Prosthetic mitral valve Aspergillus fumigatus endocarditis

Aspergillus endocarditis is a fatal source of valvular infection with a near 100 % mortality rate if pharmacotherapy and valve-replacement surgery are not initiated swiftly after diagnosis. Complicating its diagnosis is the low yield for growth on standard blood culture and time requirements for molecular diagnostic tools to return a result. Aspergillus endocarditis of the mitral valve presents as valvular vegetations that reduce the caliber of the mitral valve and can cause syncope as in the case of mitral stenosis with subsequent valve failure, left atrial enlargement, and prospective cardiovascular failure. Reports of the management of Aspergillus endocarditis after serial mitral valve replacement are not prominent in the literature. We report the case of a 41-year-old female with previous mitral valve prosthesis who received a second prosthetic mitral valve after a syncopal episode. Vegetations resembling thrombi were noted on transesophageal echocardiogram, diagnosed as Aspergillus fumigatus endocarditis, and successfully treated with antifungal therapy in conjunction with removal of her dysfunctional prosthesis

Vascular Endothelial Growth Factor Signaling in Hypoxia and Inflammation

Infection, cancer and cardiovascular diseases are the major causes for morbidity and mortality in the United States according to the Center for Disease Control. The underlying etiology that contributes to the severity of these diseases is either hypoxia induced inflammation or inflammation resulting in hypoxia. Therefore, molecular mechanisms that regulate hypoxia-induced adaptive responses in cells are important areas of investigation. Oxygen availability is sensed by molecular switches which regulate synthesis and secretion of growth factors and inflammatory mediators. As a consequence, tissue microenvironment is altered by reprogramming metabolic pathways, angiogenesis, vascular permeability, pH homeostasis to facilitate tissue remodeling. Hypoxia inducible factor (HIF) is the central mediator of hypoxic response. HIF regulates several hundred genes and vascular endothelial growth factor (VEGF) is one of the primary target genes. Understanding the regulation of HIF and its influence on inflammatory response offers unique opportunities for drug development to modulate inflammation and ischemia in pathological conditions