosis) is liable to occur.
So we see there are two very obvious ways in which learning to relax can help to prevent a devastating disease which is liable to attack one man in three (and one woman in two) during middle age. Control of high blood pressure can stop the artery disease developing in the vessel walls to such an extent that an angina-producing patch can grow. Secondly, regular relaxation can coax the blood out of its high clotting tendency which produces the blood clot that forms coronary thrombosis.