The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Sep 2010
Tissue-engineered pro-angiogenic fibroblast scaffold improves myocardial perfusion and function and limits ventricular remodeling after infarction.
Microvascular malperfusion after myocardial infarction leads to infarct expansion, adverse remodeling, and functional impairment. Native reparative mechanisms exist but are inadequate to vascularize ischemic myocardium. We hypothesized that a 3-dimensional human fibroblast culture (3DFC) functions as a sustained source of angiogenic cytokines, thereby augmenting native angiogenesis and limiting adverse effects of myocardial ischemia. ⋯ Application of a bioengineered 3DFC augments native angiogenesis through delivery of angiogenic cytokines to ischemic myocardium. This yields improved microvascular perfusion, limits infarct progression and adverse remodeling, and improves ventricular function.
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J. Thorac. Cardiovasc. Surg. · Sep 2010
Simulation-based training delivered directly to the pediatric cardiac intensive care unit engenders preparedness, comfort, and decreased anxiety among multidisciplinary resuscitation teams.
Resuscitation of pediatric cardiac patients involves unique and complex physiology, requiring multidisciplinary collaboration and teamwork. To optimize team performance, we created a multidisciplinary Crisis Resource Management training course that addressed both teamwork and technical skill needs for the pediatric cardiac intensive care unit. We sought to determine whether participation improved caregiver comfort and confidence levels regarding future resuscitation events. ⋯ We developed a Crisis Resource Management training program in a pediatric cardiac intensive care unit to teach technical resuscitation skills and improve team function. Participants found the experience useful and reported improved ability to function in a code. Further work is needed to determine whether participation in the Crisis Resource Management program objectively improves team function during real resuscitations.
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J. Thorac. Cardiovasc. Surg. · Sep 2010
Early outcomes of deliberate nonoperative management for blunt thoracic aortic injury in trauma.
Traumatic blunt aortic injury has traditionally been viewed as a surgical emergency, whereas nonoperative therapy has been reserved for nonsurgical candidates. This study reviews our experience with deliberate, nonoperative management for blunt thoracic aortic injury. ⋯ This experience suggests that deliberate, nonoperative management of carefully selected patients with traumatic blunt aortic injury may be a reasonable alternative in the polytrauma patient; however, serial imaging and long-term follow-up are necessary.
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J. Thorac. Cardiovasc. Surg. · Sep 2010
Cardiac dysfunction induced by experimental myocardial infarction impairs the host defense response to bacterial infection in mice because of reduced phagocytosis of Kupffer cells.
This study was undertaken to investigate the effects of cardiac dysfunction induced by experimental myocardial infarction on the host defense response to bacterial infection and the role of Kupffer cells in mediating this response. ⋯ Cardiac dysfunction induced by myocardial infarction renders mice susceptible to bacterial infection and increases mortality because of a reduced ability of Kupffer cells to clear infectious bacteria. C-reactive protein-enhanced phagocytic activity of Kupffer cells may improve the poor prognosis after bacterial infection in mice with myocardial infarction.
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J. Thorac. Cardiovasc. Surg. · Sep 2010
Single double-lumen venous-venous pump-driven extracorporeal lung membrane support.
We sought to investigate the safety and feasibility of obtaining total respiratory support during 72 hours using a pump-driven (Levitronix CentriMag; Levitronix LLC, Waltham, Mass) venous-venous extracorporeal lung membrane (Novalung; Novalung GmbH, Hechingen, Germany) attached through a single double-lumen cannula (Novalung) into the femoral or jugular vein in pigs. ⋯ This circuit provides total respiratory support over 72 hours without inducing significant hemodynamic, coagulatory, cellular, or inflammatory responses.