INTRODUCTION: Endomyocardial fibrosis with apical obliteration is the best known involvement among heart lesions induced by hypereosinophilia. However, hypereosinophilic heart disease may involve all three heart layers, with a polymorphic clinical and echocardiographic presentation. METHODS: Retrospective descriptive study of five patients highlighting the various manifestations of hypereosinophilic heart disease. RESULTS: We report five cases illustrating the variety of hypereosinophilic heart disease and review the pathophysiology of this potentially severe illness: cytotoxicity of eosinophils is mediated by the release of granular proteins that primarily damage the endocardium, leading to thrombosis and embolic complications, then to fibrosis and valvular complications; myocardial involvement may induce a dreadful acute eosinophilic myocarditis; finally, pericardial involvement may cause tamponade. CONCLUSION: These observations highlight the whole spectrum of the heart manifestations of hypereosinophilia, remind that the vital prognosis may be involved in the acute phase and underline that functional prognosis depends on early detection and treatment to reduce the risk of early thromboembolic and late fibrotic complications.
INTRODUCTION:Endomyocardial fibrosis with apical obliteration is the best known involvement among heart lesions induced by hypereosinophilia. However, hypereosinophilic heart disease may involve all three heart layers, with a polymorphic clinical and echocardiographic presentation. METHODS: Retrospective descriptive study of five patients highlighting the various manifestations of hypereosinophilic heart disease. RESULTS: We report five cases illustrating the variety of hypereosinophilic heart disease and review the pathophysiology of this potentially severe illness: cytotoxicity of eosinophils is mediated by the release of granular proteins that primarily damage the endocardium, leading to thrombosis and embolic complications, then to fibrosis and valvular complications; myocardial involvement may induce a dreadful acute eosinophilic myocarditis; finally, pericardial involvement may cause tamponade. CONCLUSION: These observations highlight the whole spectrum of the heart manifestations of hypereosinophilia, remind that the vital prognosis may be involved in the acute phase and underline that functional prognosis depends on early detection and treatment to reduce the risk of early thromboembolic and late fibrotic complications.