Diabetes mellitus and obesity are both related to the risk of cardiovascular disease and sudden death. In hypertensive guidelines, diabetes and obesity, especially abdominal obesity, are regarded as high-risk factors. Ambulatory blood pressure monitoring (ABPM) is an established method for the management of hypertension. However, ABPM is not a standard tool for the management of hypertension in diabetes and obesity. In this paper, recent data on the use of ABPM in diabetes and obesity will be discussed. In patients with diabetes, the ambulatory BP level has been shown to be better than clinic BP in predicting cardiovascular events. A riser pattern has been associated with increased risk of cardiovascular disease. White-coat hypertension and masked hypertension in diabetics constitute a moderate risk. A nondipping pattern is very common in obese hypertensive patients. In this paper, we will summarize the findings on the use of ABPM in patients with diabetes and obesity. 1. Introduction There have been increasing numbers of diabetic and obese patients in recent years. Hypertension coexisting with diabetes and obesity has a major impact on cardiovascular prognosis. Patients with diabetes and obesity usually have other risk factors, such as dyslipidemia, sleep apnea syndrome, and metabolic syndrome. Strict control of BP has been recommended in these patients. The ACCORD trial proved that aggressive BP control has no such benefit on cardiovascular prognosis in patients with diabetes [1], but a new target level of BP in diabetes has not yet been established in response to these findings. Therefore, individualized control of BP is becoming more important in this post-ACCORD era. In this paper, we summarized the data on ABPM in diabetes and obesity. 2. Ambulatory Blood Pressure Monitoring in Diabetes Diabetes itself is classified as a high-risk factor for cardiovascular disease, and when hypertension coexists with diabetes, not only is the cardiovascular risk magnified, but cardiovascular target organ damages such as silent cerebral infarcts (SCIs) and left ventricular hypertrophy (LVH) may progress. This is why the target level of blood pressure in diabetes is set as low as 130/80?mmHg. In a seminal paper by de la Sierra et al. based on findings from 42,947 patients included in the Spanish Society of Hypertension, ABPM registry has shown that diabetes was associated with nondipping status [2]. In clinical practice, it is sometimes very hard to identify the true blood pressure level when the BP variability is very large. In such cases, 24-hour BP monitoring
References
[1]
W. C. Cushman, G. W. Evans, R. P. Byington et al., “Effects of intensive blood-pressure control in type 2 diabetes mellitus,” The New England Journal of Medicine, vol. 362, no. 17, pp. 1575–1585, 2010.
[2]
A. de la Sierra, J. Redon, J. R. Banegas et al., “Prevalence and factors associated with circadian blood pressure patterns in hypertensive patients,” Hypertension, vol. 53, no. 3, pp. 466–472, 2009.
[3]
P. Home, “Global guideline for type 2 diabetes: recommendations for standard, comprehensive, and minimal care,” Diabetic Medicine, vol. 23, no. 6, pp. 579–593, 2006.
[4]
T. Ogihara, K. Kikuchi, H. Matsuoka et al., “The Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2009),” Hypertension Research, vol. 32, no. 1, pp. 3–107, 2009.
[5]
American Diabetes Association, “Diagnosis and classification of diabetes mellitus,” Diabetes Care, vol. 34, supplement 1, pp. S62–S69, 2010.
[6]
S. Lehto, T. R?nnemaa, K. Py?r?l?, and M. Laakso, “Predictors of stroke in middle-aged patients with non-insulin-dependent diabetes,” Stroke, vol. 27, no. 1, pp. 63–68, 1996.
[7]
R. Turner, R. Holman, I. Stratton et al., “Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38,” British Medical Journal, vol. 317, no. 7160, pp. 703–713, 1998.
[8]
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.
[9]
K. Eguchi, J. Ishikawa, S. Hoshide, S. Ishikawa, K. Shimada, and K. Kario, “Impact of blood pressure vs. glycemic factors on target organ damage in patients with type 2 diabetes mellitus,” Journal of Clinical Hypertension, vol. 8, no. 6, pp. 404–410, 2006.
[10]
K. Eguchi, T. G. Pickering, S. Hoshide et al., “Ambulatory blood pressure is a better marker than clinic blood pressure in predicting cardiovascular events in patients with/without type 2 diabetes,” American Journal of Hypertension, vol. 21, no. 4, pp. 443–450, 2008.
[11]
S. Nakano, K. Konishi, K. Furuya et al., “A prognostic role of mean 24-h pulse pressure level for cardiovascular events in type 2 diabetic subjects under 60 years of age,” Diabetes Care, vol. 28, no. 1, pp. 95–100, 2005.
[12]
K. Eguchi, J. Ishikawa, S. Hoshide, T. G. Pickering, K. Shimada, and K. Kario, “Masked hypertension in diabetes mellitus: a potential risk,” Journal of Clinical Hypertension, vol. 9, no. 8, pp. 601–607, 2007.
[13]
K. Eguchi, T. G. Pickering, and K. Kario, “Why is blood pressure so hard to control in patients with type 2 diabetes?” Journal of the Cardiometabolic Syndrome, vol. 2, no. 2, pp. 114–118, 2007.
[14]
C. Cuspidi, S. Meani, L. Lonati et al., “Short-term reproducibility of a non-dipping pattern in type 2 diabetic hypertensive patients,” Journal of Hypertension, vol. 24, no. 4, pp. 647–653, 2006.
[15]
S. Nakano, M. Fukuda, F. Hotta et al., “Reversed circadian blood pressure rhythm is associated with occurrences of both fatal and nonfatal vascular events in NIDDM subjects,” Diabetes, vol. 47, no. 9, pp. 1501–1506, 1998.
[16]
E. Lurbe, J. Redon, A. Kesani et al., “Increase in nocturnal blood pressure and progression to microalbuminuria in type 1 diabetes,” The New England Journal of Medicine, vol. 347, no. 11, pp. 797–805, 2002.
[17]
K. Kario, T. G. Pickering, T. Matsuo, S. Hoshide, J. E. Schwartz, and K. Shimada, “Stroke prognosis and abnormal nocturnal blood pressure falls in older hypertensives,” Hypertension, vol. 38, no. 4, pp. 852–857, 2001.
[18]
K. Eguchi, K. Kario, and K. Shimada, “Greater impact of coexistence of hypertension and diabetes on silent cerebral infarcts,” Stroke, vol. 34, no. 10, pp. 2471–2474, 2003.
[19]
K. Kario and T. G. Pickering, “White-coat hypertension or white-coat hypertension syndrome: which is accompanied by target organ damage?” Archives of Internal Medicine, vol. 160, no. 22, pp. 3497–3498, 2000.
[20]
K. Eguchi, S. Hoshide, J. Ishikawa et al., “Cardiovascular prognosis of sustained and white-coat hypertension in patients with type 2 diabetes mellitus,” Blood Pressure Monitoring, vol. 13, no. 1, pp. 15–20, 2008.
[21]
C. K. Kramer, C. B. Leit?o, L. H. Canani, and J. L. Gross, “Impact of white-coat hypertension on microvascular complications in type 2 diabetes,” Diabetes Care, vol. 31, no. 12, pp. 2233–2237, 2008.
[22]
C. B. Leit?o, L. H. Canani, C. K. Kramer, J. C. Boza, A. F. Pinotti, and J. L. Gross, “Masked hypertension, urinary albumin excretion rate, and echocardiographic parameters in putatively normotensive type 2 diabetic patients,” Diabetes Care, vol. 30, no. 5, pp. 1255–1260, 2007.
[23]
V. Kotsis, S. Stabouli, M. Bouldin, A. Low, S. Toumanidis, and N. Zakopoulos, “Impact of obesity on 24-hour ambulatory blood pressure and hypertension,” Hypertension, vol. 45, no. 4, pp. 602–607, 2005.
[24]
M. O. Hassan, D. Jaju, S. Albarwani et al., “Non-dipping blood pressure in the metabolic syndrome among Arabs of the Oman family study,” Obesity, vol. 15, no. 10, pp. 2445–2453, 2007.
[25]
E. J. Diamantopoulos, E. Andreadis, G. Tsourous et al., “Insulin resistance and blood pressure circadian variation in an obese hypertensive population,” Clinical and Experimental Hypertension, vol. 28, no. 7, pp. 625–630, 2006.
[26]
A. Kagan, H. Faibel, G. Ben-Arie, Z. Granevitze, and J. Rapoport, “Gender differences in ambulatory blood pressure monitoring profile in obese, overweight and normal subjects,” Journal of Human Hypertension, vol. 21, no. 2, pp. 128–134, 2007.
[27]
R. C. Hermida, L. Chayán, D. E. Ayala et al., “Association of metabolic syndrome and blood pressure nondipping profile in untreated hypertension,” American Journal of Hypertension, vol. 22, no. 3, pp. 307–313, 2009.
[28]
Z. Tartan, H. Uyarel, H. Kasikcioglu et al., “Metabolic syndrome as a predictor of non-dipping hypertension,” Tohoku Journal of Experimental Medicine, vol. 210, no. 1, pp. 57–66, 2006.
[29]
G. P. Vyssoulis, E. A. Karpanou, S. M. G. Kyvelou et al., “Nocturnal blood pressure fall and metabolic syndrome score in hypertensive patients,” Blood Pressure Monitoring, vol. 12, no. 6, pp. 351–356, 2007.
[30]
D. E. Ayala, R. C. Hermida, L. Chayán, A. Mojón, M. J. Fontao, and J. R. Fernández, “Circadian pattern of ambulatory blood pressure in untreated hypertensive tatients with and without metabolic syndrome,” Chronobiology International, vol. 26, no. 6, pp. 1189–1205, 2009.
[31]
O. Ukkola, R. L. Vasunta, and A. Y. Kes?niemi, “Non-dipping pattern in ambulatory blood pressure monitoring is associated with metabolic abnormalities in a random sample of middle-aged subjects,” Hypertension Research, vol. 32, no. 11, pp. 1022–1027, 2009.