Visualizing the vascular effects of smoking

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Smoking is a well-established risk factor for coronary artery disease (CAD). In the year 2000, 11% of all cardiovascular deaths world-wide (corresponding to around 1.6 million) were estimated to be caused by smoking, of which CAD accounts for the majority 1.
Smoking has been shown to promote endothelial dysfunction, inflammation, and unfavorable changes in lipoprotein levels, which may in turn cause atherosclerosis development and progression 2. Clinical studies have reported an increased prevalence of subclinical markers of atherosclerosis including higher coronary artery calcium, higher carotid intima-media thickness, and lower ankle–brachial index in smokers 3. Smoking is also associated with the presence and severity of CAD as determined by coronary computed tomography angiography (CTA) and coronary angiography 4,5. Although these studies demonstrate a higher burden of atherosclerosis in smokers, smoking may also independently influence the cardiovascular prognosis. In a prospective study the prognostic value of significant CAD (≥50% stenosis) in smokers and nonsmokers referred for coronary CTA was evaluated 6. They found a nine times higher risk of death and nonfatal myocardial infarction in smoking patients with significant CAD compared with smoking patients with nonsignificant CAD. In contrast, this risk was only two times increased in their nonsmoking counterparts (P<0.05 for interaction from smoking). This suggests that smokers are at higher risk of adverse cardiac events than nonsmokers, in spite of similar levels of CAD. Whether this may be caused by the presence of a certain malignant type of atherosclerosis in smokers is unknown.
In an autopsy study, Glagov et al.7 described coronary artery positive remodeling (CAPR) as a compensatory enlargement of the vessel to an increase in plaque area. Since then it has become evident that plaques may also develop and grow in the absence of arterial expansion. The presence of CAPR is a high-risk plaque feature 8. CAPR indicates the presence of a fibroatheroma, and the extent to which the artery has been enlarged is proportional to the volume of the lipid-rich necrotic core 9. When these features are present, the plaque may be vulnerable to rupture and at a high-risk of causing coronary thrombosis 8. In contrast, in the absence of CAPR, the plaque is considered to be stable.
In the current issue of Coronary Artery Disease, Alani and colleagues report the findings of a cross-sectional study on 358 symptomatic patients with documented CAD by coronary CTA. CAPR was present in 178 of these patients, most often located in the proximal segments of the coronary artery tree. The major finding of the study was that smoking patients had three times higher odds of CAPR compared with nonsmoking patients. Among former smoking patients a nonsignificant trend was observed in the same direction as for current smokers.
Although the exploratory and cross-sectional nature of the study caution the interpretation of the findings, CAPR by coronary CTA is an important marker of high-risk plaques, as was also observed in previous histological studies. An adverse plaque morphology including low-attenuation plaque (representing lipid-cores) and CAPR are reliably determined by coronary CTA 10,11, and have been shown to predict acute coronary events in patients undergoing coronary CTA for suspected or known CAD 12. In fact, these features have also been associated with lesion-specific ischemia in stable plaques as measured by fractional flow reserve 13. Therefore, the present study may provide an anatomical explanation for the increased risk of cardiac events in smoking patients.
It is not answered by this study whether CAPR in smokers reflects an increased burden of coronary atherosclerosis per se or if CAPR may be a phenomenon of a more malignant type of atherosclerosis in smoking patients.

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