pISSN 1738-5520 eISSN 1738-5555
Indexed in PubMed, SCIE and Scopus
Open Access, Peer-reviewed, Monthly
    Korean Circ J. 2008 Apr;38(4):220-226. Korean.
    Published online Apr 30, 2008.
    https://doi.org/10.4070/kcj.2008.38.4.220
    Copyright © 2008 The Korean Society of Cardiology
    Original Article

    The Effect of Hyperglycemia Induced by Oral Glucose Loading on Coronary Flow Reserve

    Mi-Jin Song, MD,1,2 Nam-Ho Kim, MD,1,2,3 An Saeng Lee, RN,2 Jun-Ho Choi, MD,1,2 Yong Cheol Kim, MD,1,2 Seung Hwan Kim, MD,1,2 Eun Mi Park, MD,1,2 Sang Jae Rhee, MD,1,2 Kyeong Ho Yun, MD,1,2,3 Eun Mi Lee, MD,1 Nam Jin Yoo, MD,1 Seok Kyu Oh, MD,1,2,3 and Jin-Won Jeong, MD1,2,3
      • 1Department of Internal Medicine, Wonkwang University School of Medicine, Iksan, Korea.
      • 2Cardiovascular Center, Wonkwang University School of Medicine, Iksan, Korea.
      • 3Wonkwang Institute of Medical Science, Wonkwang University School of Medicine, Iksan, Korea.
    • Correspondence: Nam-Ho Kim, MD, Department of Internal Medicine, Wonkwang University School of Medicine, 344-2 Sinyong-dong, Iksan 570-711, Korea. Tel: 82-63-859-2523, Fax: 82-63-855-2025, Email: cardionh@wonkwang.ac.kr
    Received November 16, 2007; Revised December 21, 2007; Accepted February 08, 2008.

    Abstract

    Background and Objectives

    Patients with chronic diabetes mellitus (DM) have an increased risk of cardiac dysfunction and mortality. There is some evidence that suggests acute hyperglycemia may cause vascular dysfunction. However, it is unknown whether acute, short-term hyperglycemia affects coronary microcirculation function in healthy subjects. The present study was undertaken to explore this issue.

    Subjects and Methods

    We evaluated 20 healthy males who had no history of DM or impaired glucose tolerance, ranging in age from 23 to 36 years (25.9±3.3 years). We checked blood sugar, 12-lead electrocardiography, pulse wave velocity, and coronary flow reserve using echocardiography during fasting, and 30, 60, 90, and 120 minutes after ingestion of 75 g of glucose orally.

    Results

    Non-significant prolongation of the QTc dispersion was observed after the 75 g glucose loading. No significant difference in the pulse wave velocity of the carotid-to-femoral artery, carotid-to-radial artery, or femoral-to-dorsalis pedis artery was observed after the 75 g glucose loading. There was a significant reduction in the coronary flow reserve at 60 (4.06±0.75 vs. 3.54±0.82, p=0.021) and 90 minutes (4.06±0.75 vs. 3.59±0.63, p=0.021) after the 75 g glucose loading compared to that on fasting.

    Conclusion

    The results of this study suggest that acute exposure to high circulating glucose levels does not affect heterogeneity of the ventricular repolarization or arterial stiffness, but it does reduce the coronary flow reserve in healthy young men.

    Keywords
    Glucose; Coronary vessels; Blood flow velocity

    Figures

    Fig. 1
    Coronary flow reserve in a subject with 24 years old. At baseline (A), resting peak diastolic velocity was 16 cm/sec (top) and hyperemic peak diastolic velocity was 86 cm/sec. Calculated coronary flow reserve at baseline was 86/16=5.38; At 60 min after ingestion of 75 g glucose (B), resting peak diastolic velocity was 20 cm/sec (top) and hyperemic peak diastolic velocity was 92 cm/sec. Calculated coronary flow reserve at baseline was 103/22=4.60.

    Fig. 2
    Changes of coronary flow reserve after ingestion of 75 g glucose. *p<0.05 compare to baseline.

    Tables

    Table 1
    Baseline clinical characteristics

    Table 2
    Changes of hemodynamic, electrocardiographic, and pulse wave velocity parameters after oral glucose loading

    Table 3
    Changes of coronary blood flow after oral glucose loading

    Table 4
    Correlation between change (Δ) of glucose and change of other parameters after 1 hour of oral glucose loading

    References

      1. DCCT Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1993;329:977–986.
      1. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998;352:837–853.
      1. Umpierrez GE, Isaacs SD, Bazargan N, You X, Thaler LM, Kitabchi AE. Hyperglycemia: an independent marker of in-hospital mortality in patients with undiagnosed diabetes. J Clin Endocrinol Metab 2002;87:978–982.
      1. Capes SE, Hunt D, Malmberg K, Gerstein HC. Stress hyperglycemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview. Lancet 2000;355:773–778.
      1. Ceriello A. Acute hyperglycemia: a 'new' risk factor during myocardial infarction. Eur Heart J 2005;26:328–331.
      1. Nishikawa T, Edelstein D, Du XL, et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycemia damage. Nature 2000;404:787–790.
      1. Gutterman DD. Vascular dysfunction in hyperglycemia: is protein kinase C the culprit? Circ Res 2002;90:5–7.
      1. Gresele P, Guglielmini G, De Angelis M, et al. Acute, short-term hyperglycemia enhances shear stress-induced platelet activation in patients with type II diabetes mellitus. J Am Coll Cardiol 2003;41:1013–1020.
      1. Marfella R, Esposito K, Giunta R, et al. Circulating adhesion molecules in humans: role of hyperglycemia and hyperinsulinemia. Circulation 2000;101:2247–2251.
      1. Esposito K, Nappo F, Marfella R, et al. Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress. Circulation 2002;106:2067–2072.
      1. Akbari CM, Saouaf R, Barnhill DF, Newman PA, LoGerfo FW, Veves A. Endothelium-dependent vasodilatation is impaired in both microcirculation and macrocirculation during acute hyperglycemia. J Vasc Surg 1998;28:687–694.
      1. Kawano H, Motoyama T, Hirashima O, et al. Hyperglycemia rapidly suppresses flow-mediated endothelium-dependent vasodilation of brachial artery. J Am Coll Cardiol 1999;34:146–154.
      1. Title LM, Cummings PM, Giddens K, Nassar BA. Oral glucose loading acutely attenuates endothelium-dependent vasodilation in healthy adults without diabetes: an effect prevented by vitamins C and E. J Am Coll Cardiol 2000;36:2185–2191.
      1. Beckman JA, Goldfine AB, Gordon MB, Creager MA. Ascorbate restores endothelium-dependent vasodilation impaired by acute hyperglycemia in humans. Circulation 2001;103:1618–1623.
      1. Youn HJ, Foster E. Demonstration of coronary artery flow using transthoracic Doppler echocardiography. J Am Soc Echocardiogr 2004;17:178–185.
      1. Park JH, Kang DH, Lee SW, et al. Detection of coronary restenosis by serial Doppler echocardiographic assessment of coronary flow velocity reserve after percutaneous intervention. Korean Circ J 2004;34:660–669.
      1. Choi CU, Shim WJ, Kim SH, et al. Factors affecting coronary flow reserve: measured by transthoracic Doppler echocardiography. Korean Circ J 2002;32:958–964.
      1. Bazett HC. An analysis of the time-relations of electrocardiograms. Heart 1918;7:353–370.
      1. Capaldo B, Galderisi M, Turco AA, et al. Acute hyperglycemia does not affect the reactivity of coronary microcirculation in humans. J Clin Endocrinol Metab 2005;90:3871–3876.
      1. Fusimoto K, Hozumi T, Watanabe H, et al. Acute hyperglycemia induced by oral glucose loading suppresses coronary micocirculation on transthoracic doppler echocardiography in healthy young adults. Echocardiography 2006;23:829–834.
      1. Weiss D. Hyperglycemia during physical stress. Am J Med 1996;100:374.
      1. Galderisi M, de Simone G, Cicala S, et al. Coronary flow reserve in hypertensive patients with appropriate or inappropriate left ventricular mass. J Hypertens 2003;21:2183–2188.
      1. Youn HJ, Park CS, Cho EJ, et al. Analysis of coronary artery flow patterns in patients with chest pain and normal coronary angiogram: study using transthoracic Doppler echocardiography. Korean Circ J 2003;33:205–211.
      1. Nemes A, Forster T, Csanady M. Decreased aortic distensibility and coronary flow velocity reserve in patients with significant aortic valve stenosis with normal epicardial coronary arteries. J Heart Valve Dis 2004;13:567–573.
      1. Kim HK, Kim YJ, Sohn DW, Park YB, Choi YS. Transthoracic echocardiographic evaluation of coronary flow reserve in patients with hypertrophic cardiomyopathy. Int J Cardiol 2004;94:167–171.
      1. Ceriello A, Quagliaro L, D'Amico M, et al. Acute hyperglycemia induces nitrotyrosine formation and apoptosis in perfused heart from rat. Diabetes 2002;51:1076–1082.
      1. Gupta S, Sussman I, McArtliur CS, Tornheim K, Cohen RA, Ruderman NB. Endothelium-dependent inhibition of Na+-K+ ATP ase activity in rabbit aorta by hyperglycemia: possible role of endothelium-derived nitric oxide. J Clin Invest 1992;90:727–732.
      1. Joffe II, Travers KE, Perreault-Micale CL, et al. Abnormal cardiac function in the streptozocin-induced non-insulin-dependent diabetic rat: non-invasive assessment with Doppler echocardiography and contribution of nitric oxide pathway. J Am Coll Cardiol 1999;34:2111–2119.
      1. McVeigh G, Brennan G, Hayes R, Cohn J, Finkelstein S, Johnston D. Vascular abnormalities in non-insulin-dependent diabetes mellitus identified by arterial waveform analysis. Am J Med 1993;95:424–430.
      1. Eckel RH, Wassef M, Chait A, et al. Diabetes and cardiovascular disease: writing group II: pathogenesis of atherosclerosis in diabetes. Circulation 2002;105:e138–e143.
    MeSH Terms
    Arteries
    Blood Flow Velocity
    Blood Glucose
    Coronary Vessels
    Diabetes Mellitus
    Eating
    Echocardiography
    Electrocardiography
    Fasting
    Glucose
    Humans
    Hyperglycemia
    Male
    Microcirculation
    Population Characteristics
    Pulse Wave Analysis
    Vascular Stiffness
    Metrics
    Share
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    Tables
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