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The Sweet Spot: Continued Search for the Glycemic Threshold for Macrovascular Disease—A Retrospective Single Center Experience

DOI: 10.5402/2012/874706

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Abstract:

Background. Atherosclerotic cardiovascular disease (ASCVD) is a common complication of diabetes mellitus and impaired fasting glucose (IFG). We hypothesized that the relation of fasting glucose levels to ASCVD is linear, with the prevalence of clinical ASCVD beginning to increase even among individuals currently categorized as normoglycemic. Methods. Patient charts were retrospectively reviewed from our Dyslipidemic Preventive Cardiology Clinic. We evaluated the prevalence of ASCVD relative to fasting glucose levels in a cross-section of patients at high risk for ASCVD. Results. In 558 dyslipidemic patients, ASCVD prevalence increased with increasing fasting glucose levels. A significantly higher prevalence of ASCVD was observed among patients with fasting glucose levels between 90 and 99?mg/dL versus lower levels. As glucose levels increased from 90 to 125?mg/dL, the prevalence of ASCVD continued to rise in parallel. Logistic regression analysis with forward likelihood ratio stepwise selection indicated that individuals with fasting blood glucose of 90–99?mg/dL were 2.6 times more likely to have ASCVD than those with lower levels of fasting blood glucose. Conclusion. Our findings suggest that the current cutoff for impaired fasting glucose of 100?mg/dL may be somewhat conservative and that a level above 90?mg/dL may be more appropriate as an ASCVD risk factor, particularly in patients with a lipid disorder. 1. Introduction Atherosclerotic cardiovascular disease (ASCVD) is a common complication of diabetes mellitus (DM). Atherosclerosis is the primary reason for the decreased life expectancy of a newly diagnosed diabetic compared to an age and gender-matched nondiabetic [1, 2]. The risk of having a myocardial infarction over a period of seven years in the middle-aged diabetic patient without identified preexisting coronary heart disease (CHD) is the same as that in nondiabetic individual with existing CHD [3]. It is generally accepted that improved glycemic control decreases the onset and progression of microvascular complications, including nephropathy and retinopathy, and yet it does not reduce the risk of ASCVD and all-cause mortality [4, 5]. In the Prospective Pioglitazone Clinical Trial in macrovascular events (PROActive) study, however, improved glycemic control with pioglitazone reduced the composite endpoint of all-cause mortality, nonfatal myocardial infarction, and stroke in patients with type-2 diabetes and atherosclerosis [6]. In part, this may be due to the favorable effect of pioglitazone on the high-density lipoprotein (HDL),

References

[1]  “Diabetes Mellitus: a major risk factor for cardiovascular disease: a joint editorial statement by the American Diabetic Association, The National Heart, Lung, and Blood Institute, The Juvenile Diabetes Foundation International: The National Institute of Diabetes and Digestive and Kidney Disease: and The American Heart Association,” Circulation, vol. 100, pp. 1132–1133, 1999.
[2]  N. A. Roper, R. W. Bilous, W. F. Kelly, N. C. Unwin, and V. M. Connolly, “Excess mortality in a population with diabetes and the impact of material deprivation: longitudinal, population based study,” British Medical Journal, vol. 322, no. 7299, pp. 1389–1393, 2001.
[3]  S. M. Haffner, S. Lehto, T. R?nnemaa, K. Py?r?l?, and M. Laakso, “Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction,” The New England Journal of Medicine, vol. 339, no. 4, pp. 229–234, 1998.
[4]  The Diabetes Control and Complications Trial Research Group, “The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus,” The New England Journal of Medicine, vol. 329, pp. 977–986, 1993.
[5]  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, vol. 352, no. 9131, pp. 837–853, 1998.
[6]  J. A. Dormandy, B. Charbonnel, D. J. Eckland et al., “Secondary prevention of macrovascular events in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial in macroVascular Events): a randomised controlled trial,” Lancet, vol. 366, no. 9493, pp. 1279–1289, 2005.
[7]  “Report of the expert committee on the diagnosis and classification of diabetes mellitus,” Diabetes Care, vol. 26, supplement 1, pp. S5–S20, 2003.
[8]  The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, “Follow-up report on the diagnosis of diabetes mellitus,” Diabetes Care, vol. 26, no. 11, pp. 3160–3167, 2003.
[9]  Heart Protection Study Collaborative Group, “MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: a randomised placebo-controlled trial,” Lancet, vol. 360, no. 9326, pp. 7–22, 2002.
[10]  “National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). Third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III) final report,” Circulation, vol. 106, no. 25, pp. 3143–3421, 2002.
[11]  R. W. Nesto, “Correlation between cardiovascular disease and diabetes mellitus: current concepts,” American Journal of Medicine, vol. 116, supplement 5, pp. S11–S22, 2004.
[12]  W. A. Hsueh, C. J. Lyon, and M. J. Qui?ones, “Insulin resistance and the endothelium,” American Journal of Medicine, vol. 117, no. 2, pp. 109–117, 2004.
[13]  S. V. Edelman, “The role of the thiazolidinediones in the practical management of patients with type 2 diabetes and cardiovascular risk factors,” Reviews in Cardiovascular Medicine, vol. 4, no. 6, pp. S29–S37, 2003.
[14]  B. Balkau, M. Shipley, R. J. Jarrett et al., “High blood glucose concentration is a risk factor for mortality in middle-aged nondiabetic men: 20-year follow-up in the Whitehall Study, the Paris Prospective Study, and the Helsinki Policemen Study,” Diabetes Care, vol. 21, no. 3, pp. 360–367, 1998.
[15]  J. Sung, Y. M. Song, S. Ebrahim, and D. A. Lawlor, “Fasting blood glucose and the risk of stroke and myocardial infarction,” Circulation, vol. 119, no. 6, pp. 812–819, 2009.
[16]  I. M. Stratton, A. I. Adler, H. A. W. Neil et al., “Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study,” British Medical Journal, vol. 321, no. 7258, pp. 405–412, 2000.
[17]  R. B. Goldberg, D. M. Kendall, M. A. Deeg et al., “A comparison of lipid and glycemic effects of pioglitazone and rosiglitazone in patients with type 2 diabetes and dyslipidemia,” Diabetes Care, vol. 28, no. 7, pp. 1547–1554, 2005.
[18]  D. S. Fredrickson, “An international classification of hyperlipidemias and hyperlipoproteinemias,” Annals of Internal Medicine, vol. 75, no. 3, pp. 471–472, 1971.
[19]  S. C. Port, M. O. Goodarzi, N. G. Boyle, and R. I. Jennrich, “Blood glucose: a strong risk factor for mortality in nondiabetic patients with cardiovascular disease,” American Heart Journal, vol. 150, no. 2, pp. 209–214, 2005.
[20]  National Institute of Health (NIH), Clinical Guidelines on the Identification, Evaluation and Treatment of Overweight and Obesity in Adults: The Evidence Report, Government Printing Office, Washington, DC, USA, 1998.
[21]  E. Barrett-Connor, “Does hyperglycemia really cause coronary heart disease?” Diabetes Care, vol. 20, no. 10, pp. 1620–1623, 1997.

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