mitral valve insufficiency/tyrosine

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Severe mitral regurgitation caused by eosinophilic endocarditis.

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We describe a patient with symptoms of heart failure caused by severe mitral regurgitation. Echocardiography revealed an intracardiac mass embedding the posterior mitral valve leaflet, and cardiac magnetic resonance imaging showed two intracardiac thrombi and endomyocardial fibrosis. Eosinophil

Sympathetic activation causes focal adhesion signaling alteration in early compensated volume overload attributable to isolated mitral regurgitation in the dog.

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We reported that left ventricular (LV) dilatation after 4 weeks of isolated mitral regurgitation (MR) in the dogs is marked by extracellular matrix loss and an increase in adrenergic drive. Given that extracellular matrix proteins and their receptor integrins influence beta-adrenergic receptor

Loeffler endocarditis in a pediatric patient.

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Loefler endocarditis is a potential fatal adverse event of hypereosinophilic syndrome. We report a case of a 5-year-old girl diagnosed with peripheral hypereosinophilia refractory to corticosteroid therapy who developed eosinophilia-related endocarditis. Echocardiography revealed infiltration of the

Critical Structural Defects Explain Filamin A Mutations Causing Mitral Valve Dysplasia.

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Mitral valve diseases affect ∼3% of the population and are the most common reasons for valvular surgery because no drug-based treatments exist. Inheritable genetic mutations have now been established as the cause of mitral valve insufficiency, and four different missense mutations in the filamin A

Histopathological characteristics and oxidative injury secondary to atrial fibrillation in the left atrial appendages of patients with different forms of mitral valve disease.

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BACKGROUND The prevalence of atrial fibrillation (AF) and the frequency cardioversion of AF postoperatively are different in different forms of mitral valve disease. We hypothesized that these differences would relate to different extent of histopathological characteristics and oxidative injury in

CD45 Expression in Mitral Valve Endothelial Cells After Myocardial Infarction.

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BACKGROUND Ischemic mitral regurgitation, a complication after myocardial infarction (MI), induces adaptive mitral valve (MV) responses that may be initially beneficial but eventually lead to leaflet fibrosis and MV dysfunction. We sought to examine the MV endothelial response and its potential

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