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(Hypertension. 2001;37:1053.)
© 2001 American Heart Association, Inc.
Review Article |
From the SUNY Downstate Medical Center and VAMC (J.R.S.), Brooklyn, NY; the Alton Ochsner Medical Foundation (E.D.F.), New Orleans, La; and VAMC (M.E.), Miami, Fla.
Correspondence to James R. Sowers, MD, Professor of Medicine and Cell Biology, Director, Endocrinology, Diabetes and Hypertension, SUNY HSC at Brooklyn, 450 Clarkson Ave, Box 1205, Brooklyn, NY 11203. E-mail jsowers{at}netmail.hscbklyn.edu
AbstractCardiovascular diseases (CVDs) are the major causes of mortality in persons with diabetes, and many factors, including hypertension, contribute to this high prevalence of CVD. Hypertension is approximately twice as frequent in patients with diabetes compared with patients without the disease. Conversely, recent data suggest that hypertensive persons are more predisposed to the development of diabetes than are normotensive persons. Furthermore, up to 75% of CVD in diabetes may be attributable to hypertension, leading to recommendations for more aggressive treatment (ie, reducing blood pressure to <130/85 mm Hg) in persons with coexistent diabetes and hypertension. Other important risk factors for CVD in these patients include the following: obesity, atherosclerosis, dyslipidemia, microalbuminuria, endothelial dysfunction, platelet hyperaggregability, coagulation abnormalities, and "diabetic cardiomyopathy." The cardiomyopathy associated with diabetes is a unique myopathic state that appears to be independent of macrovascular/microvascular disease and contributes significantly to CVD morbidity and mortality in diabetic patients, especially those with coexistent hypertension. This update reviews the current knowledge regarding these risk factors and their treatment, with special emphasis on the cardiometabolic syndrome, hypertension, microalbuminuria, and diabetic cardiomyopathy. This update also examines the role of the renin-angiotensin system in the increased risk for CVD in diabetic patients and the impact of interrupting this system on the development of clinical diabetes as well as CVD.
Key Words: diabetes cardiovascular diseases hypertension, essential blood pressure
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J. F. Kincer, A. Uittenbogaard, J. Dressman, T. M. Guerin, M. Febbraio, L. Guo, and E. J. Smart Hypercholesterolemia Promotes a CD36-dependent and Endothelial Nitric-oxide Synthase-mediated Vascular Dysfunction J. Biol. Chem., June 21, 2002; 277(26): 23525 - 23533. [Abstract] [Full Text] [PDF] |
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J. R. Sowers Hypertension, Angiotensin II, and Oxidative Stress N. Engl. J. Med., June 20, 2002; 346(25): 1999 - 2001. [Full Text] [PDF] |
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J. A. Beckman, M. A. Creager, and P. Libby Diabetes and Atherosclerosis: Epidemiology, Pathophysiology, and Management JAMA, May 15, 2002; 287(19): 2570 - 2581. [Abstract] [Full Text] [PDF] |
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M. GLICK Screening for traditional risk factors for cardiovascular disease: A review for oral health care providers J Am Dent Assoc, March 1, 2002; 133(3): 291 - 300. [Abstract] [Full Text] [PDF] |
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E. D. Motley, S. M. Kabir, C. D. Gardner, K. Eguchi, G. D. Frank, T. Kuroki, M. Ohba, T. Yamakawa, and S. Eguchi Lysophosphatidylcholine Inhibits Insulin-Induced Akt Activation Through Protein Kinase C-{alpha} in Vascular Smooth Muscle Cells Hypertension, February 1, 2002; 39(2): 508 - 512. [Abstract] [Full Text] [PDF] |
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E. Nicolaides and C. J. Jones Review: Type 2 diabetes -- implications for macrovascular mechanics and disease The British Journal of Diabetes & Vascular Disease, January 1, 2002; 2(1): 9 - 12. [Abstract] [PDF] |
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W. A. Hsueh and R. E. Law PPAR{gamma} and Atherosclerosis: Effects on Cell Growth and Movement Arterioscler Thromb Vasc Biol, December 1, 2001; 21(12): 1891 - 1895. [Abstract] [Full Text] [PDF] |
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E. D. Frohlich Local Hemodynamic Changes in Hypertension: Insights for Therapeutic Preservation of Target Organs Hypertension, December 1, 2001; 38(6): 1388 - 1394. [Abstract] [Full Text] [PDF] |
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F. H. Messerli, E. Grossman, and J. R. Sowers Diabetes, Hypertension, and Cardiovascular Disease: An Update Response Hypertension, September 1, 2001; 38 (3): e11 - e11. [Full Text] [PDF] |
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