Cigarette smoking and coronary disease

Cigarette smoking and coronary disease

FORUM-LIETTERS CIGARETTE DISEASE SMOKING TO THE EDITOR AND CORONARY To the Editor: Recent editorials by Seltzer (AM HEART J 100275, 1980) and Bur...

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To the Editor: Recent editorials by Seltzer (AM HEART J 100275, 1980) and Burch (AM HEART J 100:421, 1980) referred to our study of characteristics of ex-cigarette smokers before they stopped smoking.’ Compared to persons who later persisted in the lhabit, the ex-smokers-to-be aplpeared in general at lower risk of developing coronary heart In our article we suggested that for a more accurate assessment of the net effect of quitting smoking on coronary disease rislk, such baseline differences should be considered. I would like the readers of the JOURNAL to know that we are not content simply to have published our findings and raised this issue. We are presently conducting a follow-up study on the same individuals to assess the differences between persistent smokers and quitters relative to total mortality and mortality due to coronary heart disease, taking into account the baseline differences in risk characteristics that we noted. These results will be available in the near future. Gary D. Friedman, M.D. Dept. of Medical Methods Research Kaiser-Permanente Medical Care Program Oakland, CA 94611

of oral propranolol, she developed cardiogenic shock. Cardiac output was 2.7 Lfmin with profound peripheral vasoconstriction. Dopamine was ineffective but isoproterenol infusion (1 pg/min) resulted in cardiac output rise to 4.2 L/mti accompanied by stable clinical improvement. In the report by Swedberg et al.,’ rather than propranolol, cardioselective beta-l antagonists such as metoprolol or less potent noncardioselective agents with sympathomimetic agonist activity were utilized. In the presence of circulating catecholamine excess described in COCM,’ it is postulated that propranolol might induce “epinepbrine to norepinephrine reversal,” thereby producing potent alpha-adrenergic mediated generalized vasoconstriction,” in addition to depression of myocardial contractility by propranolol. The detrimental hemodynamic effects that occurred in our patients and others*. Li with propranolol might be partially avoided by the use of cardioselective beta blockers. Meir Brezis Ruth Stalnikowicz Jonathan Hasin Depts. of Medicine and Cardiology Hadassah University Hospital Jerusalem, Israel REFERENCES 1.


Friedman GD, Siegelaub AB, Dales LG, Seltzer CC:Characteristica predictive of coronary heart disease in ex-smokers before they stopped smoking: Comparison with persistent smokers and non-smokers. J Chronic Dis 32:175, 1979.


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Swedberg K, Hjalmarson A, Waagstein F, Wallentin I: Prolongation of survival in congestive cardiomyopathy by beta-receptor blockade. Lancet 1:1374, 1979. Kuhn H: Discussion (Workshop on Multicenter Research Project on Congestive Cardiomyopathy, London, 1978). Postgrad Med J 54:475, 1978. Siipson FO: /3-adrenergic receptor blocking drugs in hypertension. Drugs 7:85, 1974. Hoffbrand BI: Beta-adrenergic blockade in congestive cardiomyopathy. Lancet 1:1031, 1980.

BETA BLOCKADE IN CONGESTIVE CARDIOMYOPATHY To the Editor: Beta-blocking agents have recently* been claimed to have a salutary effect in congestive cardiomyopathy (COCM). The following patients are reported to warn against the use of propranolol in this condition. Case NO. 1. A 31-year-old man had been suffering for 3 years from dyspnea and Ipalpitations. Clinical and echocardiographic findings suggested the diagnosis of COCM. Two episodes of decompensated cardiac failure responded to bed rest, digitalis, and short-term corticosteroids. His persistent tachycardia was controlled with alprenolol, 80 mg, and thereafter oxprenolol, 80 mg daily. Three weeks before admission oxprenolol was discontinued and the day prior to admission b’ecause of severe fatigue, propranolol, 80 mg per day, was administered for 2 days. During the first hospital day, his cardiovascular status deteriorated rapidly with biventricular failure, which responded to dopamine infusion (2.5 gg/kg/min). Cardiac catherterization revealed low cardiac output (2.1 L/min) with markedl systemic and pulmonary vasoconstriction. By the second hospital day, one day postpropranolol, vasoconstriction was relieved and cardiac output improved to 5.9 L/min. Three months later, the patient died in intractable heart failure and autopsy confirmed COCM with multiple pulmonary infarctions. Case NO. 2. A 50-year-old woman suffering from idiopathic COCM on the basis of clinical and echocardiographic findings, was admitted because of persistent sinus tachycardia. After 20 mg




To the Editor: The recent article on cardiovascular manifestations of tricyclic antidepressant overdose by Langou et al.’ is of considerable interest. It was gratifying to note that lidocaine was successfully used to treat ventricular ectopic beats. Lidocaine, an antiarrhythmic agent which enhances electrical conduction velocity, also mildly depresses cardiac contractility, but to a lesser degree than tricyclic antidepressants (TCA).’ Since the untoward cardiac manifestations of TCA are similar to those of quinidine toxicity, disopyramide, procainamide, and quinidine appear relatively contraindicated because of possible further depression of both conduction and myocardial contractility.?. a In the event of ventricular tachycardia occurring in the preterminal phase of severe intoxication, it would appear that bretylium tosylate might be useful in TCA poisoning. In addition, verapamil should be valuable in abating supraventricular tachycardiasP Alkalinization is often efficacious in treating TCA cardiovascular complications, and is best achieved by sodium bicarbonate 1 to 3 mEq/kg.* While physostigmine is used primarily to reverse central nervous system depression, the agent also may be helpful in correcting cardiac arrhythmias due to TCA pois0ning.j Some authorities recommend the combination of physostigmine and 357