title: Acute hyperglycemia reduces myocardial blood flow reserve and the magnitude of reduction is associated with insulin resistance: a study in nondiabetic humans using contrast echocardiography.
abstract: The effect of acute hyperglycemia per se on coronary perfusion in humans is undefined. We evaluated the effects of short-term hyperglycemia on myocardial blood flow reserve (MBFR) in healthy nondiabetic volunteers. Twenty-one nondiabetic volunteers (76 % females, mean ± SD, age 48 ± 5 years) had noninvasive MBFR assessment while exposed to pancreatic clamp with somatostatin and replacement glucagon and growth hormone infusions, with frequent interval plasma glucose (PG) monitoring. Insulin was infused at 0.75 mU/kg/min to mimic postprandial plasma insulin concentrations, and glucose was infused to maintain euglycemia (PG 93.9 ± 7.3 mg/dl) followed by hyperglycemia (PG 231.5 ± 18.1 mg/dl). Myocardial contrast echocardiography (MCE) was performed during each glycemic steady state using continuous infusion of Definity at rest and during regadenoson (Lexiscan 5 ml (400 μg) intravenous bolus) infusion to quantify myocardial blood flow (MBF) and determine MBFR. Insulin resistance (IR) was assessed by glucose infusion rate (GIR; mg/kg/min) at euglycemia. Median stress MBF, MBFR, and β reserve were significantly reduced during acute hyperglycemia versus euglycemia (stress MBF 3.9 vs 5.4, P = 0.02; MBFR 2.0 vs 2.7, P < 0.0001; β reserve 1.45 vs 2.4, P = 0.007). Using a median threshold GIR of 5 mg/kg/min, there was a correlation between GIR and hyperglycemic MBFR (r = 0.506, P = 0.019). MBFR, as determined noninvasively by MCE, is significantly decreased during acute hyperglycemia in nondiabetic volunteers, and the magnitude of this reduction is modulated by IR.
authors.affiliation: Mayo Clinic, Division of Cardiovascular Diseases and Internal Medicine, 200 First street SW, Rochester, MN, 55905, USA, abdelmoneim.sahar@mayo.edu.
authors.forename: Sahar S
authors.initials: SS
authors.lastname: Abdelmoneim
authors.forename: Mary E
authors.initials: ME
authors.lastname: Hagen
authors.forename: Edward
authors.initials: E
authors.lastname: Mendrick
authors.forename: Vishwanath
authors.initials: V
authors.lastname: Pattan
authors.forename: Benjamin
authors.initials: B
authors.lastname: Wong
authors.forename: Barbara
authors.initials: B
authors.lastname: Norby
authors.forename: Tamara
authors.initials: T
authors.lastname: Roberson
authors.forename: Troy
authors.initials: T
authors.lastname: Szydel
authors.forename: Rita
authors.initials: R
authors.lastname: Basu
authors.forename: Ananda
authors.initials: A
authors.lastname: Basu
authors.forename: Sharon L
authors.initials: SL
authors.lastname: Mulvagh
mesh_terms: D000208:Acute Disease; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D003287:Contrast Media; D003326:Coronary Circulation; D004452:Echocardiography; D005260:Female; D005466:Fluorocarbons; D015309:Glucose Clamp Technique; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D011237:Predictive Value of Tests; D011687:Purines; D011720:Pyrazoles; D015203:Reproducibility of Results; D013997:Time Factors; D014665:Vasodilator Agents
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D003287:Contrast Media; D005466:Fluorocarbons; D011687:Purines; D011720:Pyrazoles; D014665:Vasodilator Agents; C430916:regadenoson; C042852:perflutren