Chest
Volume 93, Issue 1, January 1988, Pages 14-19
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Cardiovascular Effects of Smoking in Patients with Ischemic Heart Disease

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The cardiovascular effects of smoking, including the occurrence of ventricular arrhythmias, were examined in 52 patients with ischemic heart disease. The study was a randomized, crossover comparison between smoking six cigarettes and nonsmoking with observer-blinded primary outcome measurements. Continuous Holter ECG recording for four hours showed no significant differences in the proportion of patients experiencing ventricular ectopy or the total number and complexity of ventricular premature beats during smoking vs nonsmoking. Aside from the first cigarette, smoking did not significantly alter blood pressure or heart rate. Mean (± SEM) plasma epinephrine (pg/ml) increased (p = 0.02) from baseline (52 ± 4) to a maximum of 64 ± 6 at 240 minutes with younger subjects exhibiting a more marked rise (p = 0.02) than subjects over 55 years of age. Plasma norepinephrine was unchanged by smoking. A power calculation confirmed the conclusion that the resumption of smoking after overnight abstention does not acutely increase the occurrence of ventricular ectopic activity in patients with ischemic heart disease.

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Patient Population

Patients who were regular cigarette smokers were entered into the study if they had ischemic heart disease (Table 1) (myocardial infarction, stable or unstable angina) as defined previously.13 Patients over the age of 75 years were excluded because of the known decreased adrenergic sensitivity in the elderly. Patients receiving cardiovascular medication were eligible for entry, but these drugs were withheld on the study mornings. Patients receiving antiarrhythmic drugs for ventricular

Ventricular Arrhythmias

On the control day, 31 of the 52 patients (60 percent) exhibited ventricular ectopy compared with 29 (56 percent) on the smoking day (Table 2). The numbers of patients with ventricular couplets and those with greater than ten ventricular premature complexes during the four-hour observation period were similar on both days. Individual patients tended to have the same number of ventricular premature complexes on both the smoking and control days (Fig 1): 16 patients had an increase in the number

Discussion

Several factors may be responsible for the adverse effects of smoking on the heart,17, 18, 19 including increased myocardial oxygen consumption,20 accelerated atherosclerosis,1, 3 coronary artery vasospasm,21 and increased platelet adhesiveness and blood coagulability.1, 3, 22 A smoking-induced increase in cardiac arrhythmias could also be of major importance in the occurrence of sudden death in smokers with ischemic heart disease.23

To examine this latter possibility further, we performed

Acknowledgements

The authors thank A.G. Caves, P. Parsons, A. Madapallimattam, and E. Roberts for technical and secretarial assistance, and Dr. J. Szalai for statistical advice.

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  • Cited by (0)

    This study was supported by project grants from the Ontario Heart Foundation and the National Institute of Health (HL 29476, DA 02277) and the Heart and Stroke Foundation of Ontario (M.G.M. and M.J.S.).

    Manuscript received April 19; revision accepted July 13.

    Reprint requests: Dr. Myers, Division of Cardiology, Sunnybrook Hospital, Toronto, Ontario, Canada M4N 3M5

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