Pablo R. Lopez, MD; Alan N. Peiris, MD, PhD, MRCP(UK)

Disclosures

South Med J. 2010;103(11):1148-1155. 

In This Article

Abstract and Introduction

Abstract

The association between acute coronary events and acute allergic reactions has been recognized for several years. The first reported case occurred in 1950, during an allergic reaction to penicillin. In 1991, Kounis and Zavras described the syndrome of allergic angina and allergic myocardial infarction, currently known as Kounis syndrome. Two subtypes have been described: type I, which occurs in patients without predisposing factors for coronary artery disease and is caused by coronary artery spasm, and type II, which occurs in patients with angiographic evidence of coronary disease when the allergic events induce plaque erosion or rupture. This syndrome has been reported in association with a variety of medical conditions, environmental exposures, and medication exposures. Entities such as Takotsubo cardiomyopathy, drug-eluted stent thrombosis, and coronary allograft vasculopathy appear to be associated with this syndrome. In this review, we discuss the pathobiology, clinical features, associated entities, and management of Kounis syndrome.

Introduction

Allergic phenomena in predisposed subjects can trigger not only anginal episodes, but also acute myocardial infarction.[1] This was first reported in the American Heart Journal in 1950 with a case of a prolonged allergic reaction to penicillin.[2] In 1991, Kounis and Zavras initially described a syndrome of allergic angina as the coincidental occurrence of chest pain associated with an allergic insult. The chest pain would present as classical angina pectoris, and if severe enough, this allergic angina could progress to an allergic myocardial infarction.[3–7] In 1995, Constantinides raised the possibility that even ordinary allergic reactions could promote atheromatous plaque disruption, and in an editorial in 1998 Braunwald noted that vasospastic angina can be induced by allergic reactions, with mediators such as histamine and leukotrienes acting on coronary vascular smooth muscle.[8,9] Thus, allergic angina and allergic myocardial infarction have become recognized as the Kounis syndrome.[6,7]

Kounis syndrome (KS), or the concurrence of acute coronary events with allergic or hypersensitivity reactions, has increasingly been reported in the medical literature. The true frequency of KS is unknown. However, during a diagnostic insect sting challenge study Brown et al reported that 9.5% of healthy volunteers developed chest pain with electrocardiographic abnormalities consistent with acute myocardial ischemia.[10]

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