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Stanford, CA, United States

Carter W.H.,Charleston Area Medical Center | Trotter C.C.,Texas A&M University | Kowalski T.E.,University of Cincinnati | Modak A.,Center for Health Services and Outcomes Research | And 5 more authors.
Journal of Electrocardiology | Year: 2012

Background: Atrial fibrillation occurs in 20% to 40% of patients post cardiac surgery. Prophylactic amiodarone decreases the incidence of atrial fibrillation, especially in those not taking β-blockers. Studies, however, vary in dosage, duration of treatment, and route of administration. Limited studies evaluating short duration use of oral amiodarone show conflicting results. We hypothesize that an order set for use of short duration, oral amiodarone started the night before surgery and continued for 4 to 6 days will decrease atrial fibrillation after heart surgery. Methods: The Society of Thoracic Surgeons database was used to identify 471 patients who received amiodarone per order set and 151 patients that did not receive amiodarone. The amiodarone order set included amiodarone 600 mg the night before surgery and 400 mg twice daily for 4 to 6 days post heart surgery. After propensity matching, 112 patients remained in each group. We compared outcomes for the 2 groups as a case-controlled, retrospective, study. Results: Atrial fibrillation occurred in 43% (48 of 112) of the patients that did not receive amiodarone vs 23% (26 of 112) receiving prophylactic amiodarone (P = <.001). There was no increased incidence of hemodynamic, pulmonary, or other adverse outcomes observed between the 2 groups. Conclusions: This practical order set for, short duration, oral amiodarone, with or without adjunct β-blocker therapy started the night before heart surgery and continued for up to six days post surgery, appears to be a safe and effective treatment for reducing the incidence of atrial fibrillation following heart surgery. © 2012 Elsevier Inc.

Taniguchi C.M.,Center for Clinical science Research | Finger E.C.,Center for Clinical science Research | Krieg A.J.,University of Kansas Medical Center | Wu C.,Center for Clinical science Research | And 7 more authors.
Nature Medicine | Year: 2013

Signaling initiated by hypoxia and insulin powerfully alters cellular metabolism. The protein stability of hypoxia-inducible factor-1 alpha (Hif-1α) and Hif-2α is regulated by three prolyl hydroxylase domain-containing protein isoforms (Phd1, Phd2 and Phd3). Insulin receptor substrate-2 (Irs2) is a critical mediator of the anabolic effects of insulin, and its decreased expression contributes to the pathophysiology of insulin resistance and diabetes. Although Hif regulates many metabolic pathways, it is unknown whether the Phd proteins regulate glucose and lipid metabolism in the liver. Here, we show that acute deletion of hepatic Phd3, also known as Egln3, improves insulin sensitivity and ameliorates diabetes by specifically stabilizing Hif-2α, which then increases Irs2 transcription and insulin-stimulated Akt activation. Hif-2α and Irs2 are both necessary for the improved insulin sensitivity, as knockdown of either molecule abrogates the beneficial effects of Phd3 knockout on glucose tolerance and insulin-stimulated Akt phosphorylation. Augmenting levels of Hif-2α through various combinations of Phd gene knockouts did not further improve hepatic metabolism and only added toxicity. Thus, isoform-specific inhibition of Phd3 could be exploited to treat type 2 diabetes without the toxicity that could occur with chronic inhibition of multiple Phd isoforms.© 2013 Nature America, Inc. All rights reserved.

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