We report a rare case of native valve endocarditis caused by Staphylococcus warneri in an immunocompetent 79-year-old man with known degenerative valvular heart disease but no previous risk factors such as recent invasive treatment or medical implant. The patient presented with heart failure, due to perforation of the mitral valve, and lacked any signs of infection. The diagnosis of endocarditis with S. warneri was established by echocardiography and positive blood cultures.
Testosterone exerts an important regulation of cardiovascular function through genomic and nongenomic pathways. It produces several changes in cardiomyocytes, the main actor of cardiomyopathies, which are characterized by pathological remodeling, eventually leading to heart failure. Testosterone is involved in contractility, in the energy metabolism of myocardial cells, apoptosis, and the remodeling process. In myocarditis, testosterone directly promotes the type of inflammation that leads to fibrosis, and influences viremia with virus localization. At the same time, testosterone exerts cardioprotective effects that have been observed in different studies. There is increasing evidence that low endogenous levels of testosterone have a negative impact in some cardiomyopathies and a protective impact in others. This review focuses on the interrelationships between testosterone and cardiomyopathies and heart failure.
We report the case of a previously healthy young woman, who developed a severe form of COVID-19 with massive pneumonia and acute pericarditis in whom constrictive physiology developed rapidly. To our knowledge, this represents the second reported case of SARS-CoV-2 constrictive pericarditis, a rare, but severe cardiac complication.
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