Acute Bioprosthetic Mitral Valve Thrombosis During Venoarterial Extracorporeal Membrane.

Bioprosthetic valve thrombosis is a rare complication. Left atrial dilatation, atrial fibrillation, hypercoagulability and low cardiac output are known risk factors. We report the case of a patient undergoing a bioprosthetic mitral valve replacement who required postoperative circulatory support with extracorporeal membrane oxygenation and presented acute bioprosthetic valve thrombosis. Some aspects regarding pathogenesis, diagnosis and treatment are discussed.

Neuroprotective effects of dexmedetomidine conditioning strategies: Evidences from an in vitro model of cerebral ischemia.

AIMS: Dexmedetomidine is a selective agonist of α2-adrenergic receptors with clinical anesthetic and analgesic properties that has also shown neuroprotective effects on several models of brain injury. Because perioperative stroke and brain damage are frequent causes of death in critical care units, we aimed to investigate neuroprotective properties of dexmedetomidine using an in vitro model of cerebral ischemia. MAIN METHODS: Primary mixed rat brain cortical cultures were subjected to oxygen and glucose deprivation and treated with different doses of dexmedetomidine in order to analyze three conditioning strategies: preconditioning, intraconditioning and postconditioning. KEY FINDINGS: All dexmedetomidine pre-, intra- and postconditioning treatments showed neuroprotective effects reducing brain cell necrosis, although only preconditioning showed antiapoptotic effects. Dexmedetomidine treatments also reduced IL-6 and TNF-α levels, especially in the preconditioning groups. Oxidative stress was attenuated with all dexmedetomidine preconditioning treatments, but only with the higher dose in the intraconditioning group, and no effects were observed in the postconditioning. All conditioning strategies increased BDNF levels. SIGNIFICANCE: Dexmedetomidine-mediated neuroprotective effects in an in vitro model of cerebral ischemia involve the attenuation of inflammation and oxidative stress and the increment of BDNF expression.