Effects of glucose-insulin-potassium infusion on chronic ischaemic left ventricular dysfunction.
BACKGROUND
Glucose-insulin-potassium (GIK) infusion improves cardiac function and outcome during acute ischaemia.


OBJECTIVE
To determine whether GIK infusion benefits patients with chronic ischaemic left ventricular dysfunction, and if so whether this is related to the presence and nature of viable myocardium.


METHODS
30 patients with chronic ischaemic left ventricular dysfunction had dobutamine echocardiography and were given a four hour infusion of GIK. Segmental responses were quantified by improvement in wall motion score index (WMSI) and peak systolic velocity using tissue Doppler. Global responses were assessed by left ventricular volume and ejection fraction, measured using a three dimensional reconstruction. Myocardial perfusion was determined in 15 patients using contrast echocardiography.


RESULTS
WMSI (mean (SD)) improved with dobutamine (from 1.8 (0.4) to 1.6 (0.4), p < 0.001) and with GIK (from 1.8 (0.4) to 1.7 (0.4), p < 0.001); there was a similar increment for both. Improvement in wall motion score with GIK was observed in 55% of the 62 segments classed as viable by dobutamine echocardiography, and in 5% of 162 classed as non-viable. There was an increment in peak systolic velocity after both dobutamine echocardiography (from 2.5 (1.8) to 3.2 (2.2) cm/s, p < 0.01) and GIK (from 3.0 (1.6) to 3.5 (1.7) cm/s, p < 0.001). The GIK effects were not mediated by changes in pulse, mean arterial pressure, lactate, or catecholamines, nor did they correlate with myocardial perfusion. End systolic volume improved after GIK (p = 0.03), but only in 25 patients who had viable myocardium on dobutamine echocardiography.


CONCLUSIONS
In patients with viable myocardium and chronic left ventricular dysfunction, GIK improves wall motion score, myocardial velocity, and end systolic volume, independent of effects on haemodynamics or catecholamines. The response to GIK is observed in areas of normal and abnormal perfusion assessed by contrast echocardiography.
Khoury
V K
VK
University of Queensland, Brisbane, Queensland, Australia.
Haluska
B
B
Prins
J
J
Marwick
T H
TH
D000368:Aged; D002316:Cardiotonic Agents / Q000008:administration & dosage*; D002908:Chronic Disease; D003925:Diabetic Angiopathies / Q000188:drug therapy* / Q000503:physiopathology; D004298:Dopamine; D004338:Drug Combinations; D004452:Echocardiography / Q000379:methods; D005260:Female; D005947:Glucose / Q000008:administration & dosage*; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D007262:Infusions, Intravenous; D007328:Insulin / Q000008:administration & dosage*; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D011188:Potassium / Q000008:administration & dosage*; D013318:Stroke Volume / Q000187:drug effects; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology
D002316:Cardiotonic Agents; D004338:Drug Combinations; D007004:Hypoglycemic Agents; D007328:Insulin; C030396:glucose-insulin-potassium cardioplegic solution; D005947:Glucose; D011188:Potassium; D004298:Dopamine