Although an association between high blood eosinophil counts and endomyocardial disease has been known for nearly a hundred years, the reasons for this were not understood. Brockington, Luzzatto and Osunkoya (1970) suggested that eosinophil leucocytes, in susceptible persons, by some unknown mechanisms, cause endomyocardial damage. Evidence to support this possibility has come from three sources: (1) Clinical studies have shown that very high blood eosinophil counts, from any cause, can be associated with endomyocardial disease, and in some patients it has been possible to show that eosinophilia preceded the onset of heart disease. (2) The development of heart disease has been associated with the presence of degranulated eosinophils in the blood and tissues, including damaged endomyocardium, and raised serum levels of eosinophil granule basic proteins have been found in many of these patients. (3) Low concentrations of eosinophil secretion products (which contain these eosinophil granule basic proteins) have been found to injure isolated heart cells in vitro. Studies with purified eosinophil granule basic proteins have shown that cardiac cell damage is the result of a specific toxic effect of eosinophil cationic protein on the plasma membrane and two enzyme complexes (pyruvate dehydrogenase and 2-oxoglutarate dehydrogenase) involved in mitochondrial respiration. These results support the suggestion that under certain conditions, eosinophils may damage the heart, leading to endomyocardial disease, and they offer new approaches for the early diagnosis and treatment of endomyocardial disease both in temperate and tropical countries.
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