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.
Wegener's granulomatosis, first characterized as a clinical syndrome in 1936, is a rare form of vasculitis of the small-and medium-sized blood vessels affecting mainly the upper and lower respiratory tracts as well as the kidneys. This review article describes the case of a 45-year-old man who developed aortic regurgitation and third degree heart block secondary to Wegener's granulomatosis. He subsequently presented to our institution 3 years later with pulmonary hemorrhage. The ensuing literature review reveals that historically clinical cardiac involvement in Wegener's has been rare, particularly with valvular lesions. However, recent literature has shown an increase in reported cases of cardiac valvular lesions in Wegener's. The presented case report along with recently reported case reports highlight the morbidity and mortality associated with such cardiac lesions. We believe routine cardiovascular supervision including echocardiography and electrocardiograms are important for the screening and monitoring of patients with Wegener's granulomatosis.
Prinzmetal angina or vasospastic angina is a clinical phenomenon that is often transient and self-resolving. Clinically it is associated with ST elevations on the electrocardiogram, and initially it may be difficult to differentiate from an acute myocardial infarction. The vasospasm induced in this setting occurs in normal or mildly to moderately diseased vessels and can be triggered by a number of etiologies including smoking, changes in autonomic activity, or drug ingestion. While the ischemia induced is usually transient, myocardial infarction and life-threatening arrhythmias can occur in 25% of cases. We present the case of a 65-year-old female where repetitive intermittent coronary vasospasm culminated in transmural infarction in the setting of gastrointestinal bleeding. This case highlights the mortality associated with prinzmetal angina and the importance of recognizing the underlying etiology.
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