Glucose-insulin therapy, plasma substrate levels and cardiac recovery after cardiac ischemic events.
BACKGROUND
The potential usefulness of glucose-insulin therapy relies to a large extent on the premise that it prevents hyperglycemia and hyperlipidemia following cardiac ischemic events.


METHODS
In this review we evaluate the literature concerning plasma glucose and free fatty acids levels during and following cardiac ischemic events.


RESULTS
The data indicate that hyperlipidemia and hyperglycemia most likely occur during acute coronary ischemic syndromes in the conscious state (e.g. acute myocardial infarction) and less so during reperfusion following CABG reperfusion. This is in accordance with observations that glucose-insulin therapy during early reperfusion post CABG may actually cause hypolipidemia, because substantial hyperlipidemia does not appear to occur during that stage of cardiac surgery.


CONCLUSIONS
Considering recent data indicating that hypolipidemia may be detrimental for cardiac function, we propose that free fatty acid levels during reperfusion post CABG with the adjunct glucose-insulin therapy need to be closely monitored.


CONCLUSIONS
From a clinical point of view, a strategy directed at monitoring and thereafter maintaining plasma substrate levels in the normal range for both glucose (4-6 mM) and FFA (0.2-0.6 mM) as well as stimulation of glucose oxidation, promises to be the most optimal metabolic reperfusion treatment following cardiac ischemic episodes. Future (preclinical and subsequently clinical) investigations are required to investigate whether the combination of glucose-insulin therapy with concomitant lipid administration may be beneficial in the setting of reperfusion post CABG.
Zuurbier
C J
CJ
Department of Anesthesiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. c.j.zuurbier@amc.uva.nl
Van Wezel
H B
HB
D001786:Blood Glucose / Q000378:metabolism*; D004359:Drug Therapy, Combination; D005230:Fatty Acids, Nonesterified / Q000097:blood / Q000378:metabolism; D005947:Glucose / Q000378:metabolism / Q000627:therapeutic use*; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use*; D017202:Myocardial Ischemia / Q000097:blood / Q000188:drug therapy*; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007004:Hypoglycemic Agents; D007328:Insulin; D005947:Glucose