Margaret A.WinkerMD, Senior EditorIndividualAuthorPhil B.FontanarosaMD, Senior EditorIndividualAuthor
To the Editor.— Dr Howard et al1 conclude, "Atherosclerosis progression appears to be largely related to the pack-years of cigarette exposure and not to present smoking status" and "the impact of exposure to ETS [environmental tobacco smoke] was 34% (5.9/17.1) as great as the impact of active smoking on the progression of atherosclerosis." The first conclusion is in stark contradiction with 2 huge bodies of literature, the mechanisms underlying the atherosclerotic process2 and measured alterations in atherogenic and atherothrombotic markers of risk seen in current smokers but not in ex-smokers. Many studies in current smokers, but not ex-smokers, have reported elevated low-density lipoprotein cholesterol levels and lower high-density lipoprotein cholesterol levels; increased fibrinogen levels; acute platelet aggregation and peripheral white blood cell counts; transient increases in blood pressure, heart rate, and vasoconstriction; increased blood viscosity via elevations in red blood cells, hematocrit, and hemoglobin; and increases in oxidative stress. In summary, the growth rate of plaque in ex-smokers would be expected to be less than the plaque growth rate found in smokers currently experiencing the large number of atherogenic stimuli listed above. If the normalization of these changes in ex-smokers has no impact on the progression of atherosclerosis, then a conceptual paradigm shift regarding the biochemical and hemodynamic stimuli of atherosclerotic plaque growth is in order.
Smith CJ, Ogden MW. Tobacco Smoke and Atherosclerosis Progression. JAMA. 1998;280(1):32-33. doi:10-1001/pubs.JAMA-ISSN-0098-7484-280-1-jbk0701