Department of Molecular and Comparative Pathobiology, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.
Published: June 2024
AI Article Synopsis
Article Abstract
is a protozoan parasite that causes human and animal African trypanosomiases (HAT and AAT). Cardiac symptoms are commonly reported in HAT patients, and intracardiac parasites with accompanying myocarditis have been observed in both natural hosts and animal models of infection. Despite the importance of as a cause of cardiac dysfunction and the dramatic socioeconomic impact of African trypanosomiases in sub-Saharan Africa, there are currently no reproducible murine models of -associated cardiomyopathy. We present the first clinically relevant, reproducible murine model of cardiac dysfunction in chronic infection. Similar to humans, mice showed histological evidence of myocarditis and elevation of serum NT-proBNP with electrocardiographic abnormalities. Serum NT-proBNP levels were elevated prior to the development of severe ventricular dysfunction. On flow cytometry, myocarditis was associated with an increase of most myocardial immune cell populations, including multiple T cell and macrophage subsets, corroborating the notion that -associated cardiac damage is an immune-mediated event. This novel mouse model represents a powerful and practical tool to investigate the pathogenesis of -mediated heart damage and supports the development of therapeutic options for -associated cardiac disease.
From the Robarts Research Institute, Department of Medical Biophysics, Division of Respirology, Department of Medicine, and School of Biomedical Engineering, Western University, 1151 Richmond St N, Rm 5235, London, ON, Canada N6A 5B7 (G.P.); and Centre for Heart Lung Innovation, St. Paul's Hospital, BC Children's Hospital Research Institute, Department of Radiology, Department of Pediatrics, University of British Columbia, Vancouver, Canada (R.L.E.).
The renin-angiotensin system (RAS) is a classically known circulatory regulatory system. In addition to the previously known multi-organ circulatory form of the RAS, the existence of tissue RASs in individual organs has been well established. Skeletal muscle has also been identified as an organ with a distinct RAS.
The incidence of hyperuricemia has increased recently, posing a serious threat to public health. Hyperuricemia is associated with an increased risk of gout, chronic kidney disease (CKD), obesity, metabolic syndrome, type 2 diabetes mellitus, hypertension, hypertriglyceridaemia, metabolic dysfunction‑associated steatotic liver disease, acute kidney injury, coronary heart disease and cardiovascular disease (CVD). These diseases are commonly accompanied by varying degrees of kidney damage.
This case report presents the management of tachycardiomyopathy (TCM) in a patient with Friedreich ataxia, a hereditary disorder characterized by progressive neurodegeneration and associated cardiac complications. The patient exhibited severe tachycardia-induced cardiac dysfunction, complicating the clinical picture due to the overlapping neurological symptoms of Friedreich ataxia. Utilizing a 3D mapping system, catheter ablation was performed to accurately identify and target the arrhythmogenic foci contributing to the patient's TCM.
