Skip to main content
Download PDF
Download ePub

Blood pressure control and components of the metabolic syndrome: the GOOD survey

Cardiovascular Diabetology volume 8, Article number: 51 (2009) Cite this article

Abstract

Background

The GOOD (Global Cardiometabolic Risk Profile in Patients with Hypertension Disease) survey showed that blood pressure control was significantly worse in hypertensive patients with metabolic syndrome and/or diabetes mellitus than in those with essential hypertension only. This analysis aimed to investigate which components of the metabolic syndrome are primarily associated with poor blood pressure control.

Methods

The GOOD survey was designed as an observational cross-sectional survey in 12 European countries to assess the cardiometabolic risk profile in patients with essential hypertension. Investigators were randomly selected from a list of general practitioners (70% of investigators) and a list of specialists such as internists, cardiologists and hypertension specialists (30% of investigators). Data from 3,280 outpatients with hypertension, aged at least 30 years who were receiving antihypertensive treatment or had newly diagnosed hypertension according to the European Society of Hypertension and the European Society of Cardiology criteria, were included in the analyses. Blood pressure control, body mass index (BMI), waist circumference, serum triglycerides, total and high density lipoprotein (HDL) cholesterol measurements were compared in patients with diabetes mellitus and metabolic syndrome, with diabetes mellitus only, with metabolic syndrome only, and with neither metabolic syndrome nor diabetes mellitus.

Results

The highest blood pressure values were found in patients with metabolic syndrome with or without diabetes mellitus. Blood pressure was significantly lower in patients with diabetes mellitus only. The highest BMI, waist circumference and serum triglycerides, and the lowest HDL cholesterol levels among the groups studied occurred in patients with metabolic syndrome, either with or without diabetes mellitus.

Conclusion

Among the components of the metabolic syndrome, it is not impaired glucose tolerance which is associated with the poor response to antihypertensive treatment. Instead, visceral obesity and dyslipidemia components of the metabolic syndrome, i.e. hypertriglyceridemia and low HDL cholesterol levels, are associated with resistance to antihypertensive treatment.

Background

In a previous paper, in which the principal results of the Global Cardiometabolic Risk Profile in Patients with Hypertension Disease (GOOD) survey were reported, the main finding was that blood pressure control was significantly worse in hypertensive patients with diabetes mellitus and/or metabolic syndrome [1]. The prevalence of metabolic syndrome and type 2 diabetes was significantly higher in patients with uncontrolled blood pressure compared with those with controlled blood pressure. Ninety five percent of patients with both metabolic syndrome and type 2 diabetes had uncontrolled blood pressure. Diabetes mellitus and metabolic syndrome present with partly overlapping features. Of note, patients with metabolic syndrome without diabetes mellitus were associated with a similarly poor blood pressure control as those with diabetes mellitus. The components of the metabolic syndrome, besides hypertension, are impaired glucose tolerance, dyslipidemia and obesity, especially central obesity, as measured by waist circumference. Therefore, in view of the principal results of the GOOD survey, we aimed to investigate which components of the metabolic syndrome are primarily associated with poor blood pressure control.

Methods

The GOOD survey was designed as an observational cross-sectional survey in 12 European countries to assess the cardiometabolic risk profile in patients with essential hypertension [1]. The study was conducted in Belgium, Germany, Hungary, Italy, the Netherlands, Norway, Portugal, Slovenia, Spain, Sweden, Turkey and the United Kingdom between 6 October, 2006 and 16 May, 2007. Investigators were randomly selected from a list of general practitioners (70% of investigators) and a list of specialists such as internists, cardiologists and hypertension specialists (30% of investigators). The lists contained 3- to 10-fold the number of investigators needed.

The first patient to be seen by physicians each working day who fulfilled the inclusion criteria were asked to participate. In the case of decline the next patient was asked to participate. Maximally two patients per day were recruited. Further details of the selection procedure have been published earlier [1].

Patients included in the survey were outpatients with hypertension, aged at least 30 years, who were receiving antihypertensive treatment or had newly diagnosed hypertension according to the European Society of Hypertension and European Society of Cardiology (ESH/ESC) criteria [2, 3], which was confirmed on the day of inclusion in the study.

Exclusion criteria were pregnancy, menstruation, hospitalization, secondary hypertension, fever, known renal disease (serum creatinine > 177 μmol/l) and current drug treatment and/or concomitant conditions that could affect microalbuminuria measurements.

Data collection

The following data were collected during the patients' visits: weight, height, waist circumference, seated blood pressure (two measurements taken after at least 3 minutes' rest), heart rate at rest, urinary albumin excretion, cardiometabolic risk factors, including duration of hypertension, history of diabetes, cardiovascular disease or stroke, lifestyle factors including alcohol consumption, physical exercise and smoking habits, and laboratory measurements of fasting blood glucose, fasting lipid profile and serum creatinine. Furthermore, data on current antihypertensive medications, other cardiovascular, antithrombotic, lipid, glucose and uric acid-lowering drugs were collected. Patients with incomplete records were not excluded. Metabolic syndrome was diagnosed according to the National Cholesterol Education Program Adult Treatment Panel III (ATP III) criteria [4], i.e. at least three of the following had to be present: blood pressure ≥ 130/85 mmHg; waist circumference ≥ 102 cm (men) or ≥ 88 cm (women); triglycerides ≥ 1.69 mmol/l or on drug treatment for elevated triglycerides; HDL cholesterol < 1.03 mmol/l (men) or < 1.29 mmol/l (women) or on drug treatment for reduced HDL cholesterol; fasting glucose ≥ 5.55 mmol/l or on drug treatment for elevated glucose. In this study, history or treatment of hypertension were not counted as criteria for metabolic syndrome as they applied to all patients.

The study was conducted in accordance with the principles laid down by the 18th World Medical Assembly (Helsinki, 1964) and all subsequent amendments. The study was also conducted in accordance with the European guidelines for Good Epidemiology Practice (GEP), and Proper Conduct in Epidemiologic Research (European Federation, IEA and "societies", 2004). Each participating country ensured that all necessary regulatory submissions (e.g., IRB/IEC) were performed in accordance with local regulations including local data protection regulations.

Statistics

Among the hypertensive patients studied, four groups were compared: patients with metabolic syndrome and diabetes mellitus, with metabolic syndrome but no diabetes mellitus, with diabetes mellitus but no metabolic syndrome, and with neither diabetes mellitus nor metabolic syndrome. The haemodynamic, clinical and metabolic parameters were tested for significance using analysis of variance with Tukey's test as a post-hoc test.

Results

In total, 3,464 outpatients were recruited in the survey and of these 3,280 were included in these analyses. The regional distribution of the patients has been described earlier [2]. Figure 1 and Table 1 show systolic blood pressure in hypertensive patients with metabolic syndrome (n = 1033), with diabetes mellitus (n = 206), with both (n = 864), and with none of these (n = 1177). Systolic blood pressure was highest in patients with metabolic syndrome with or without diabetes mellitus. Furthermore, systolic blood pressure was significantly higher in patients with metabolic syndrome only, than in patients with diabetes mellitus only.

Figure 1
figure 1

Systolic blood pressure (mean ± SD) in patients with metabolic syndrome, but no diabetes mellitus (MS ∅DM), with metabolic syndrome and diabetes mellitus (MS+DM), with neither metabolic syndrome nor diabetes mellitus (∅MS ∅DM), and with diabetes mellitus only (∅MS DM); *** p < 0.001.

Full size image
Table 1 Systolic and diastolic blood pressure (P sys, P dia), body mass index (BMI), waist circumference and serum lipids (mean ± SD) in the different groups studied.
Full size table

Similar findings were obtained with diastolic blood pressure (Figure 2, Table 1). Diastolic blood pressure was significantly higher in patients with metabolic syndrome alone, than in those with only diabetes mellitus. Moreover, patients with metabolic syndrome only showed a higher diastolic blood pressure than those with metabolic syndrome and diabetes mellitus.

Figure 2
figure 2

Diastolic blood pressure (mean ± SD) in patients with metabolic syndrome, but no diabetes mellitus (MS ∅DM), with metabolic syndrome and diabetes mellitus (MS+DM), with neither metabolic syndrome nor diabetes mellitus (∅MS ∅DM), and with diabetes mellitus only (∅MS DM); *** p < 0.001.

Full size image

The number of different antihypertensive therapies the patients were receiving is shown in Table 2. The percentage of patients receiving 1, 2 or ≥3 different treatments was similar in those with metabolic syndrome alone and in those with diabetes alone, with 34.4% and 38.8%, respectively, receiving ≥3 treatments. More patients (48.4%) with metabolic syndrome and diabetes, and fewer (28.0%) with neither metabolic syndrome nor diabetes were receiving ≥3 treatments.

Table 2 Number of antihypertensive therapies received by patients according to the presence or absence of metabolic syndrome and diabetes.
Full size table

The next question to arise was which component of the metabolic syndrome, except blood glucose, may be associated with blood pressure. Figure 3 and Table 1 show body mass index (BMI) depending on the presence or absence of metabolic syndrome and diabetes mellitus. BMI was higher in patients with metabolic syndrome and diabetes than in those with metabolic syndrome alone. BMI in patients with metabolic syndrome only was significantly higher than in those with diabetes mellitus alone.

Figure 3
figure 3

BMI (mean ± SD) in patients with metabolic syndrome, but no diabetes mellitus (MS ∅DM), with metabolic syndrome and diabetes mellitus (MS+DM), with neither metabolic syndrome nor diabetes mellitus (∅MS ∅DM), and with diabetes mellitus only (∅MS DM); *** p < 0.001.

Full size image

Waist circumference was highest in patients with metabolic syndrome whether or not they had concomitant diabetes mellitus. Patients with diabetes mellitus alone showed significantly lower waist circumference than those with metabolic syndrome alone (Figure 4, Table 1).

Figure 4
figure 4

Waist circumference (mean ± SD) in patients with metabolic syndrome, but no diabetes mellitus (MS ∅DM), with metabolic syndrome and diabetes mellitus (MS+DM), with neither metabolic syndrome nor diabetes mellitus (∅MS ∅DM), and with diabetes mellitus only (∅MS DM); *** p < 0.001.

Full size image

Next, we examined the lipid parameters obtained for their association with diabetes mellitus and the metabolic syndrome. Figure 5 and Table 1 show serum triglycerides, total and HDL cholesterol levels depending on the presence or absence of metabolic syndrome and diabetes mellitus. Serum triglycerides were highest in patients with metabolic syndrome with diabetes mellitus. Patients with metabolic syndrome only, had significantly higher serum triglycerides than patients with diabetes mellitus only (Figure 5A, Table 1). Similarly, serum cholesterol was highest in patients with metabolic syndrome only, whereas patients with diabetes mellitus only, had the lowest serum cholesterol (Figure 5B, Table 1). Serum HDL cholesterol levels showed a pattern largely inverse to that of serum triglycerides, with the lowest levels in patients with metabolic syndrome, either with or without diabetes mellitus, which were significantly lower than in patients with diabetes mellitus but no metabolic syndrome (Figure 5C, Table 1). Thus, the lipid parameters studied showed a similar pattern to those of systolic and diastolic blood pressure among the four groups of patients.

Figure 5
figure 5

Serum lipids (mean ± SD; A: triglycerides, B: total cholesterol, C: HDL cholesterol) in patients with metabolic syndrome, but no diabetes mellitus (MS ∅DM), with metabolic syndrome and diabetes mellitus (MS+DM), with neither metabolic syndrome nor diabetes mellitus (∅MS ∅DM), and with diabetes mellitus only (∅MS DM); *** p < 0.001.

Full size image

Discussion

The findings show that blood pressure is influenced by the metabolic syndrome, irrespective of the presence or absence of diabetes mellitus. This finding was not a reflection of the antihypertensive treatments received by the patients, as those with metabolic syndrome alone and those with diabetes alone were receiving a similar number of treatments. Other factors may be more important for conferring resistance to antihypertensive treatment, since patients with diabetes mellitus alone, without accompanying metabolic syndrome, showed much lower blood pressure than patients with metabolic syndrome with or without diabetes mellitus. In addition, resistance to antihypertensive treatment may also reflect some doubts about target blood pressure values and low physician compliance in prescribing further therapy for patients with metabolic syndrome[1].

As disturbed glucose metabolism is present in both metabolic syndrome and diabetes mellitus, other factors of the metabolic syndrome are likely to be responsible for the tendency towards higher blood pressure in patients with metabolic syndrome. Indeed, when we evaluated the other components of the metabolic syndrome with respect to their impact on blood pressure, it was BMI and waist circumference which showed the closest association with blood pressure, both systolic and diastolic. On the other hand, the presence or absence of diabetes mellitus was not a major determinant of blood pressure. The above analyses were based on blood pressure values instead of blood pressure control rates. This seemed appropriate since blood pressure control rates were much lower in patients with diabetes mellitus than in patients with metabolic syndrome due to the fact that in patients with metabolic syndrome without diabetes mellitus the blood pressure target was < 140/90 mm Hg, but in patients with diabetes mellitus with or without metabolic syndrome the blood pressure target was < 130/80 mm Hg. Due to the different blood pressure targets, blood pressure control rates differed markedly depending on the presence or absence of diabetes mellitus.

These findings suggest that among the components of the metabolic syndrome, it is central obesity which affects blood pressure most. These findings are in line with the newer concepts on the pathophysiology of hypertension. The role of adipocytokines in the pathogenesis of hypertension has been of increasing interest in the last decade, and has markedly extended our view on the humoral mechanisms of hypertension [3–6]. Among the adipocytokines involved in the pathogenesis of hypertension, adiponectin and leptin have been most extensively studied. Recently, in a 5-year prospective study, serum adiponectin levels have been shown to be independent predictors of incident hypertension in a population normotensive at baseline [7].

Adiponectin, besides its effects on insulin sensitivity, may also act on the vasculature directly. Hypoadiponectinemia was found to be associated with an impaired endothelium-dependent vasodilation in humans and mice [8–10]. Conversely, adiponectin is a stimulator of nitric oxide (NO) production in endothelial cells [11, 12]. In addition to adiponectin, other adipocytokines, such as leptin, have also been linked with the development of hypertension. Leptin increases peripheral sympathetic tone, and leptin-deficient mice show lower arterial blood pressure [13, 14]. Among the many known adipocytokines, angiotensinogen has been found to be produced by adipocytes, and angiotensinogen can promote the development of hypertension by stimulating the production of angiotensin II [15, 16].

There is also ample epidemiological evidence that obesity is one of the major causes of essential hypertension. Excess weight gain has been repeatedly shown to be one of the best predictors for the development of hypertension [17–19]. Moreover, from the Framingham Heart study it has been estimated that about 65% to 75% of the risk for hypertension can be attributed to excess weight [20].

Recent results from the National Health and Nutrition Examination Survey (NHANES) support the eminent role of obesity in the development of hypertension [21]: between NHANES II (1988-1994) and NHANES 1999-2004, the age-standardized hypertension prevalence increased from 24.4% to 28.9%. Depending on gender and ethnicity, between 20% and 80% of this increase could be attributed to increasing BMI. Although the authors did not report control rates depending on BMI, blood pressure distribution within the population was shifted towards higher values with increasing BMI.

The relative contributions of subcutaneous and visceral fat to the development of hypertension have been elucidated in further studies. It is visceral fat which has been identified as the more prominent factor inducing hypertension [22]: quantification of adipose tissue in different locations by computer tomography revealed that, in a group of 300 Japanese Americans, the amount of visceral fat, but not subcutaneous fat, conferred a risk of incident hypertension during the follow-up of up to 11 years.

Blood pressure is also associated with humoral components of the metabolic syndrome. Low HDL levels are known to confer an increased cardiovascular risk. Moreover, a direct association between low serum HDL levels and blood pressure has been shown in elderly hypertensive patients [23]. The mechanistic background of this association may be that HDL contains important lipid mediators such as sphingosine-1-phosphate, sphingosylphosphorylcholine, and lysosulphatide which induce NO-dependent vasorelaxation via the lysophospholipid receptor S1P3 [24]. Thereby HDL restores endothelial function by improving NO availability and hence favours vasorelaxation.

As in the present survey we studied patients receiving antihypertensive treatment, the results do not imply a higher prevalence of hypertension with increasing BMI, but show less effective blood pressure control in obese patients. This finding infers that in obesity-related hypertension other pathogenetic mechanisms may be involved than occur in other forms of essential hypertension.

The data in this survey show that metabolic syndrome is not only associated with higher blood pressure but also with the poor response to treatment. Interestingly, among the components of the metabolic syndrome, it is not impaired glucose tolerance which is associated with the response to antihypertensive treatment. Instead, both visceral obesity and the dyslipidemia of the metabolic syndrome, i.e. hypertriglyceridemia and low HDL cholesterol levels, are associated with resistance to antihypertensive treatment.

There have been few studies addressing the relative contributions of single components of the metabolic syndrome to the development of hypertension and vascular disease [25]. The GOOD registry offers an appropriate database to answer these questions. Earlier publications of the GOOD data focused on the control of blood pressure depending on the co-occurrence of the metabolic syndrome [1] and on regional differences in blood pressure control [2]. The DIG study addressed a similar question as the present study; Hanefeld et al. [26] studied the relative contributions of the different components of the metabolic syndrome to the development of atherosclerotic vascular disease. In contrast to the present study, the DIG study did not assess the impact of the components of the metabolic syndrome on the development of hypertension. Similarly to the present study, diabetes mellitus alone did not contribute significantly to the development of atherosclerotic vascular disease, whereas the combination of diabetes mellitus with hypertension and dyslipidemia was closely associated with vascular disease.

Conclusion

Among the components of the metabolic syndrome, impaired glucose tolerance is not associated with the poor response to antihypertensive treatment. Instead, other components of the metabolic syndrome, viz. visceral obesity and dyslipidemia, hypertriglyceridemia and low HDL cholesterol levels, are associated with resistance to antihypertensive treatment.

References

  1. Kjeldsen SE, Naditch-Brule L, Perlini S, Zidek W, Farsang C: Increased prevalence of metabolic syndrome in uncontrolled hypertension across Europe: the Global Cardiometabolic Risk Profile in Patients with hypertension disease survey. J Hypertens. 2008, 26: 2064-2070. 10.1097/HJH.0b013e32830c45c3.

    CAS  Article  PubMed  Google Scholar 

  2. Farsang C, Naditch-Brule L, Perlini S, Zidek W, Kjeldsen SE: Inter-regional comparisons of the prevalence of cardiometabolic risk factors in patients with hypertension in Europe: the GOOD survey. J Hum Hypertens. 2009, 23: 316-324. 10.1038/jhh.2008.136.

    CAS  Article  PubMed  Google Scholar 

  3. Ritchie SA, Ewart MA, Perry CG, Connell JM, Salt IP: The role of insulin and the adipocytokines in regulation of vascular endothelial function. Clin Sci (Lond). 2004, 107: 519-532.

    CAS  Article  Google Scholar 

  4. Aldhahi W, Hamdy O: Adipokines, inflammation, and the endothelium in diabetes. Curr Diab Rep. 2003, 3: 293-298. 10.1007/s11892-003-0020-2.

    Article  PubMed  Google Scholar 

  5. Guerre-Millo M: Adipose tissue and adipokines: for better or worse. Diabetes Metab. 2004, 30: 13-19. 10.1016/S1262-3636(07)70084-8.

    CAS  Article  PubMed  Google Scholar 

  6. Lau DC, Dhillon B, Yan H, Szmitko PE, Verma S: Adipokines: molecular links between obesity and atheroslcerosis. Am J Physiol Heart Circ Physiol. 2005, 288: H2031-2041. 10.1152/ajpheart.01058.2004.

    CAS  Article  PubMed  Google Scholar 

  7. Chow WS, Cheung BM, Tso AW, Xu A, Wat NM, Fong CH, Ong LH, Tam S, Tan KC, Janus ED: Hypoadiponectinemia as a predictor for the development of hypertension: a 5-year prospective study. Hypertension. 2007, 49: 1455-1461. 10.1161/HYPERTENSIONAHA.107.086835.

    CAS  Article  PubMed  Google Scholar 

  8. Ouchi N, Ohishi M, Kihara S, Funahashi T, Nakamura T, Nagaretani H, Kumada M, Ohashi K, Okamoto Y, Nishizawa H: Association of hypoadiponectinemia with impaired vasoreactivity. Hypertension. 2003, 42: 231-234. 10.1161/01.HYP.0000083488.67550.B8.

    CAS  Article  PubMed  Google Scholar 

  9. Ouedraogo R, Gong Y, Berzins B, Wu X, Mahadev K, Hough K, Chan L, Goldstein BJ, Scalia R: Adiponectin deficiency increases leukocyte-endothelium interactions via upregulation of endothelial cell adhesion molecules in vivo. J Clin Invest. 2007, 117: 1718-1726. 10.1172/JCI29623.

    PubMed Central  CAS  Article  PubMed  Google Scholar 

  10. Tan KC, Xu A, Chow WS, Lam MC, Ai VH, Tam SC, Lam KS: Hypoadiponectinemia is associated with impaired endothelium-dependent vasodilation. J Clin Endocrinol Metab. 2004, 89: 765-769. 10.1210/jc.2003-031012.

    CAS  Article  PubMed  Google Scholar 

  11. Hattori Y, Hattori S, Akimoto K, Nishikimi T, Suzuki K, Matsuoka H, Kasai K: Globular adiponectin activates nuclear factor-kappaB and activating protein-1 and enhances angiotensin II-induced proliferation in cardiac fibroblasts. Diabetes. 2007, 56: 804-808. 10.2337/db06-1405.

    CAS  Article  PubMed  Google Scholar 

  12. Chen H, Montagnani M, Funahashi T, Shimomura I, Quon MJ: Adiponectin stimulates production of nitric oxide in vascular endothelial cells. J Biol Chem. 2003, 278: 45021-45026. 10.1074/jbc.M307878200.

    CAS  Article  PubMed  Google Scholar 

  13. Quehenberger P, Exner M, Sunder-Plassmann R, Ruzicka K, Bieglmayer C, Endler G, Muellner C, Speiser W, Wagner O: Leptin induces endothelin-1 in endothelial cells in vitro. Circ Res. 2002, 90: 711-718. 10.1161/01.RES.0000014226.74709.90.

    CAS  Article  PubMed  Google Scholar 

  14. Bouloumie A, Marumo T, Lafontan M, Busse R: Leptin induces oxidative stress in human endothelial cells. FASEB J. 1999, 13: 1231-1238.

    CAS  PubMed  Google Scholar 

  15. Esposito K, Pontillo A, Di Palo C, Giugliano G, Masella M, Marfella R, Giugliano D: Effect of weight loss and lifestyle changes on vascular inflammatory markers in obese women: a randomized trial. JAMA. 2003, 289: 1799-1804. 10.1001/jama.289.14.1799.

    CAS  Article  PubMed  Google Scholar 

  16. Ahima RS, Flier JS: Adipose tissue as an endocrine organ. Trends Endocrinol Metab. 2000, 11: 327-332. 10.1016/S1043-2760(00)00301-5.

    CAS  Article  PubMed  Google Scholar 

  17. Jones DW, Kim JS, Andrew ME, Kim SJ, Hong YP: Body mass index and blood pressure in Korean men and women: the Korean National Blood Pressure Survey. J Hypertens. 1994, 12: 1433-1437. 10.1097/00004872-199412000-00018.

    CAS  Article  PubMed  Google Scholar 

  18. Hall JE, Hildebrandt DA, Kuo J: Obesity hypertension: role of leptin and sympathetic nervous system. Am J Hypertens. 2001, 14: 103S-115S. 10.1016/S0895-7061(01)02077-5.

    CAS  Article  PubMed  Google Scholar 

  19. Hall JE, Crook ED, Jones DW, Wofford MR, Dubbert PM: Mechanisms of obesity-associated cardiovascular and renal disease. Am J Med Sci. 2002, 324: 127-137. 10.1097/00000441-200209000-00003.

    Article  PubMed  Google Scholar 

  20. Garrison RJ, Kannel WB, Stokes J, Castelli WP: Incidence and precursors of hypertension in young adults: the Framingham Offspring Study. Prev Med. 1987, 16: 235-251. 10.1016/0091-7435(87)90087-9.

    CAS  Article  PubMed  Google Scholar 

  21. Cutler JA, Sorlie PD, Wolz M, Thom T, Fields LE, Roccella EJ: Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between 1988-1994 and 1999-2004. Hypertension. 2008, 52: 818-827. 10.1161/HYPERTENSIONAHA.108.113357.

    CAS  Article  PubMed  Google Scholar 

  22. Hayashi T, Boyko EJ, Leonetti DL, McNeely MJ, Newell-Morris L, Kahn SE, Fujimoto WY: Visceral adiposity is an independent predictor of incident hypertension in Japanese Americans. Ann Intern Med. 2004, 140: 992-1000.

    Article  PubMed  Google Scholar 

  23. Wildman RP, Sutton-Tyrrell K, Newman AB, Bostom A, Brockwell S, Kuller LH: Lipoprotein levels are associated with incident hypertension in older adults. J Am Geriatr Soc. 2004, 52: 916-921. 10.1111/j.1532-5415.2004.52258.x.

    Article  PubMed  Google Scholar 

  24. Nofer JR, Giet van der M, Tolle M, Wolinska I, von Wnuck Lipinski K, Baba HA, Tietge UJ, Godecke A, Ishii I, Kleuser B: HDL induces NO-dependent vasorelaxation via the lysophospholipid receptor S1P3. J Clin Invest. 2004, 113: 569-581.

    PubMed Central  CAS  Article  PubMed  Google Scholar 

  25. Redon J, Cifkova R, Laurent S, Nilsson P, Narkiewicz K, Erdine S, Mancia G: The metabolic syndrome in hypertension: European society of hypertension position statement. J Hypertens. 2008, 26: 1891-1900. 10.1097/HJH.0b013e328302ca38.

    CAS  Article  PubMed  Google Scholar 

  26. Hanefeld M, Koehler C, Gallo S, Benke I, Ott P: Impact of the individual components of the metabolic syndrome and their different combinations on the prevalence of atherosclerotic vascular disease in type 2 diabetes: the Diabetes in Germany (DIG) study. Cardiovasc Diabetol. 2007, 6: 13-10.1186/1475-2840-6-13.

    PubMed Central  Article  PubMed  Google Scholar 

Download references

Acknowledgements

We acknowledge the contribution of the members of the Global CardiOMetabOlic Risk Profile in Patients with Hypertension Disease (GOOD) Scientific Council and the Study Investigators to this study. The study was sponsored by Bristol-Myers Squibb and Sanofi-Aventis. Editorial support for this article was provided by Bristol-Myers Squibb and Sanofi-Aventis.

Author information

Authors and Affiliations

  1. Medizinische Klinik IV (Endocrinology and Nephrology), Charité, Berlin, Germany

    Walter Zidek

  2. Sanofi Aventis, Paris, France

    Lisa Naditch-Brûlé

  3. Department of Internal Medicine, Fondazione IRCCS San Matteo, Università di Pavia, Pavia, Italy

    Stefano Perlini

  4. The Cardiometabolic Centre, St Imre Hospital, Budapest, Hungary

    Csaba Farsang

  5. Department of Cardiology, Ullevaal Hospital, Norway

    Sverre E Kjeldsen

Authors
  1. Walter Zidek
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Lisa Naditch-Brûlé
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Stefano Perlini
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Csaba Farsang
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Sverre E Kjeldsen
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Walter Zidek.

Additional information

Competing interests

Dr Naditch-Brûlé declares to be an employee of Sanofi-Aventis. All other authors have attended advisory boards and have held lectures for a number of pharmaceutical companies including the sponsor.

Authors' contributions

WZ prepared the manuscript, LN-B provided statistical expertise, SP created the database, CF developed the hypotheses tested, SEK significantly contributed to the design of the GOOD trial. All authors read and approved the final manuscript.

Authors’ original submitted files for images

Rights and permissions

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and Permissions

About this article

Cite this article

Zidek, W., Naditch-Brûlé, L., Perlini, S. et al. Blood pressure control and components of the metabolic syndrome: the GOOD survey. Cardiovasc Diabetol 8, 51 (2009). https://doi.org/10.1186/1475-2840-8-51

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/1475-2840-8-51

Keywords

  • Metabolic Syndrome
  • Waist Circumference
  • Blood Pressure Control
  • Antihypertensive Treatment
  • Blood Pressure Target

Comments

Cardiovascular Diabetology

ISSN: 1475-2840