This case report illustrates a challenging case of worsening heart failure in a previously well-compensated patient with unclear etiology. Further workup revealed the patient’s cardiac resynchronization therapy-defibrillator (CRT-D) left ventricle (LV) lead was losing capture during positional changes. This case demonstrates the importance of device optimization, as well as electrocardiogram (ECG) monitoring to elucidate possible causes of acute systolic heart failure.
Giant cell myocarditis is a rare condition first described in 1905. It has a reported incidence range from 0.007% to 0.051%. It affects female and male individuals, equally, and usually occurs in young and middle-aged persons. The underlying aetiology of giant cell myocarditis is unknown but it is thought to be mediated by T-lymphocytes. Diagnosis is made via histological examination of myocardial tissue and is characterized by a mixed inflammatory cell infiltrate with multinucleated giant cells and cardiomyocyte necrosis, predominantly affecting the ventricles. The following report describes a rare case of giant cell myocarditis in a 71-year-old man with a history of hypertension and heart failure, who died while waiting to be seen in the emergency department. Autopsy findings revealed an enlarged, dilated heart with histologic features in keeping with giant cell myocarditis, along with features of heart failure. Diagnosis of giant cell myocarditis is less common in the elderly age group, possibly due to a less severe disease process in this age group and it may be misdiagnosed because older individuals may have other cardiovascular diseases (CVDs).
Sudden death is the principal cause of fatality in Chagas disease, afflicting to non-symptomatic patients younger than 50-years. For this, sudden death associated with chagasic malignant arrhythmias is underdiagnosed and their pathophysiological basis is poorly understood.
In this sense, this work aimed to analyze the histopathological alterations in cardiac structures specialized in the generation/conduction of action potential in an anatomopathological case of non-diagnosed sudden death living in a Chagasic endemic area.
The donor was a woman, 62-year-old, which ingressed without vital signs to the emergency room of “Antonio María Pineda” hospital, without any apparent antecedents of cardiac disease. The gross examination was normal, with no external evidence of structural/ischemic disease.
Microscopic examination revealed nodal like cell depopulation, microvascular disturbances, chronic myocarditis with mononuclear and mast cell infiltrate plus extracellular matrix reaction, and profuse damage of neural structures placed in nodal region. amastigote nest of Trypanosoma cruzi (T. cruzi) was detected.
These findings suggest a complex association among parasite persistence, sinus disease, micro-ischemia foci, and neural inflammation in the genesis of malignant arrhythmias of Chagas disease despite the absence of structural disease or massive necrosis. It is important to perform a protocol of examination for no explained sudden death cases in chagasic endemic countries, to avoid misdiagnosed of sudden death associated with Chagas disease.