Loeffler's endocarditis Complicating Crohn's Disease-Associated Hypereosinophilia: A Fatal Case of Eosinophil-Mediated Restrictive Cardiomyopathy

Abstract

Background: Cardiac elastomyofibrosis represents the irreversible fibrotic end-stage of Loeffler's endocarditis, an uncommon restrictive cardiomyopathy driven by eosinophil-mediated endomyocardial injury. While most often associated with hypereosinophilic syndromes, its occurrence in the context of chronic inflammatory disorders such as inflammatory bowel disease (IBD) remains exceptionally rare. We report a fatal case of Loeffler's endocarditis progressing to elastomyofibrosis in a patient with Crohn's disease-associated hypereosinophilia. Case Presentation: A 46-year-old man with hypertension and Crohn's disease on intermittent corticosteroid therapy presented with acute-onset dyspnea (NYHA Class III–IV), chronic fatigue, and intermittent fever. Examination revealed elevated jugular venous pressure and bilateral pleural effusions on chest radiography. Transthoracic echocardiography demonstrated reduced global longitudinal strain with apical sparing, multivalvular regurgitation, severe pulmonary hypertension, right ventricular dilatation, and a speckled left ventricular apex with an apical mass suggestive of restrictive cardiomyopathy. Cardiac magnetic resonance imaging confirmed a left ventricular mural thrombus with extensive subendocardial fibrosis, consistent with Loeffler's endocarditis. Laboratory evaluation revealed marked peripheral eosinophilia (21%). Hematologic workup excluded clonal leukemia and lymphoma. Autoimmune markers including ANA and c-ANCA were positive, consistent with the known IBD diagnosis. Despite supportive management, the patient deteriorated rapidly, culminating in multiorgan failure and death. The clinical, laboratory, and imaging findings collectively supported a diagnosis of Crohn's disease-associated hypereosinophilia leading to eosinophilic endomyocardial injury and elastomyofibrosis. Discussion: This case highlights a rare cardiac manifestation of IBD-associated systemic inflammation. Eosinophil-mediated myocardial injury in Loeffler's endocarditis progresses sequentially from necrosis to thrombosis and irreversible fibrosis, resulting in restrictive physiology, valvular dysfunction, and pulmonary hypertension. Multimodality imaging — particularly transthoracic echocardiography and cardiac MRI — was essential for diagnosis in the absence of histopathological confirmation. Once advanced fibrosis is established, therapeutic options remain limited and prognosis is poor. Conclusion: Loeffler's endocarditis culminating in cardiac elastomyofibrosis should be considered in patients with IBD presenting with unexplained heart failure and peripheral eosinophilia. Early recognition through multimodality imaging and multidisciplinary evaluation remains critical, as this case demonstrates that delayed diagnosis can permit progression to irreversible fibrosis with a fatal outcome.