Introduction:
Age and inflammation both are considered risk factors for coronary artery disease (CAD) and the levels of inflammatory markers increase with aging. However, the role of age-induced inflammatory burden in CAD development is not fully understood. We investigated the trajectories of inflammatory markers with increasing age in subjects with or without CAD.
Hypothesis:
We hypothesized that the rate of increase in inflammatory markers as a function of age would depend on the presence of CAD and differ between subjects with and without CAD.
Methods:
Systemic inflammatory burden was assessed by levels of C-reactive protein (CRP), serum amyloid A (SAA) and fibrinogen in Caucasians (n=184) and African-Americans (n=154) (age range: 20-60 years). The presence of CAD was defined as the presence of ≥50% stenosis in any one of 15 coronary artery segments.
Results:
The prevalence of CAD was 46% (85 of 184) and 38% (58 of 154) in Caucasians and African-Americans, respectively. In both ethnic groups, subjects with CAD were older and had an atherogenic lipid profile compared to subjects without CAD. For both subjects with and without CAD, HDL cholesterol level was significantly higher and triglyceride level was significantly lower in African-Americans compared to Caucasians. The pattern of inflammatory burden over age differed across CAD status and ethnicity. Among Caucasians, the trend patterns of CRP (p<0.05), SAA (p<0.01) and fibrinogen (p<0.001) over age differed significantly between subjects with and without CAD. Levels of all three markers were elevated already at young ages and remained relatively constant over age in Caucasians with CAD. In contrast, in Caucasians without CAD, the levels of these markers were lower at young ages with a gradual increase over age. The findings for African-Americans differed from that of Caucasians. The levels of inflammatory markers increased with age with no significant differences in trends between subjects with and without CAD. In multivariate analyses adjusting for covariates, the trend pattern of fibrinogen over age differed significantly between Caucasians with and without CAD.
Conclusions:
There was a diverging pattern in age-induced inflammatory burden associated with CAD, with an early start and faster rate of increase in Caucasian patients with CAD. The findings suggest an accelerated inflammation over age in individuals with CAD with a possible modulatory role of ethnicity/race.
Role of myocardial perfusion imaging for risk stratification in suspected or known coronary artery disease
