Anti-inflammatory and profibrinolytic effect of insulin in acute ST-segment-elevation myocardial infarction.
BACKGROUND
The clinical benefits of insulin previously observed in acute ST-segment-elevation myocardial infarction (STEMI) may be partially explained by an anti-inflammatory effect. We assessed this potential effect of insulin in STEMI patients treated with fibrinolytics.


RESULTS
Thirty-two patients receiving reteplase were randomly assigned infusions of either insulin at 2.5 U/h, dextrose, and potassium (GIK) or normal saline and potassium (C) for 48 hours. Plasma concentrations of high-sensitivity C-reactive protein (CRP), serum amyloid A (SAA), plasminogen activator inhibitor-1 (PAI-1), creatine kinase (CK), and CK-MB were measured at baseline and sequentially for 48 hours. Total p47phox protein in mononuclear cells was measured in a subgroup of 13 subjects. Baseline CRP and SAA were significantly increased (2- to 4-fold) at 24 and 48 hours in each group (P<0.01). However, in the insulin group, there was a significant (P<0.05) attenuation of the absolute rise in concentration of CRP and SAA from baseline. The absolute increase of CRP and SAA was reduced by 40% (CRP) and 50% (SAA) at 24 hours and at 48 hours compared with the control group. The absolute increase in PAI-1 from baseline and the percentage increase in p47phox over 48 hours were significantly (P<0.05) lower in the insulin-treated group. CK-MB peaked earlier and tended to be lower in insulin-treated subjects, especially in patients with inferior MI.


CONCLUSIONS
Insulin has an anti-inflammatory and profibrinolytic effect in patients with acute MI. These effects may contribute to the clinical benefits of insulin in STEMI.
Chaudhuri
Ajay
A
Division of Endocrinology, Diabetes and Metabolism, State University of New York at Buffalo, and Kaleida Health, Buffalo, NY 14209, USA.
Janicke
David
D
Wilson
Michael F
MF
Tripathy
Devjit
D
Garg
Rajesh
R
Bandyopadhyay
Arindam
A
Calieri
Janeen
J
Hoffmeyer
Debbie
D
Syed
Tufail
T
Ghanim
Husam
H
Aljada
Ahmad
A
Dandona
Paresh
P
D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D001786:Blood Glucose / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D015897:Comorbidity; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D004359:Drug Therapy, Combination; D004562:Electrocardiography; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000097:blood; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D007527:Isoenzymes / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D019255:NADPH Oxidases; D010750:Phosphoproteins / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000627:therapeutic use; D000685:Serum Amyloid A Protein / Q000032:analysis; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage / Q000627:therapeutic use; D016896:Treatment Outcome
D000894:Anti-Inflammatory Agents, Non-Steroidal; D001786:Blood Glucose; D005343:Fibrinolytic Agents; D007328:Insulin; D007527:Isoenzymes; D010750:Phosphoproteins; D017395:Plasminogen Activator Inhibitor 1; D011994:Recombinant Proteins; D000685:Serum Amyloid A Protein; D002097:C-Reactive Protein; C087896:reteplase; D019255:NADPH Oxidases; C060505:neutrophil cytosolic factor 1; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form; D010959:Tissue Plasminogen Activator