Objectives. To explore the difference of glucose fluctuations between the normal subjects and diabetes mellitus (DM) patients and explore their impact on the development of CAD in type 2 DM patients. Methods. The subjects were divided into 3 groups: normal control (group A, ), type 2 DM patients without cardiovascular complications (group B, ), and type 2 DM patients with cardiovascular complications (group C, ). The SYNTAX scores were collected in group C. CGMS for 72?h was applied on all the subjects. The indexes such as MBG and the LAGE were calculated. Glycemic excursions were compared between groups A, B, and C, respectively. Results. The tested indexes had significant differences among the three groups. SYNTAX scores are related to systolic blood pressure, CRP, MAGE, and HbA1c and are significantly correlated at 6:00–8:00 and 11:00–13:00 time points in group C. Conclusions. Compared with normal subjects, T2DM patients have greater blood glucose fluctuations; T2DM patients with CAD have larger glucose fluctuations than T2DM patients without CAD. Blood glucose fluctuations are positively correlated with carotid artery intima-media thickness in T2DM patients and have a significant influence on the development of coronary artery. 1. Introduction The incidence of type 2 diabetes mellitus (T2DM) is increasing these years with the improvement of people's living standard, the changes of life style, and the increasing aging population. Yang et al. reported that the prevalence of diabetes in adults over 20 years old was 9.7% and the prevalence of prediabetes (impaired fasting glycaemia and impaired glucose tolerance) has reached 15.5% [1]. The complications of T2DM almost involved each organ of the body; 60%–80% of the patients died of vascular disease [2]. Large vascular disease affects the aorta, coronary artery, cerebral artery, renal artery, and peripheral artery mainly, which is hard to ignore; many researchers have studied the effect of blood glucose fluctuation on the vascular complications of T2DM [3–6]. Quagliaro et al. confirmed that the blood vessel endothelium was damaged greater by blood glucose fluctuation than by chronic persistent hyperglycemia [6]; recent studies have demonstrated that acute and chronic fluctuations in blood glucose levels can increase oxidative stress in type 2 diabetes mellitus patients [7], which results in cell dysfunction and tissue injury [8]. Therefore, it is important to evaluate the relationship between the blood glucose fluctuation and the coronary artery disease by dynamic glucose monitoring. Su et al. [9] have
References
[1]
Z.-J. Yang, J. Liu, J.-P. Ge, L. Chen, Z.-G. Zhao, and W.-Y. Yang, “Prevalence of cardiovascular disease risk factor in the Chinese population: the 2007-2008 China National Diabetes and Metabolic Disorders Study,” European Heart Journal, vol. 33, no. 2, pp. 213–220, 2012.
[2]
R. Huxley, F. Barzi, and M. Woodward, “Excess risk of fatal coronary heart disease associated with diabetes in men and women: meta-analysis of 37 prospective cohort studies,” British Medical Journal, vol. 332, no. 7533, pp. 73–76, 2006.
[3]
F. Cavalot, A. Petrelli, M. Traversa et al., “Postprandial blood glucose is a stronger predictor of cardiovascular events than fasting blood glucose in type 2 diabetes mellitus, particularly in women: lessons from the San Luigi Gonzaga Diabetes Study,” Journal of Clinical Endocrinology and Metabolism, vol. 91, no. 3, pp. 813–819, 2006.
[4]
M. Muggeo, G. Zoppini, E. Bonora et al., “Fasting plasma glucose variability predicts 10-year survival of type 2 diabetic patients: the Verona Diabetes Study,” Diabetes Care, vol. 23, no. 1, pp. 45–50, 2000.
[5]
G. Zoppini, G. Verlato, G. Targher, E. Bonora, M. Trombetta, and M. Muggeo, “Variability of body weight, pulse pressure and glycaemia strongly predict total mortality in elderly type 2 diabetic patients. The Verona Diabetes Study,” Diabetes/Metabolism Research and Reviews, vol. 24, no. 8, pp. 624–628, 2008.
[6]
L. Quagliaro, L. Piconi, R. Assaloni, L. Martinelli, E. Motz, and A. Ceriello, “Intermittent high glucose enhances apoptosis related to oxidative stress in human umbilical vein endothelial cells: the role of protein kinase C and NAD(P)H-oxidase activation,” Diabetes, vol. 52, no. 11, pp. 2795–2804, 2003.
[7]
C.-M. Chang, C.-J. Hsieh, J.-C. Huang, and I.-C. Huang, “Acute and chronic fluctuations in blood glucose levels can increase oxidative stress in type 2 diabetes mellitus,” Acta Diabetologica, vol. 49, supplement 1, pp. S171–S177, 2012.
[8]
A. Piwowar, M. Knapik-Kordecka, and M. Warwas, “Oxidative stress and endothelium dysfunction in diabetes mellitus type 2,” Polski Merkuriusz Lekarski, vol. 25, no. 146, pp. 120–123, 2008.
[9]
G. Su, S. Mi, H. Tao et al., “Association of glycemic variability and the presence and severity of coronary artery disease in patients with type 2 diabetes,” Cardiovascular Diabetology, vol. 10, article 19, 2011.
[10]
T. Palmerini, P. Genereux, A. Caixeta et al., “Prognostic value of the SYNTAX score in patients with acute coronary syndromes undergoing percutaneous coronary intervention: analysis from the ACUITY (Acute Catheterization and Urgent Intervention Triage StrategY) trial,” Journal of the American College of Cardiology, vol. 57, no. 24, pp. 2389–2397, 2011.
[11]
D. Y. Sahin, M. Gur, Z. Elbasan et al., “SYNTAX score is a predictor of angiographic no-reflow in patients with ST-elevation myocardial infarction treated with a primary percutaneous coronary intervention,” Coronary Artery Disease, vol. 24, no. 2, pp. 148–153, 2013.
[12]
P. G. Colman, D. W. Thomas, P. Z. Zimmet, T. A. Welborn, P. Garcia-Webb, and M. P. Moore, “New classification and criteria for diagnosis of diabetes mellitus. The Australasian Working Party on Diagnostic Criteria for Diabetes Mellitus,” New Zealand Medical Journal, vol. 112, no. 1086, pp. 139–141, 1999.
[13]
G.-D. Kang, L. Guo, Z.-R. Guo, X.-S. Hu, M. Wu, and H.-T. Yang, “Continuous metabolic syndrome risk score for predicting cardiovascular disease in the Chinese population,” Asia Pacific Journal of Clinical Nutrition, vol. 21, no. 1, pp. 88–96, 2012.
[14]
C. Cobelli, G. M. Toffolo, C. Dalla Man et al., “Assessment of β-cell function in humans, simultaneously with insulin sensitivity and hepatic extraction, from intravenous and oral glucose tests,” American Journal of Physiology, vol. 293, no. 1, pp. E1–E15, 2007.
[15]
Z. T. Bloomgarden, “Cardiovascular disease in diabetes,” Diabetes Care, vol. 31, no. 6, pp. 1260–1266, 2008.
[16]
M. Brownlee, “Biochemistry and molecular cell biology of diabetic complications,” Nature, vol. 414, no. 6865, pp. 813–820, 2001.
[17]
M. S. Joshi, L. Tong, A. C. Cook et al., “Increased myocardial prevalence of C-reactive protein in human coronary heart disease: direct effects on microvessel density and endothelial cell survival,” Cardiovascular Pathology, vol. 21, pp. 428–435, 2012.
[18]
F. Zheng, W. Lu, C. Jia, H. Li, Z. Wang, and W. Jia, “Relationships between glucose excursion and the activation of oxidative stress in patients with newly diagnosed type 2 diabetes or impaired glucose regulation,” Endocrine, vol. 37, no. 1, pp. 201–208, 2010.
[19]
A. Patel, S. MacMahon, J. Chalmers et al., “Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes,” The New England Journal of Medicine, vol. 358, no. 24, pp. 2560–2572, 2008.
[20]
H. C. Gerstein, M. E. Miller, R. P. Byington, et al., “Effects of intensive glucose lowering in type 2 diabetes,” The New England Journal of Medicine, vol. 358, no. 24, pp. 2545–2559, 2008.
[21]
M. Hanefeld, S. Fischer, U. Julius et al., “Risk factors for myocardial infarction and death in newly detected NIDDM: the Diabetes Intervention Study, 11-year follow-up,” Diabetologia, vol. 39, no. 12, pp. 1577–1583, 1996.
[22]
A. Ceriello, K. Esposito, L. Piconi et al., “Oscillating glucose is more deleterious to endothelial function and oxidative stress than mean glucose in normal and type 2 diabetic patients,” Diabetes, vol. 57, no. 5, pp. 1349–1354, 2008.
[23]
K. Torimoto, Y. Okada, H. Mori, and Y. Tanaka, “Relationship between fluctuations in glucose levels measured by continuous glucose monitoring and vascular endothelial dysfunction in type 2 diabetes mellitus,” Cardiovascular Diabetology, vol. 12, article 1, 2013.
[24]
C. Colette and L. Monnier, “Acute glucose fluctuations and chronic sustained hyperglycemia as risk factors for cardiovascular diseases in patients with type 2 diabetes,” Hormone and Metabolic Research, vol. 39, no. 9, pp. 683–686, 2007.
[25]
X. Geng, W. Cui, X. H. Yang, R. Q. Xie, J. D. Zhang, and H. M. Zheng, “The efficacy of antihypertensive treatment on diabetes mellitus or impaired glucose tolerance patients with blood pressure below 140/90?mm Hg: a meta-analysis,” Zhonghua Nei Ke Za Zhi, vol. 51, pp. 875–879, 2012.
[26]
E. S. Kilpatrick, A. S. Rigby, and S. L. Atkin, “For debate. Glucose variability and diabetes complication risk: we need to know the answer,” Diabetic Medicine, vol. 27, no. 8, pp. 868–871, 2010.
[27]
S. E. Siegelaar, F. Holleman, J. B. L. Hoekstra, and J. H. DeVries, “Glucose variability; does it matter?” Endocrine Reviews, vol. 31, no. 2, pp. 171–182, 2010.