Abstract 9726: Cigarette Smoking: Association Between Inflammation, Subclinical Atherosclerosis and Cardiovascular Events. The Multi-Ethnic Study of Atherosclerosis (MESA)

Abstract

Background: Cigarette smoking is known to increase cardiovascular event risk. Whether smoking continues to be associated with adverse events after taking into account the burden of subclinical atherosclerosis and vascular inflammation is unclear. Methods: MESA is a population-based study of 6815 adults free of baseline cardiovascular disease. We stratified participants based on smoking status into 3 groups: Never (NS), Former (FS), and Current Smokers (CS). FS and CS were further stratified into quartiles of pack-year history of tobacco exposure (PYH). We excluded 28 participants with missing information on smoking (n=23) or follow-up events (n=5). We analyzed the association of smoking status with CHD (coronary heart disease) and CVD (cardiovascular disease) events after taking into account traditional risk factors, CRP, as well as burden of CAC. Results: A total of 6787 participants were followed for median 5.8 years. CS comprised 887 (13%, mean age 58yrs), FS 2484 (37%, 63yrs) and NS 3416 (50%, 62yrs). Significantly more CS suffered both CHD and CVD events than NS (4.5% vs 3.3% [p=0.003] and 6.5% vs 4.9% [p=0.019], respectively). Multivariable HRs of 1.8 (CHD, p=0.004) and 1.9 (CVD, p<0.001) were found in CS, compared to NS. These findings were increased with higher PYH, suggesting a dose-response effect of smoking on events. Incremental reductions in these HRs were found on addition of CRP (e.g. CVD HR=1.8, p<0.001) and then CAC (e.g. CVD HR=1.5, p=0.012) to the multivariable adjusted regression model. No differences in event HRs were found between FS and NS. Conclusions: CS, but not FS, was strongly associated with events. This association weakened slightly with the inclusion of CRP, and more significantly with the inclusion of CAC. However, the persistent association of smoking with events even after accounting for the burden of inflammation and CAC confirms the importance of additional pathways contributing to the cardiovascular risk associated with smoking.