Exploring Cardiac Variability in Hypereosinophilia: Clinical Insights and Echocardiographic Findings

Introduction: The cardiac manifestations of hypereosinophilia include mainly endomyocardial fibrosis, which is the most frequently observed form. However, eosinophilic cardiopathy can manifest itself in different ways, affecting the various layers of the heart and presenting a variety of clinical and echocardiographic presentations.

Aim: The aim of our study is to describe the various aspects of cardiac involvement observed in hypereosinophilia, based on our case series and data from the literature.

Methods: This is a retrospective, descriptive study of five observations illustrating the diversity of eosinophilic cardiopathy, from the cardiology department of the Mohammed VI University Hospital in Marrakech, over a period of 12 months.

Results: Over the period of the study, five patients presented with cardiac damage in the context of hypereosinophilia. The mean age was 53.8 years, with a predominance of women (sex ratio 0.66). In the majority of cases, the discovery of cardiac involvement was incidental to a cardiovascular check-up requested during the course of their medical condition. All cases had high levels of hypereosinophilia, with an average of 5681. These observations illustrate the wide variety of aetiologies of hypereosinophilia, all of which were represented: 3 cases of Churg-Strauss syndrome, 1 case of idiopathic hypereosinophilia syndrome, and 1 case of DRESS syndrome. The cardiac disorders observed were hypokinetic cardiomyopathy at the dilated stage in 60% of cases, acute eosinophilic myocarditis in 20%, and acute pericarditis in the remaining cases. The outcome was marked by an improvement in the FE in 60% of cases, stabilisation in 20%, and a fatal outcome in the remainder. Treatment is based on symptomatic therapy of the CHF and treatment of the underlying aetiology.

Discussion and Conclusion: Eosinophils are cytotoxic through the release of granular proteins that initially attack the endocardium, leading to thrombosis and embolic events. Subsequently, this aggression contributes to fibrosis and valvular complications. Cardiac damage can also manifest itself as potentially serious acute myocarditis or pericarditis, which can progress to cardiac tamponade. These cardiac disorders and the diversity of possible aetiologies serve as a reminder that vital prognosis may be at stake in the acute phase, and to emphasise that functional prognosis depends on early echocardiographic screening and rapid initiation of treatment to limit the risk of thrombo-embolic and fibrosing complications.