The Annals of thoracic surgery
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Neurocognitive decline, often produced by atherosclerotic plaque embolization, remains a frequent complication of cardiopulmonary bypass. Plaque fragments may initiate local thrombosis, which, in turn, aggravates the embolic insult. Prothrombotic genetic factors may exacerbate this process. We investigated whether the PlA2 polymorphism of platelet GPIIIa, a prothrombotic risk factor in other cardiovascular settings, is associated with early neurocognitive decline after cardiopulmonary bypass. ⋯ This study demonstrates a link between the PlA2 allele of platelet GPIIIa and more severe neurocognitive decline after cardiopulmonary bypass. Although the mechanism is unknown, it could represent exacerbation of platelet-dependent thrombotic processes associated with plaque embolism.
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Cardiopulmonary bypass is associated with a systemic inflammatory response, a spectrum of pathophysiologic changes ranging from mild organ dysfunction to multisystem organ failure. Complications include coagulation disorders (bleeding diathesis, hyperfibrinolysis) from platelet defects and plasmin activation, as well as pulmonary dysfunction from neutrophil sequestration and degranulation. Diverse injuries are a consequence of multiple inflammatory mediators (complement, kinins, kallikrein, cytokines). ⋯ Specifically, inhibition of factor XII, bradykinin, C5a, neutrophil integrin expression, elastase activity, and airway nitric oxide production are observed. Clinical correlates include reduced capillary leak, preserved systemic vascular resistance and blood pressure, and improved myocardial recovery following ischemia. Overall, evidence indicates that aprotinin attenuates the systemic inflammatory response associated with cardiopulmonary bypass.
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The purpose of this study was to evaluate the early and late outcome after repair of tetralogy of Fallot in the first year of life. ⋯ These data strongly support the concept of early repair of tetralogy of Fallot. It is associated with an acceptable operative risk and a low incidence of significant arrhythmias, and provides long-term survival similar to that observed in the general population. Late complications may, however, develop, and long-term follow-up for their early recognition is essential.
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Acquired methemoglobinemia occurs rarely in clinical practice. We present a case of a 57-year-old man who developed severe drug-induced methemoglobinemia after exposure to benzocaine spray and lidocaine jelly during intubation for an elective thoracoscopic lung biopsy. Information regarding the classifications, pathophysiology, diagnosis, and treatment of this entity is reviewed.
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Postpneumonectomy syndrome, a late complication of pneumonectomy, is secondary to shift of the mediastinum and remaining lung toward the pneumonectomy side, leading to tracheobronchial compression between the vertebral body and the aorta or pulmonary artery. Obstructive airway symptoms are usually due to tracheobronchial tree compression, however, secondary airway malacia may develop. We report herein a case of postpneumonectomy syndrome with secondary bronchomalacia after left pneumonectomy in a patient with normal mediastinal vascular anatomy.