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An Experimental Series Investigating the Effects of Euglycaemic Hyperinsulinaemia on Myocardial Blood Flow Reserve in Healthy Individuals and Perfusion Defect Size in Patients Presenting With Acute Myocardial Infarction
Abstract   Peer reviewed

An Experimental Series Investigating the Effects of Euglycaemic Hyperinsulinaemia on Myocardial Blood Flow Reserve in Healthy Individuals and Perfusion Defect Size in Patients Presenting With Acute Myocardial Infarction

Michael C Y Nam, Annelise L Meneses, C Anstey, Christopher D Askew, I Hickman, Tom G Bailey, J Quah, R Senior, S Cox, R Poulter, …
Heart, Lung and Circulation, Vol.27(Supplement 2), pp.S298-S299
Cardiac Society of Australia and New Zealand Annual Scientific Meeting, the International Society for Heart Research Australasian Section Annual Scientific Meeting and the 12th Annual Australia and New Zealand Endovascular Therapies Meeting, 66th (Brisbane, Australia, 02-Aug-2018–05-Aug-2018)
2018
url
https://doi.org/10.1016/j.hlc.2018.06.570View
Published Version

Abstract

Cardiovascular Medicine and Haematology Public Health and Health Services
Background: Euglycaemic hyperinsulinaemia increases myocardial blood flow reserve (MBFR) and may reduce myocardial ischaemia. Using insulin-dextrose infusions, a two-phase study was conducted to determine: 1) how insulin duration, dose, and diabetes affect MBFR response; 2) the effect of insulin-dextrose on perfusion in the immediate period following revascularisation of ST-elevation myocardial infarction (STEMI). Methods: MBFR was determined using vasodilator myocardial contrast echocardiography (MCE). Twelve participants received insulin-dextrose or saline infusion. MBFR was measured at four time-points. Twenty-two received one of three insulin doses (0.5, 1.5, 3.0 mU/kg/minute), and 11 insulin-resistant participants (five metabolic syndrome, six type-2 diabetes) received 1.5 mU/kg/minute for 60 minutes. Baseline and 60-minute MBFRs were determined. Immediately following revascularisation for STEMI, 20 participants received 1.5 mU/kg/minute insulin-dextrose infusion or standard care for 120 minutes. MCE was performed at four time points to quantify percentage contrast defect length over total left ventricular endocardial border (CDL). Results: Insulin duration: MBFR increased with time in the insulin-dextrose group. Insulin dose: from baseline, MBFR increased in the 1.5 mU/kg/minute (2.42±0.39 to 3.25±0.77, p = 0.002), did not change in 0.5 mU/kg/minute, and decreased in 3.0 mU/kg/minute (2.64±0.25 to 2.16±0.33, p = 0.02) groups. Diabetes: from baseline, MBFR increased in healthy and metabolic syndrome (1.98±0.33 to 2.59±0.45, p = 0.04), but was borderline significant in diabetes (1.67±0.35 to 2.14±0.21, p = 0.05). STEMI: Baseline CDL was similar in both groups. It decreased with time and was significantly lower at 60 minutes with insulin-dextrose. Conclusion: Insulin infusion duration, dose, and diabetes are important factors that affect MBFR. When given after revascularisation for STEMI, insulin-dextrose reduces CDL.

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