Eosinophilic myocarditis is a rather rare condition found in 0.5% of autopsies with heart failure and in 0.1% of biopsies in suspected myocarditis. It consists of myocardial inflammation with eosinophilic infiltration and often eosinophilia. It has been reported in association with hypersensitivity reactions; immune-mediated disorders; HES; infections but often the causes remain unknown. Eosinophilic degranulation in response to triggers is believed to release cardiotoxic proteins with fibrosis or myocardial dysfunction. The diagnosis is essentially histological. Acute events include arrhythmias with a risk of sudden death and are unrelated to the degree of myocardial injury; probably because even limited involvement of conduction tissue can lead to a fatal arrhythmia. There is no definite information on mortality rates. Our case involves a 17-year-old male subject who entered the emergency room apyretic with chest pain, dispnea, hypertensive spike, dysuria. In history: obesity, hepatic steatosis, PAH, hyperinsulinism, hypercholesterolaemia and DM; all untreated. On laboratory analysis: neutrophilic leukocytosis (eosinophils and PCT normal), hyperglycaemia, hyposodidaemia; severe metabolic acidosis, lactic-ketotic, with respiratory compensation; ketonuria, haematuria, proteinuria, glycosuria; negative urine culture. ECG: abnormal IV conduction and QRS, no Q progression in right precordial. Insulin therapy was administered with discrete benefit of metabolic imbalances. After about 48 hours, though, she died of sudden cardiac arrest. An autopsy was performed on suspicion of inadequate management of diabetic ketoacidosis. However, the clinical- laboratory and anatomopathological data showed that the arrhythmic event was due to myopericarditis, in a subject with probable viral infection triggering ketoacidotic decompensation. The autopsy showed a picture of acute heart failure with signs of pericarditis, pulmonary edema, and polyvisceral congestion. Histological examination confirmed the diagnosis of eosinophilic myocardiopericarditis, also involving the conduction tissue (atrioventricular node). The case appears interesting due to the clinical-laboratory picture, the differential diagnostic difficulties, the particular histological pattern and the absence of established etiological factors. It is also useful for statistical-epidemiological purposes given the extreme rarity of the pathology and the current limited scientific knowledge.
MIOCARDITE EOSINOFILA UN CASO DI DIFFICILE DIAGNOSI DIFFERENZIALE TRA COMORBIDITÀ E LACUNE SCIENTIFICHE / Albore, M.; Del Prete, S.; D’Antonio, G.; Sorace, L.. - (2023). (Intervento presentato al convegno Convegno Roma 8-9 Giugno 2023 ‘Gli Scenari Gestionali E Assicurativi Nella Sanità Italiana tenutosi a Roma).
MIOCARDITE EOSINOFILA UN CASO DI DIFFICILE DIAGNOSI DIFFERENZIALE TRA COMORBIDITÀ E LACUNE SCIENTIFICHE
Albore M.;Del Prete S.;D’Antonio G.;
2023
Abstract
Eosinophilic myocarditis is a rather rare condition found in 0.5% of autopsies with heart failure and in 0.1% of biopsies in suspected myocarditis. It consists of myocardial inflammation with eosinophilic infiltration and often eosinophilia. It has been reported in association with hypersensitivity reactions; immune-mediated disorders; HES; infections but often the causes remain unknown. Eosinophilic degranulation in response to triggers is believed to release cardiotoxic proteins with fibrosis or myocardial dysfunction. The diagnosis is essentially histological. Acute events include arrhythmias with a risk of sudden death and are unrelated to the degree of myocardial injury; probably because even limited involvement of conduction tissue can lead to a fatal arrhythmia. There is no definite information on mortality rates. Our case involves a 17-year-old male subject who entered the emergency room apyretic with chest pain, dispnea, hypertensive spike, dysuria. In history: obesity, hepatic steatosis, PAH, hyperinsulinism, hypercholesterolaemia and DM; all untreated. On laboratory analysis: neutrophilic leukocytosis (eosinophils and PCT normal), hyperglycaemia, hyposodidaemia; severe metabolic acidosis, lactic-ketotic, with respiratory compensation; ketonuria, haematuria, proteinuria, glycosuria; negative urine culture. ECG: abnormal IV conduction and QRS, no Q progression in right precordial. Insulin therapy was administered with discrete benefit of metabolic imbalances. After about 48 hours, though, she died of sudden cardiac arrest. An autopsy was performed on suspicion of inadequate management of diabetic ketoacidosis. However, the clinical- laboratory and anatomopathological data showed that the arrhythmic event was due to myopericarditis, in a subject with probable viral infection triggering ketoacidotic decompensation. The autopsy showed a picture of acute heart failure with signs of pericarditis, pulmonary edema, and polyvisceral congestion. Histological examination confirmed the diagnosis of eosinophilic myocardiopericarditis, also involving the conduction tissue (atrioventricular node). The case appears interesting due to the clinical-laboratory picture, the differential diagnostic difficulties, the particular histological pattern and the absence of established etiological factors. It is also useful for statistical-epidemiological purposes given the extreme rarity of the pathology and the current limited scientific knowledge.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.