Israel Medical Association Journal

Eosinophilic myocarditis (EM) is a rare form of myocardial inflammation defined by eosinophilic infiltration with associated myocyte injury. Its clinical expression is heterogeneous, ranging from subtle symptoms of heart failure to fulminant cardiogenic shock. Because these features often overlap with other types of myocarditis and systemic conditions, establishing the diagnosis can be difficult. In such cases, endomyocardial biopsy (EMB) remains the reference standard.

Amyloid transthyretin (ATTR) cardiac amyloidosis is an infiltrative cardiomyopathy marked by amyloid fibril deposition in the heart's extracellular space. It usually presents with signs of heart failure, and echocardiography often shows concentric left ventricular hypertrophy (LVH), restrictive physiology, and a distinctive pattern of apical strain sparing. In recent years, the development of non-invasive diagnostic methods, as well as the availability of disease-modifying treatments, has significantly improved diagnosis and management.

To the best of our knowledge, the coexistence of ATTR cardiac amyloidosis and EM has not been previously reported. Such overlap presents distinct diagnostic and therapeutic challenges. These conditions may have synergistic effects on the structure and function of the myocardium. We describe a case of concurrent ATTR cardiac amyloidosis and EM, highlighting the role of multimodality imaging and multidisciplinary management of these overlapping pathologies.

Peripartum cardiomyopathy (PPCM) is an idiopathic cardiomyopathy presenting with heart failure (HF) secondary to left ventricular systolic dysfunction (defined as left ventricular ejection fraction [LVEF]) < 45% toward the end of pregnancy or in the months following delivery, where no other cause of HF is found. Complete understanding of the etiology is lacking, with higher incidence seen in advanced maternal age, multiple gestations, preeclampsia, and anemia [1]. Potential suggested causes include pathological immune response, hormonal abnormalities, stress cytokines, and nutritional deficiencies. Genetic predisposition was demonstrated in some PPCM, most commonly pathogenic loss-of-function truncating variants in Titin gene (TTN) [1]. Other causative genes reported are DMD, LAMP2, DSP, MYH6, SYNM, TPM1, and VCL [1].