Is Inflammatory Bowel Disease a Risk Factor for Coronary Artery Disease?

Abstract

Purpose: Chronic inflammation may act independently or synergistically with traditional atherosclerotic risk factors in the pathogenesis of atherosclerosis. The association between inflammatory bowel disease (IBD) and coronary artery disease (CAD) has not been clearly studied. The purpose of this study is to assess whether IBD is a risk factor for CAD. Methods: This is a cross-sectional, single-center study aimed at evaluating the presence of traditional atherosclerotic risk factors in patients with IBD and CAD compared with the control (CAD alone) population. The medical records of 112 consecutive patients with documented IBD and CAD discharged from our hospital between October 2007 and September 2009 were reviewed for the Framingham risk factors. The Framingham risk score (FRS) was calculated based on age, sex, hypertension, diabetes, tobacco use, total cholesterol and HDL values. FRS of patients with IBD and CAD was compared with the FRS of 100 randomly selected age- and sex-matched patients with CAD alone. Values were expressed as mean±standard deviation. The effects of age and gender on FRS were controlled using analysis of covariance (ANCOVA). Student's t-test was used to analyze continuous variables and χ2 test or Fisher's exact test for categorical variables. A p value of ≤0.05 was considered significant. Results: 79 patients with complete laboratory data and confirmed IBD and CAD diagnosis were enrolled into the study group. 46 (58.2%) patients had ulcerative colitis, and 52% were males in the study group, compared to 40% males in control group (p=0.13). Mean age in IBD+CAD group was 61.39±10.1 years compared to mean age of 63.71±11.4 years in CAD alone group (p=0.16). There was no significant difference in the treatment for CAD between the two groups (p=0.81). Mean (unadjusted) FRS in IBD+CAD group was 7.51±3.48 compared to 8.56±3.93 in CAD alone group (p=0.06). After adjusting FRS for group with age and gender as a covariate, the adjusted total FRS score was significantly lower in patients with IBD and CAD as compared to those with CAD alone (7.88±3.29 vs. 9.34±3.85; p=0.008). Conclusion: FRS is lower in patients with IBD and CAD compared with the control, implying that IBD is an independent risk factor for CAD. Recurrent flares of intestinal mucosal inflammation leads to presence of excess pro-inflammatory cytokines and serum soluble adhesion molecules in IBD that could promote atherosclerosis-related inflammation, alter lipid metabolism, and contribute to plaque instability and rupture. Our results are in accordance with those published by smaller studies. Further prospective cohort studies are needed to accurately study the incidence of CAD in patients with IBD.