Abstract 2801: Systemic Inflammation is Associated with Reduced Coronary Collateral Support in Patients with Stable Angina
Introduction: The heterogeneity in the degree of collateralization among patients with coronary disease is poorly understood. We sought to determine whether chronic subclinical inflammation is related to coronary collateral development in patients with chronic stable angina.
Methods: High sensitivity C-reactive protein (CRP) levels were measured prior to coronary angiography in 177 patients with stable angina who had a stenosis of 90% or more in at least one coronary vessel. Collaterals were graded according to the Rentrop classification
Results: Coronary collaterals were present in 90 patients (50.8%), with 26 (14.7%), 42 (23.7%) and 22 (12.4%) patients having Rentrop grade 1, 2 and 3, respectively. Median CRP levels were significantly lower among patients with coronary collaterals (Rentrop 1 to 3) than among patients without ([2.4 mg/L [interquartile range 1.0 to 4.6] vs. 3.9 mg/L interquartile range 1.8 to 5.9]; Mann-Whitney P = 0.028). There were 35 (60.3%), 32 (54.2%) and 23 (38.3%) patients with coronary collaterals in the first, second, and third CRP tertile, respectively (P for trend = 0.017). In a univariate logistic regression, compared with patients in the first CRP tertile, the odds ratios for the presence of coronary collaterals was 0.78 (95% CI, 0.37 to 1.62; P = 0.50) for patients in the second CRP tertile and 0.41 (95% CI, 0.20 to 0.86; P = 0.018) for patients in the third CRP tertile (P for trend = 0.017). In a multivariate logistic regression adjusted for age, gender, body mass index, history of hypertension and diabetes, current smoking, number of diseased vessels, and statins therapy, CRP remained a significant independent predictor of the presence of coronary collaterals (Table⇓).
Conclusions: An inverse graded association exists between CRP levels and the presence of coronary collaterals in patients with stable angina. These findings suggest that subclinical inflammation may exert a detrimental effect on coronary collateral formation.