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(Circulation. 2006;114:I-245 I-250.)
© 2006 American Heart Association, Inc.
Myocardial Protection and Vascular Biology |
From Department of Cardiothoracic Surgery, University Hospital Birmingham, Edgbaston, Birmingham, UK.
Correspondence to Robert Bonser, Department of Cardiothoracic Surgery, University Hospital Birmingham, Edgbaston, Birmingham, B15 2TH, UK. E-mail robert.bonser{at}uhb.nhs.uk
Background Both glucose-insulin-potassium (GIK) and tri-iodothyronine (T3) may improve cardiovascular performance after coronary artery surgery (CABG) but their effects have not been directly compared and the effects of combined treatment are unknown.
Methods and Results In 2 consecutive randomized double-blind placebo-controlled trials, in patients undergoing first time isolated on-pump CABG between January 2000 and September 2004, 440 patients were recruited and randomized to either placebo (5% dextrose) (n=160), GIK (40% dextrose, K+ 100 mmol · L1, insulin 70 u · L1) (0.75 mL · kg1 h1) (n=157), T3 (0.8 µg · kg1 followed by 0.113 µg · kg1 h1) (n=63) or GIK+T3 (n=60). GIK/placebo therapy was administered from start of operation until 6 hours after removal of aortic cross-clamp (AXC) and T3/placebo was administered for a 6-hour period from removal of AXC. Serial hemodynamic measurements were taken up to 12 hours after removal of AXC and troponin I (cTnI) levels were assayed to 72 hours. Cardiac index (CI) was significantly increased in both the GIK and GIK/T3 group in the first 6 hours compared with placebo (P<0.001 for both) and T3 therapy (P=0.009 and 0.029, respectively). T3 therapy increased CI versus placebo between 6 and 12 hours after AXC removal (P=0.01) but combination therapy did not. Release of cTnI was lower in all treatment groups at 6 and 12 hours after removal of AXC.
Conclusions Treatment with GIK, T3, and GIK/T3 improves hemodynamic performance and results in reduced cTnI release in patients undergoing on-pump CABG surgery. Combination therapy does not provide added hemodynamic effect.
Key Words: glucose hemodynamics insulin myocardial injury thyroid troponin I
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