Passive smoking and atherosclerosis - IESC/UFRJ

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Figure 1 – Natural History of Atherosclerosis Lesion: Fatty streaks Fibrous plaques Raised lesions Occlusion by thrombus Clinical expression: Decade of life: None None May cause symptoms if lumen is narrowed, e.g., intermittent claudication, angina pectoris 1 st / 2 nd / 3 rd 4 th / 5 th 6 th + Heart attack, stroke, etc. (2) What is the relevance of the natural history of atherosclerotic disease in relation to its primary prevention? In addition to hypertension, high serum cholesterol levels and diabetes, active smoking has been consistently identified as a strong determinant of atherosclerosis; it appears to be particularly important in the more advanced stages of atherosclerosis (Sharrett et al, Am J Epidemiol 1999;149:843-52.) . For example, active smoking cessation leads to the elimination of virtually all excess risk of sudden coronary death in about one year after cessation. . (3) What does this fact tell you about the mechanism whereby active smoking causes sudden coronary death? Is it appropriate to calculate rate per persontime using a long follow-up interval to study the relationship of active smoking to sudden coronary death? Sudden coronary death is usually defined as an unexpected out-of-hospital death occurring within 24 hours of the onset of symptoms (typically chest pain) and is caused by acute thrombosis leading to massive myocardial ischemia. E8-2
The concern that environmental tobacco exposure may be related to atherosclerosis was a logical outgrowth of the role of active smoking, and has been explored in numerous studies. Glantz & Parmley (Circulation 1991;83:1-12) showed that, of ten published studies conducted both in the U.S. and abroad (Japan, Scotland, China), only one (by Lee et al) did not yield a relative risk greater than 1.0 using clinical coronary heart disease death as an outcome (Figure 2). (4) Does the outcome used in these studies (mortality) allow firm conclusions on whether the association of environmental tobacco smoke with coronary heart disease risk is causal? Why? (5) Which causality criterion is met by the demonstration that all but one study showed a positive association between environmental tobacco smoke and death? (6) When conducting a review of the literature such as that reported by Glantz and Parmley, what possible bias may interfere with the interpretation of this causality criterion? Are there situations when this criterion is not met, and yet the association is still causal? What are these situations? Wells (Environ Int 1988;14:249-65) estimated a pooled risk of coronary heart disease death in persons exposed to environmental tobacco smoke relative to that in those not exposed of 1.3 (95% confidence interval, 1.1-1.6) for men and 1.2 (95% confidence interval, 1.0 – 1.4) for women. These estimates are consistent with those arrived at by Glantz & Palmer of 1.3 for both genders (95% confidence interval 1.2 – 1.4), and have been confirmed by the 2006 report of the Surgeon General. (7) A relative risk close to one is often referred to as a “small effect”. Is that statement always true? Why? Using a relative risk estimate of 1.2 and an environmental tobacco smoke prevalence of approximately 26% (Howard et al, Arch Intern Med 1994;154:1277-82), estimate the percentage of total clinical coronary deaths due to environmental tobacco smoking in women. E8-3
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Passive smoking and atherosclerosis - IESC/UFRJ

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