the most common clinical form of ischemic heart disease. Angina pectoris is caused by paroxysms of substernal or precordial constrictive pain, which often radiates to the left shouder, left arm, and neck. The disease was first described in 1768 by the English physician W. Heberden.
Angina pectoris may occur as a result of exertion or when resting. In the former case, pain is produced by walking or other physical effort, by entering the cold or wind from a warm place, or by nervous tension. The pain usually disappears after rest; if it appears while walking, the afflicted individual should stop and rest. In an attack that occurs when resting, the pain is not associated with physical exertion or nervous tension. These types of attacks frequently occur during sleep, waking the individual. In both types of angina pectoris an attack lasts several minutes and is quickly relieved by nitroglycerin and, in many cases, by Validol. It may be accompanied by temporary electrocardiographic changes and by reflex autonomic disorders, including pallor, cold sweat, and pulse inhibition. From the standpoint of prognosis, angina pectoris caused by exertion is less dangerous than that produced when resting and less frequently leads to the severe form of ischemic heart disease—myocardial infarction.
An attack of angina pectoris is a result of acute coronary insufficiency, which is a temporary disparity between the flow of blood to the heart along the coronary vessels and the requirements of cardiac muscle. In the great majority of cases, acute coronary insufficiency is caused by atherosclerosis of the coronary vessels, although it may also be caused by collagen diseases of the coronary vessels and syphilis of the aorta. These organic changes are accompanied by pain produced by functional disturbances (spasms) of the coronary vessels that occur, for example, with hypertension or an increase in the heart muscle’s demand for oxygen during physical exertion. An attack of angina pectoris may occur even in the absence of morphological changes in the blood vessels as a result of a spasm of the vessels, for example, in cases of cholecystitis and gastric and peptic ulcers.
Attacks of angina pectoris are distinguished from heartburn, or pain in the area of the heart. Many typical features of angina pectoris do not characterize heartburn. For example, unlike the pain produced by angina pectoris, heartburn pain is not paroxysmal in nature. Heartburn often accompanies various diseases of the heart and other organs and systems, including neuroses, climacteric cardiopathy, myocarditis, pericarditis, and osteochondrosis.
A regular balanced schedule of work, rest, and sleep is important in the treatment of angina pectoris. Dietetic treatment is directed against excessive weight, atherosclerosis, and hypertension. Habits that are detrimental to the health, above all smoking, should be abandoned. Sanatorium and health resort treatments are often helpful.
Drugs are used to halt and prevent attacks of angina pectoris. Validol and nitroglycerin are used for relief of attacks. In cases of severe, prolonged attacks these drugs may be ineffectual, and nonnarcotic analgesics, narcotics, and nitrous oxide may be prescribed. Attacks may be prevented and chronic ischemic heart disease treated by the use of vasodilators (papaverine, Nospa-num, Intensain, Depot-Nitroglycerine), beta adrenergic blocking agents (Propranolol hydrochloride and Proctalol), anabolic steroids (retabolil), and anginine.
N. R. PALEEV