PRIMARY PULMONARY HYPERTENSION pulmonary hypertension, with a very recent thrombus or embolus to a tertiary right lower lobe pulmonary artery. Cardiac catheterization is generally indicated in order to establish a definite diagnosis of pulmonary hypertension and to narrow down the causes of this hypertension. Caution should b e exercised when pulmonary angiography is undertaken to exclude atrial myxoma or thrombi in large pulmonary arteries in patients who have severe pulmonary hypertension. T h e examinations should be selective and the amounts of contrast medium injected should b e kept to a minimum.
1 Goff AM, Gaensler EA: Respiratory pathophysiology in
3 4 5 6
chronic progressive pulmonary vascular disease. Ir J Med Sci 497 :213-226, 1967 Caldini P, Gensini G, Hoffman MS: Primary pulmonary hypertension with death during right heart catheterization. Am J Cardiol4:519-527Oct. 1959 Cooperative study on cardiac catheterization. ( Braunwald E, et al, eds. ) Circulation 37: ( May) 1968 Watson H: Severe pulmonary hypertensive episode following angiocardiography with sodium metrizoate. Lancet 2:732-733, 1964 deBono AHB: Pulmonary hypertension following angiocardiography with sodium metrizoate. Lancet 2:860-861, 1964 Goodale F, Thomas WA: Primary pulmonary arterial disease. Observation with special reference to medial thickening of small arteries and arterioles. Arch Pathol 58:568575, 1954 Wagenvoort CA: The morphology of certain vascular lesions in pulmonary hypertension. J Pathol 78:503, 1959
What Price The alarming high mortality from lung cancer due to cigarette smoking might obscure awareness of the latter's other possible fateful implications. Authoritative statistical, clinical, autopsy and experimental studies attest to the excess incidence of coronary heart disease in cigarette smokers as compared with nonsmokers. Men of the former group have a threefold increase in the incidence of myocardial infarction. Men with angina pectoris who smoke develop myocarhal infarction more frequently than persons with angina who don't smoke. Death from coronary heart disease is substantially higher in smokers than in nonsmokers. It is estimated that one-half of excess death rate is due to smoking. Spain et al (JAMA 224:1005, 1973) reported autopsy findings, noting that in women who died suddenly 62 percent of those who died of coronary heart disease were heavy smokers versus 28 percent of heavy smokers in the group in which the cause of sudden death was other than coronary heart disease. Several investigators ascertained that atherosclerotic changes are substantially greater in smokers than in nonsmokers. According to Auerbach et a1 (New England J Med 273:775, 1965) the incidence and severity of coronary atherosclerosis in autopsies paralleled the number of cigarettes smoked by the individual and the length of time of smoking. Deposition and accumulation of cholesterol-lipid, the essential feature of vascular atherosclerosis, are aided and accelerated by high serum levels of these compounds in smokers. Too, it is well documented that animals kept on atherogenic diet, when subjected to various types of stress, develop atherosclerosis at an accelerated rate. Nicotine exerts an identical influence. In volunteers as well as in experimental animals there was significant increase in plasma corticosteroids after cigarette smoking or intravenously given nicotine, with consequent vascular atherogenesis. Corticosteroids render myocardial cells more susceptible to the adverse influence of catecholamines. As stated by Lord (JAMA 191:249, 1965), "heavy cigarette smoking may favor atherogenesis by at least four mechanisms, namely ( 1) tobacco hypersensitivity with the arterial wall as target organ, (2) by altering the clotting-fibrin-
CHEST, VOL. 64, NO. 5, NOVEMBER, 1973
olytic balance by shortening platelet survival, (3) by elevation of the free fatty acids in the serum, and ( 4 ) by lowering the lateral wall pressure associated with increased velocity of blood flow." In subjects with coronary atherosclerosis the precise cybernetics and functional adaptability of the heart become restricted, with consequent oxygen deficit in areas supplied by atherosclerotic vessels. In subjects with coronary atherosclerosis, smoking reduces coronary blood flow. Nicotine in cigarette smoke exerts a positive inotropic influence with consequent enhanced contractile action of the myocardium. Thus systole becomes prolonged and diastole shortened, with consequent reduction of coronary blood flow and oxygen supply. The latter is aggravated by high carboxyhemoglobin levels in smokers and also by hydrogen cyanide in cigarette smoke, which interferes with the enzymatic utilization of oxygen. Norepinephrine released by the action of nicotine increases oxygen consumption by myocardial cells. Norepinephrine has great affinity to myocardial cells (cardiotropism ) . Nicotine induces an increased supply of norepinephrine. The latter, through enhancement of serum free fatty acids increases their deposition in myocardial cells. The inability of these cells to convert the free fatty acids into energy results in impairment of myocardial contractility. C o n h a t o r y evidence of myocardial damage caused by smoking was recorded by Reece et a1 (Arch Environ Health 24:262, 1972). Dogs subjected to chamber exposure to cigarette smoke and treadmill exercise daily for about one year developed enlargement of both ventricles, decreased activity of enzymes: glutamic oxaloacetic transaminase, lactic dehydrogenase and creatine phosphokinase. It may be added that cardiac function may be weakened by nicotine-induced arrhythmias and conduction disturbances. It seems that the campaign against smoking is an enormous challenge as far as the community and the average individual are concerned. Alas, sometimes even sophisticated attitudes may give way to the urge of euphoria through smoking. Andrew L. Banyai, M.D.