title: Diastolic dysfunction after coronary artery bypass grafting--the effect of glucose-insulin-potassium infusion.
abstract: BACKGROUND
  Glucose-insulin-potassium (GIK) infusion improves clinical outcome after coronary artery bypass surgery (CABG). The mechanism of benefit is unclear, but GIK limits ischemia and reperfusion injury. This study was designed to assess whether the clinical benefit of perioperative GIK infusion is mediated through reduction in the severity of diastolic dysfunction that occurs after CABG.
  
  
  RESULTS
  Thirty-one patients undergoing CABG were randomized to GIK infusion (n = 14) or no-GIK (n = 17). Left ventricular compliance, using pressure-area relationships, was assessed by simultaneous transesophageal echocardiographic measurement of LV end-diastolic area (LVEDA) and pulmonary capillary wedge pressure (PCWP) at baseline prior to CABG, early post cardiopulmonary bypass (CPB), after sternal closure, and 3 hours postoperatively. Measures of LVEDA were made at a constant PCWP and a decrease in LVEDA reflects a leftward shift in the pressure-area relationship consistent with decreased compliance. Both study groups demonstrated progressive and consistent worsening of LV compliance, as evidenced by a reduction of LVEDA from 17.0 +/- 3.9 cm(2) at baseline to 15.3 +/- 3.6 cm(2) after CPB, 14.6 +/- 2.9 cm(2) after sternal closure, and 14.1 +/- 3.2 cm(2) (p < 0.0001) at three hours postoperatively. LVEDA decreased from a baseline of 16.3 +/- 2.8 to 13.8 +/- 2.9 cm(2) in the GIK group, while the non-GIK group demonstrated a reduction of LVEDA from 17.5 +/- 4.6 to 14.3 +/- 3.5 cm(2). Doppler transmitral E wave deceleration time shortened as well, which is consistent with more restrictive LV filling due to rapid equilibration of LA and LV pressures. GIK infusion did not alter either measure of diastolic function significantly.
  
  
  CONCLUSIONS
  Diastolic dysfunction occurs nearly universally after CABG, worsens with chest closure, persists for up to 3 hours postoperatively, and is unaffected by GIK. Despite theoretical reasons why GIK might limit ischemia and reperfusion injury, the clinical benefits do not appear to be related to amelioration of diastolic dysfunction.
  
  
  BACKGROUND
  The study was partially supported by Agilent Technologies/Philips Imaging.
authors.affiliation: Evans Department of Medicine Section of Cardiology, Boston University Medical Center, Boston, MA, USA.
authors.forename: Michael W
authors.initials: MW
authors.lastname: Tsang
authors.forename: Ravin
authors.initials: R
authors.lastname: Davidoff
authors.forename: Amit
authors.initials: A
authors.lastname: Korach
authors.forename: Carl S
authors.initials: CS
authors.lastname: Apstein
authors.forename: J Frederick
authors.initials: JF
authors.lastname: Hesselvik
authors.forename: Hao
authors.initials: H
authors.lastname: Nguyen
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Shemin
authors.forename: Oz M
authors.initials: OM
authors.lastname: Shapira
mesh_terms: D000368:Aged; D002317:Cardiovascular Agents / Q000008:administration & dosage*; D001026:Coronary Artery Bypass / Q000009:adverse effects*; D003971:Diastole; D005260:Female; D005947:Glucose / Q000008:administration & dosage*; D006801:Humans; D007328:Insulin / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000008:administration & dosage*; D011446:Prospective Studies; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy* / Q000209:etiology
chemical_list: D002317:Cardiovascular Agents; D007328:Insulin; D005947:Glucose; D011188:Potassium