Parikh Shailja V, Abdullah Shuaib M, Keeley Ellen C, Cigarroa Joaquin E, Addo Tayo A, Warner John J, Khera Amit, de Lemos James A, McGuire Darren K
Department of Internal Medicine, the University of Texas Southwestern Medical Center in Dallas, Texas 75235-9047, USA.
Diab Vasc Dis Res. 2007 Sep;4(3):222-5. doi: 10.3132/dvdr.2007.043.
Glucose-insulin-potassium (GIK) infusion favourably affects several biomarkers associated with risk in the setting of myocardial infarction (MI). In the context of a recent trial demonstrating no benefit of GIK, we assessed the impact of GIK on inflammation, neurohormonal activation and myonecrosis in ST elevation myocardial infarction (STEMI). In a local substudy of an international randomised trial, 25 patients with STEMI were randomised to receive a 24-hour infusion of GIK vs. no GIK. C-reactive protein (hs-CRP), N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin T (TnT) were assayed at baseline and at 24 hours. The two groups were well matched for baseline characteristics and infarct location. There were no statistically significant differences at baseline or at 24 hours in levels of hs-CRP, NT-proBNP or cTnT, with similar and significant increases in all three biomarkers by 24 hours in both groups. In conclusion, GIK had no discernible effect on biomarkers associated with inflammation, neurohormonal activation or myonecrosis, three pathways associated with adverse outcomes in STEMI.
