Inflammatory Bowel Disease as a Risk Factor for Premature Coronary Artery Disease

Abstract

BackgroundCrohn’s disease and ulcerative colitis are both systemic chronic diseases that alter bowel physiology. The central process in inflammatory bowel disease (IBD) and the associated manifestations are the result of B-cell production of IgG autoantibodies directed against self-antigens in various organ systems including coronary endothelium. Previous studies have demonstrated significant micro-vascular endothelial dysfunction in patients with IBD compared to patients not affected by the disease. We sought to analyze the relation, if any, between IBD and the development of premature coronary artery disease (CAD).MethodsWe queried our hospital database to find IBD patients admitted to the hospital from January 1, 2007 to December 31, 2008. Patients with traditional cardiovascular (CV) disease risk factors including hypertension, congestive heart failure (CHF), diabetes, age ≥ 65, hyperlipidemia, family history, end-stage renal disease (ESRD), and greater than five pack-year smoking history were excluded from the study cohort. The charts of the remaining 300 patients with diagnosed IBD were then analyzed for the incidence of CV disease events including acute myocardial infarction (MI), unstable angina, positive stress testing, and any cardiac intervention including coronary angioplasty and/or intracoronary stent implantation.ResultsOf the 300 patients included, only one patient had a CV disease event. This patient had a positive exercise stress thallium test. Otherwise, the remaining 299 patients (99.7%) did not have any reported CV disease events over the 2-year follow-up period.ConclusionMost of the clinical sequelae of CV disease events are the result of inflammatory changes at the vascular level. While IBD is associated with a chronic inflammatory state as reflected by high sedimentation rates, C-reactive protein (CRP), homocysteine levels, etc., our data seem to indicate that chronic inflammation in the absence of traditional risk factors is not associated with an increased risk of premature CV disease events. More wide-scale prospective studies should be performed to elucidate the relationship, if any, between chronic inflammation and CV disease risk.

Adiponectin promotes preadipocyte differentiation via the PPARγ pathway

“…Adipose tissue was originally thought to only store fat; however, it is now known to act as an active endocrine organ, which secretes various types of bioactive molecules, including leptin, adiponectin (APN), tumor necrosis factor α (TNF-α) and interleukin (IL)-6 (1)(2)(3)(4). Ridker and Silvertown (5) reported that aberrant secretion of endocrine substances by epicardial adipose tissue (EAT) results in the induction of inflammation (6), which is closely associated with the occurrence and development of coronary artery disease (CAD), particularly atherosclerosis (7,8). In addition, there is a close association between APN and atherosclerosis.…”

Generating Gene Ontology-Disease Inferences to Explore Mechanisms of Human Disease at the Comparative Toxicogenomics Database

“…The overlap of inferred GO-BP terms for these 2,457 disease-pairs identified a variety of pathologies exclusively on the basis of shared inferred GO-BP terms rather than specific genes using the strict filters outlined above ( Fig 4 ). Some of the disease-pairs with the greatest percentage of inferred GO-BP overlap include “brain neoplasms-chronic obstructive pulmonary disease”, “cardiomyopathies-contact dermatitis”, and “ulcerative colitis-coronary artery disease”, the latter of which has been recently confirmed in the literature [ 37 ]. Our method (using the two filters) represents just one of the many diverse ways that investigators can sort CTD’s new “GO-Disease-Gene Inference Network” files to explore mechanisms and functionality to make connections between seemingly heterogeneous pathologies.…”

Psoriasis and inflammatory bowel disease: links and risks

“… 148 , 149 On the other hand, CV is still a common cause of mortality among IBD patients although they have no different CV risk compared to the general population. 150 – 152 And this is in spite of the increased prevalence of a series of risk factors in patients with IBD, known to promote CV risk (prothrombotic state, subclinical atherosclerosis). 153 – 156 This controversy is still increasing when the role of therapeutic interventions is considered.…”