The eosinophil in myocardial disease

Abstract

During the past decade, clinical and experimental studies have enabled the earliest forms of eosinophilic endomyocardial disease to be diagnosed by endomyocardial biopsy. Experimental studies have confirmed the suggestion that eosinophil granule constituents may be toxic to the heart, and eosinophil granule secretion products have been localized within the areas of acute necrosis. Biochemical and sequencing studies on the cationic proteins within eosinophils have confirmed their potential for causing tissue injury. In addition, the association of microvascular lesions, thrombo-embolic episodes and fibrotic lesions have all been linked to the capacity of eosinophils to produce a range of products of inflammation, including leukotriene C4, platelet activating factor and fibroblast proliferating factors. It is now suggested that these may contribute to the development of endomyocardial damage in patients with hypereosinophilia, irrespective of its cause. However, the proclivity of the endocardium for this type of lesion, and the ‘silent’ preclinical phase of the disease in many patients are important issues which remain unresolved.