Letter by Cervellin et al Regarding Article, "Allergic Inflammation Is Associated With Coronary Instability and a Worse Clinical Outcome After Acute Myocardial Infarction"

We read with interest the article of Niccoli et al,who demonstrated a significant in vivo eosinophil degranulation and basophils activation during acute coronary syndrome along with a prognostic role of eosinophil cationic protein in ST-segment–elevation myocardial infarction. Indeed, the interplay between ischemic heart disease and atopy/allergy is complex and not completely revealed to date because the first report of acute coronary syndrome during a prolonged allergic reaction to penicillin was published more than half a century ago,followed by several studies supporting a role for allergic mediators in ischemic heart disease. In 1998, Eugene Braunwald described that vasospastic angina may be triggered by allergic reactions with mediators, such as histamine or leukotrienes, acting on coronary vascular smooth muscle. The results of Niccoli et al are consistent with both activation of eosinophil and basophil (both cells involved in allergic reactions) after an acute coronary event, with the additional finding of the prognostic role of elevated eosinophil cationic protein in patients with ST-segment–elevation myocardial infarction. Despite these important evidences, a causality dilemma remains. In fact, it is still unclear as to whether allergic pathway activation anticipates plaque disruption and subsequent acute thrombus formation during myocardial ischemia or, conversely, it just follows the ischemic/necrotic process. The answer to this intriguing issue would permit to recognize whether allergic reactions may be considered simple bystanders or active players in the challenging pathophysiology of myocardial ischemia