The Effect of Moxonidine on Endothelial Dysfunction in Metabolic Syndrome
- First Online:
- 28 Downloads
Endothelial dysfunction has been reported in patients with type 2 diabetes mellitus and even in healthy obese individuals with a normal metabolic profile. Sympathetic activity commonly is increased in obese hypertensive patients, and moxonidine is effective in lowering BP and improving insulin sensitivity.
To evaluate the effect of moxonidine on endothelial dysfunction in patients with metabolic syndrome.
Twenty-six patients with mild hypertension were treated with moxonidine and a hypocaloric diet for 3 months, while a second normotensive group (n = 26) were followed-up with calorie restriction alone. Anthropometric (body mass index, waist and hip circumferences, and waist-to-hip ratio) and metabolic features (fasting plasma glucose and insulin, aminotransferases, γ-glutamyl transpeptidase, triglycerides, and cholesterol levels) and flow-mediated dilatation (FMD) were evaluated. Insulin resistance was calculated by using the homeostasis model assessment formula. Insulin sensitivity was calculated according to the quantitative insulin-sensitivity check index (QUICKI).
SBP and DBP (both p < 0.001) and waist circumference (p = 0.02) were higher, and QUICKI (p = 0.043) and FMD (p = 0.01) were lower in the hypertensive group at baseline. After 3 months, nearly all the study parameters improved in both treatment groups. The decrease in BP, increase in FMD, and improvements in metabolic and anthropometric parameters were significantly greater in the moxonidine-treated group than in those treated with diet alone.
Moxonidine is proposed as a valuable option for treating mild-to-moderate hypertension in obese and insulin-resistant patients with metabolic syndrome as it appears to improve endothelial dysfunction in these patients.
- 2.Executive summary of the third report of the national cholesterol education program (NCEP) expert panel on detection, evaluation and treatment of high blood cholesterol in adults (Adults Treatment Panel III). JAMA 2001; 285: 2486–97Google Scholar
- 6.Nesto RW. The relation of insulin resistance syndromes to risk of cardiovascular disease. Rev Cardiovasc Med 2003; 4(6): 11–8Google Scholar
- 11.Cersosimo E, Defronzo RA. Insulin resistance and endothelial dysfunction: the road map to cardiovascular diseases. Diabetes Metab Res Rev. Epub 2006 Feb 28Google Scholar
- 16.Lithell O. Insulin resistance and diabetes in the context of treatment of hypertension. Blood Press 1998; Suppl. 3: 28–31Google Scholar
- 17.Haenni A, Lithell H. Moxonidine improves insulin sensitivity in insulin-resistant hypertensives. J Hypertens Suppl 1999; 17: 29–35Google Scholar
- 23.Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetes 1985; 28: 412–9Google Scholar
- 26.Corretti MC, Anderson TJ, Benjamin EJ, et al. International Brachial Artery Reactivity Task Force. Guidelines for the ultrasound assessment of endothelialdependent flow-mediated vasodilation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force. J Am Coll Cardiol 2002; 39: 257–65PubMedCrossRefGoogle Scholar
- 31.Abellan J, Leal M, Hernandez-Menarguez F, et al. Efficacy of moxonidine in the treatment of hypertension in obese, noncontrolled hypertensive patients. Kidney Int Suppl 2005; (93): 20-Google Scholar
- 36.International Diabetes Federation. The IDF consensus worldwide definition of the metabolic syndrome. April 14, 2005 [online]. Available from URL: http://www.idf.org/webdata/docs/Metac_syndrome_def.pdf [Accessed 2005 Jun 10]