Subclinical atherosclerotic plaques and significant coronary artery stenoses in stable angina patients present equivalent inflammatory activity

Background: C-reactive protein (CRP) is an important marker for coronary artery disease (CAD) in patients with acute coronary syndrome and acute myocardial infarction. Evidence of the relationship of CRP levels to the presence of CAD and subclinical atherosclerotic plaques in stable angina patients were less consistent. Methods: This study included 112 consecutive patients who received coronary angiography for stable angina. Based on coronary angiogram, patients were divided into two groups: with and without significant CAD. Patients without significant CAD were further subdivided into those with subclinical atherosclerotic plaques and those with normal coronary arteries. The Gensini scoring system was used to describe the extent of CAD. Blood samples for high-sensitivity C-reactive protein (hsCRP) measurement were taken for comparison. Results: Sixty-five (58%) patients had significant CAD. Of forty-seven (42%) patients without significant CAD, thirty-six (32%) had insignificant atherosclerotic plaques, and eleven (10%) had normal coronary arteries. The hsCRP levels in CAD patients were higher than those in patients without CAD (p = 0.049), but the difference was abolished when excluding patients with normal coronary arteries. The hsCRP levels in CAD patients with plaques were higher than in patients with normal coronary arteries (p = 0.015). No correlation between hsCRP levels and extent of CAD was noted. In the CAD group, hsCRP levels were significantly higher in patients with hyperlipidemia (p = 0.011) and lower in patients with statin treatment (p = 0.036). However, hyperlipidemia or statin treatment did not influence hsCRP levels in patients without CAD. After adjustment using multivariate regression, hyperlipidemia (p = 0.006) and statin (p = 0.048) were still independent predictors of hsCRP levels. Conclusion: CRP levels are equivalent between patients with stable CAD and subclinical atherosclerotic plaques. Hyperlipidemia and statin treatment influence CRP levels in patients with CAD but not in patients without CAD.