Endothelial progenitor cells (EPCs) are a subtype of hematopoietic stem cells, which contribute to the repair of injured endothelium. Treatment with atorvastatin has been shown to increase EPC count in patients with coronary artery disease. Therefore, we investigated whether atorvastatin augments the number of EPCs after cardiopulmonary bypass (CPB) surgery. We conducted a randomized double-blind, placebo-controlled, 2-way crossover trial in 50 patients undergoing elective coronary surgery. Patients received either 3-week treatment with atorvastatin or placebo. EPCs were quantitated by flow cytometric phenotyping on blood samples. Levels of interleukin, IL-6 and IL-8; tumor necrosis factor alpha; SDF-1alpha; granulocyte colony-stimulating factor; and vascular endothelial growth factor were determined at recruitment, preoperatively, post-CPB, and 6, 12, and 24 hours postoperatively. The atorvastatin group showed a significantly higher amount of EPCs both pre- and postoperatively compared with the placebo, with a >4-fold increase compared with the baseline values. CPB induced an increase in all cytokines, but the levels of proinflammatory cytokines were significantly lower in the atorvastatin group (P < 0.05). Statin did not affect levels of SDF-1alpha, granulocyte colony-stimulating factor, and vascular endothelial growth factor. However, no correlation was found between plasma levels of any cytokine and number of EPCs, with the exception of SDF-1alpha. Pretreatment with atorvastatin significantly increases the amount of EPCs after CPB, by a mechanism independent of plasma levels of cytokines and cholesterol.
INTRODUCTIONCardiac perforation is a rare, but potentially serious, complication of pacemaker implantation that may develop days or weeks after implantation.PRESENTATION OF CASEIn the current case, 92-year-old man underwent permanent pacemaker implantation, but he presented 3 weeks later with severe symptoms. Computed tomography showed protrusion of the tip of the ventricular electrode through the right ventricle and into the chest wall. During an urgent surgical intervention, the lead was disconnected and extracted. A sealing hemostatic device and an hemostatic patch were applied to repair the ventricle; the procedure was uneventfull.DISCUSSIONThis case demonstrates how the correct diagnosis of ventricular perforation is crucial, and should be followed immediately by surgical planning.CONCLUSIONThe hemostatic patch is a valuable alternative to sutures in patients with thin and fragile ventricular wall, unable to undergo stitching.
Preoperative atorvastatin use is associated with reduced risk of bleeding and blood products use after coronary artery bypass grafting, likely due to a reduction in the postoperative inflammatory response. Statin continuation at the highest tolerable dose should be encouraged before cardiac surgery. The preoperative use of statins in cardiac surgery as 'bleeding-preventers' might have profound clinical implications.
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