IgE and cardiac disease.

Abstract

IgE acts primarily via the high affinity IgE receptor (FcεRI) and is central to immediate hypersensitivity reactions (anaphylaxis). However, IgE is also important in the development of chronic hypersensitivity reactions (allergy). In the cardiovascular system, numerous clinical studies have investigated serum IgE levels, mainly in the context of myocardial infarction, and have established a clear association between IgE and ischemic cardiac events. While animal studies demonstrate that IgE can cause atherosclerotic plaque formation, this is complicated by clinical reports that IgE is associated with non-fatal ischemic events and not with fatal events, raising the possibility that IgE could be protective in this setting. In terms of non-ischemic cardiac disease, little information is available clinically for IgE; however, animal models also indicate that IgE promotes adverse effects in this setting as well. This review article will present the clinical studies that have established a relationship between serum IgE levels and cardiac disease, particularly myocardial infarction. This review article will also discuss animal studies that provide mechanistic understanding of how IgE can exert chronic effects in the heart. This article also attempts to address the question of whether IgE is causative of cardiac disease or is a response to cardiac disease.