Adipositas - Ursachen, Folgeerkrankungen, Therapie 2014; 08(02): 70-75
DOI: 10.1055/s-0037-1618845
Übersichtsarbeit
Schattauer GmbH

Adipositas-assoziierte Hypertonie

Obesity-associated hypertension
S. Engeli
1   Institut für Klinische Pharmakologie, Medizinische Hochschule Hannover
,
M. May
1   Institut für Klinische Pharmakologie, Medizinische Hochschule Hannover
,
J. Jordan
1   Institut für Klinische Pharmakologie, Medizinische Hochschule Hannover
› Institutsangaben
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Publikationsverlauf

Publikationsdatum:
21. Dezember 2017 (online)

Zusammenfassung

Hypertonie ist die häufigste Adipositas-assoziierte Erkrankung. Erhöhte Sympathikusaktivität, erhöhtes Blutvolumen und damit zusammenhängende hämodynamische Änderungen, renale Natriumretention, ein dennoch aktiviertes Renin-Angiotensin-Aldosteron-System und Mediatoren aus dem Fettgewebe tragen insgesamt zur Blutdruckerhöhung bei Adipositas bei. Eine Blutdruckreduktion durch Gewichtsreduktion ist möglich, aber schwer zu quantifizieren, da die vorliegenden Studien sehr heterogen sind. Dennoch ist Gewichtsreduktion sinnvoll, um das Erreichen der Zielblutdruckwerte zu unterstützen.

Im Rahmen der medikamentösen Therapie können außer den ACE-Hemmern oder AT1-Rezeptorblockern keine Medikamente bzw. Medikamentengruppen herausgehoben werden. Häufig ist ohnehin eine Kombinationstherapie notwendig bzw. Begleiterkrankungen diktieren die Substanzauswahl. Adipöse Patienten sind besonders häufig von therapieresistenter Hypertonie betroffen. Eine sorgfältige Blutdruckmessung zusammen mit der Suche nach Endorganschäden, metabolischen Störungen und Schlafapnoe helfen, die besonders gefährdeten Patienten zu identifizieren.

Summary

Hypertension is the most common obesityassociated disease. Increased sympathetic nervous system activity, increased blood volume and related hemodynamic changes, enhanced renal sodium reabsorption, increased activity of the Renin-Angiotensin-Aldosteron system, and mediators released from adipose tissue lead to rising blood pressure with obesity. Whereas weight reduction may decrease blood pressure, the relationship is difficult to quantify because clinical studies addressing the issue are rather heterogeneous. Nevertheless, blood pressure targets are more easily achieved with reduced body weight.

ACE inhibitors and AT1-receptor blockers stand out if pharmacological treatment is required, other antihypertensive drug classes do not provide specific advantages. However, combination therapy is often required and comorbidities influence the choice of antihypertensive treatment. Treatment-resistant hypertension is a common condition in obese patients. Thus, reliable blood pressure measurements and diagnosis of end-organ damage, metabolic changes and obstructive sleep will help identifying the patients at highest risk.

 
  • Literatur

  • 1 Effects of weight loss and sodium reduction intervention on blood pressure and hypertension incidence in overweight people with high-normal blood pressure. The Trials of Hypertension Prevention, phase II. The Trials of Hypertension Prevention Collaborative Research Group. Arch Intern Med 1997; 157: 657-667.
  • 2 Aburto NJ, Ziolkovska A, Hooper L. et al. Effect of lower sodium intake on health: systematic review and meta-analyses. BMJ 2013; 346: f1326.
  • 3 Aucott L, Poobalan A, Smith WC. et al. Effects of weight loss in overweight/obese individuals and long-term hypertension outcomes: a systematic review. Hypertension 2005; 45: 1035-1041.
  • 4 Bhatt DL, Kandzari DE, O’Neill WW. et al. A controlled trial of renal denervation for resistant hypertension. N Engl J Med 2014; 370: 1393-1401.
  • 5 Bisognano JD, Bakris G, Nadim MK. et al. Baroreflex activation therapy lowers blood pressure in patients with resistant hypertension: results from the double-blind, randomized, placebo-controlled rheos pivotal trial. J Am Coll Cardiol 2011; 58: 765-773.
  • 6 Bloch MJ, Viera AJ. Should patients with obesity and hypertension be treated differently from those who are not obese?. Curr Hypertens Rep 2014; 16: 418.
  • 7 Bramlage P, Pittrow D, Wittchen HU. et al. Hypertension in overweight and obese primary care patients is highly prevalent and poorly controlled. Am J Hypertens 2004; 17: 904-910.
  • 8 Doll S, Paccaud F, Bovet P. et al. Body mass index, abdominal adiposity and blood pressure: consistency of their association across developing and developed countries. Int J Obes Relat Metab Disord 2002; 26: 48-57.
  • 9 Egan BM, Zhao Y, Axon RN. et al. Uncontrolled and apparent treatment resistant hypertension in the United States, 1988 to 2008. Circulation 2011; 124: 1046-1058.
  • 10 Engeli S, Bohnke J, Gorzelniak K. et al. Weight loss and the renin-angiotensin-aldosterone system. Hypertension 2005; 45: 356-362.
  • 11 Engeli S, Jordan J. Novel metabolic drugs and blood pressure: implications for the treatment of obese hypertensive patients?. Curr Hypertens Rep 2013; 15: 470-474.
  • 12 Engeli S, Schling P, Gorzelniak K. et al. The adipose-tissue renin-angiotensin-aldosterone system: role in the metabolic syndrome?. Int J Biochem Cell Biol 2003; 35: 807-825.
  • 13 Fox CS, Massaro JM, Hoffmann U. et al. Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study. Circulation 2007; 116: 39-48.
  • 14 Grassi G, Seravalle G, Dell’Oro R. et al. Adrenergic and reflex abnormalities in obesity-related hypertension. Hypertension 2000; 36: 538-542.
  • 15 Hall JE. Hyperinsulinemia: A link between obesity and hypertension. Kidney Int 43: 1402-1417 1993
  • 16 Hall JE, Da Silva AA, do Carmo JM. et al. Obesityinduced hypertension: role of sympathetic nervous system, leptin, and melanocortins. J Biol Chem 2010; 285: 17271-17276.
  • 17 Hall JE, Henegar JR, Dwyer TM. et al. Is obesity a major cause of chronic kidney disease?. Adv Ren Replace Ther 2004; 11: 41-54.
  • 18 Haufe S, Utz W, Engeli S. et al. Left ventricular mass and function with reduced-fat or reducedcarbohydrate hypocaloric diets in overweight and obese subjects. Hypertension 2012; 59: 70-75.
  • 19 Hofso D, Nordstrand N, Johnson LK. et al. Obesity-related cardiovascular risk factors after weight loss: a clinical trial comparing gastric bypass surgery and intensive lifestyle intervention. Eur J Endocrinol 2010; 163: 735-745.
  • 20 Huang ZP, Willett WC, Manson JE. et al. Body weight, weight change, and risk for hypertension in women. Ann Intern Med 1988; 128: 81-88.
  • 21 Jordan J, Schlaich M, Redon J, Narkiewicz K, Luft FC, Grassi G, Dixon J, Lambert G, Engeli S. European Society of Hypertension Working Group on Obesity: obesity drugs and cardiovascular outcomes. J Hypertens 2011; 29: 189-193.
  • 22 Jordan J, Yumuk V, Schlaich M. et al. Joint statement of the European Association for the Study of Obesity and the European Society of Hypertension: obesity and difficult to treat arterial hypertension. J Hypertens 2012; 30: 1047-1055.
  • 23 Mancia G, Fagard R, Narkiewicz K. et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension: the Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2013; 31: 1281-1357.
  • 24 Massiera F, Bloch-Faure M, Ceiler D. et al. Adipose angiotensinogen is involved in adipose tissue growth and blood pressure regulation. FASEB J 2001; 15: 2727-2729.
  • 25 McCord J, Mundy BJ, Hudson MP. et al. Relationship between obesity and B-type natriuretic peptide levels. Arch Intern Med 2004; 164: 2247-2252.
  • 26 Mikhail N, Golub MS, Tuck ML. Obesity and hypertension. Prog Cardiovasc Dis 1999; 42: 39-58.
  • 27 Must A, Spadano J, Coakley EH. et al. The disease burden associated with overweight and obesity. JAMA 1999; 282: 1523-1529.
  • 28 Narkiewicz K, Somers VK. Sympathetic nerve activity in obstructive sleep apnoea. Acta Physiol Scand 2003; 177: 385-390.
  • 29 Neeland IJ, Winders BR, Ayers CR. et al. Higher natriuretic peptide levels associate with a favorable adipose tissue distribution profile. J Am Coll Cardiol 2013; 62: 752-760.
  • 30 Neter JE, Stam BE, Kok FJ, Grobbee DE, Geleijnse JM. Influence of weight reduction on blood pressure: a meta-analysis of randomized controlled trials. Hypertension 2003; 42: 878-884.
  • 31 O’Brien E, Asmar R, Beilin L. et al. Practice guidelines of the European Society of Hypertension for clinic, ambulatory and self blood pressure measurement. J Hypertens 2005; 23: 697-701.
  • 32 Rao RS, Yanagisawa R, Kini S. Insulin resistance and bariatric surgery. Obes Rev 2012; 13: 316-328.
  • 33 Shibao C, Gamboa A, Diedrich A. et al. Autonomic Contribution to Blood Pressure and Metabolism in Obesity. Hypertension. 2006
  • 34 Sjostrom CD, Lystig T, Lindroos AK. Impact of weight change, secular trends and ageing on cardiovascular risk factors: 10-year experiences from the SOS study. Int J Obes (Lond) 2011; 35: 1413-1420.
  • 35 Sjostrom L, Peltonen M, Jacobson P. et al. Bariatric surgery and long-term cardiovascular events. JAMA 2012; 307: 56-65.
  • 36 Straznicky N, Grassi G, Esler M. et al. European Society of Hypertension Working Group on Obesity Antihypertensive effects of weight loss: myth or reality?. J Hypertens 2010; 28: 637-643.
  • 37 Strazzullo P, Barbato A, Galletti F. et al. Abnormalities of renal sodium handling in the metabolic syndrome. Results of the Olivetti Heart Study. J Hypertens 2006; 24: 1633-1639.
  • 38 Tuck ML, Sowers J, Dornfeld L. et al. The effect of weight reduction on blood pressure, plasma renin activity, and plasma aldosterone levels in obese patients. N Engl J Med 1981; 304: 930-933.
  • 39 Wilson PW, D’Agostino RB, Sullivan L. et al. Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Arch Intern Med 2002; 162: 1867-1872.
  • 40 Engeli S, Jordan J. Neue europäische Empfehlungen zur diagnostik und Therapie der arteriellen Hypertonie. Adipositas 2014; 08: 32-36.