Skip to main content

Advertisement

SpringerLink
Log in

Cardiovascular Risk in Patients with Prehypertension and the Metabolic Syndrome

  • Hypertension and the Kidney (RM Carey, Section Editor)
  • Published:
Current Hypertension Reports Aims and scope Submit manuscript

Abstract

Prehypertension (pHTN) and metabolic syndrome (MetS) are both lifestyle diseases that are potentiated by increased adiposity, as both disease processes are closely related to weight. In the case of pHTN, increased adiposity causes dysregulation of the renin-angiotensin-aldosterone-system (RAAS) as well as adipokine- and leptin-associated increases in adrenergic tone. In MetS, excess weight potentiates hyperglycemia and insulin resistance which causes positive feedback into the RAAS system, activates an inflammatory cascade that potentiates atherosclerosis, and causes lipid dysregulation which together contribute to cardiovascular disease, especially coronary heart disease (CHD) and heart failure (HF). The relationship with all-cause mortality is not as clear-cut in part because of some protective effects associated with the obesity paradox in chronic diseases such as CHD and HF. However, in healthy populations, the absence of excess weight and its associated effects on prehypertension and MetS are associated with a longer absolute and disease-free lifespan.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1
Fig. 2

Similar content being viewed by others

Abbreviations

BMI:

Body mass index

BP:

Blood pressure

CHD:

Coronary heart disease

CVD:

Cardiovascular disease

DBP:

Diastolic blood pressure

ESH:

European Society of Hypertension

ESC:

European Society of Cardiology

FFA:

Free fatty acid

HF:

Heart failure

HTN:

Hypertension

pHTN:

Prehypertension

IR:

Insulin resistance

JNC:

Joint National Committee

LV:

Left ventricle/ventricular

MetS:

The metabolic syndrome

NCEP:

National Cholesterol Education Program

NHANES:

National Health and Nutrition Examination Survey

NO:

Nitric oxide

RAAS:

Renin-angiotensin-aldosterone system

ROS:

Reactive oxygen species

REGARDS:

The Reasons for Geographic and Racial Differences in Stroke Study

SBP:

Systolic blood pressure

WC:

Waist circumference

References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

  1. • Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. Jama. 2003;289:2560–72. An expert panel report delineating guidelines for diagnosing prehypertension.

    Article  CAS  PubMed  Google Scholar 

  2. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Bohm M, et al. 2013 ESH/ESC practice guidelines for the management of arterial hypertension. Blood Press. 2014;23(1):3–16. https://doi.org/10.3109/08037051.2014.868629.

    Article  PubMed  Google Scholar 

  3. •• Lewington S, Clarke R, Qizilbash N, Peto R, Collins R. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 2002;360:1903–13. A meta-analysis of one million patients that established increasing mortality with increasing blood pressure starting at 115/75, initiating interest in pHTN as a condition to be monitored and potentially treated.

    Article  PubMed  Google Scholar 

  4. Glasser SP, Khodneva Y, Lackland DT, Prineas R, Safford MM. Prehypertension and incident acute coronary heart disease in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study. Am J Hypertens. 2014;27(2):245–51. https://doi.org/10.1093/ajh/hpt200.

    Article  PubMed  Google Scholar 

  5. • Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002;106(25):3143. An expert panel report delineating the criteria for hyperlipidemia and cholesterol guidelines, which includes the most widely accepted definition of the metabolic syndrome.

  6. Aguilar M, Bhuket T, Torres S, Liu B, Wong RJ. Prevalence of the metabolic syndrome in the United States, 2003-2012. JAMA. 2015;313(19):1973–4. https://doi.org/10.1001/jama.2015.4260.

    Article  CAS  PubMed  Google Scholar 

  7. Ervin RB. Prevalence of metabolic syndrome among adults 20 years of age and over, by sex, age, race and ethnicity, and body mass index: United States, 2003-2006. Natl Health Stat Rep. 2009;5:1–7.

    Google Scholar 

  8. Balkau B, Charles MA, Drivsholm T, Borch-Johnsen K, Wareham N, Yudkin JS, et al. Frequency of the WHO metabolic syndrome in European cohorts, and an alternative definition of an insulin resistance syndrome. Diabetes Metab. 2002;28(5):364–76.

    PubMed  Google Scholar 

  9. Alberti KG, Zimmet PZ. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. Diabet Med. 1998;15(7):539–53. https://doi.org/10.1002/(SICI)1096-9136(199807)15:7<539::AID-DIA668>3.0.CO;2-S.

    Article  CAS  PubMed  Google Scholar 

  10. Alberti KG, Zimmet P, Shaw J. Metabolic syndrome—a new world-wide definition. A consensus statement from the International Diabetes Federation. Diabet Med. 2006;23(5):469–80. https://doi.org/10.1111/j.1464-5491.2006.01858.x.

    Article  CAS  PubMed  Google Scholar 

  11. Einhorn D, Reaven GM, Cobin RH, Ford E, Ganda OP, Handelsman Y, et al. American College of Endocrinology position statement on the insulin resistance syndrome. Endocr Pract. 2003;9:237–52.

    PubMed  Google Scholar 

  12. • Hu G, Tuomilehto J, Silventoinen K, Barengo N, Jousilahti P. Joint effects of physical activity, body mass index, waist circumference and waist-to-hip ratio with the risk of cardiovascular disease among middle-aged Finnish men and women. Eur Heart J. 2004;25:2212–9. A prospective cohort study of 18,892 Finnish men and women examining the associations of markers of obesity and physical fitness on the incidence of CVD; findings were an inverse association with levels of physical activity and direct associations of CVD risk and indicators of obesity.

    Article  PubMed  Google Scholar 

  13. Kelly RK, Magnussen CG, Sabin MA, Cheung M, Juonala M. Development of hypertension in overweight adolescents: a review. Adolesc Health Med Ther. 2015;6:171–87. https://doi.org/10.2147/AHMT.S55837.

    PubMed  PubMed Central  Google Scholar 

  14. Huang Y, Cai X, Liu C, Zhu D, Hua J, Hu Y, et al. Prehypertension and the risk of coronary heart disease in Asian and Western populations: a meta-analysis. J Am Heart Assoc. 2015;4(2):e001519. https://doi.org/10.1161/JAHA.114.001519.

    Article  PubMed  PubMed Central  Google Scholar 

  15. Huang Y, Cai X, Li Y, Su L, Mai W, Wang S, et al. Prehypertension and the risk of stroke: a meta-analysis. Neurology. 2014;82(13):1153–61. https://doi.org/10.1212/WNL.0000000000000268.

    Article  PubMed  Google Scholar 

  16. Leiba A, Twig G, Vivante A, Skorecki K, Golan E, Derazne E, et al. Prehypertension among 2.19 million adolescents and future risk for end-stage renal disease. J Hypertens. 2017;35(6):1290–6. https://doi.org/10.1097/HJH.0000000000001295.

    Article  CAS  PubMed  Google Scholar 

  17. Huang Y, Su L, Cai X, Mai W, Wang S, Hu Y, et al. Association of all-cause and cardiovascular mortality with prehypertension: a meta-analysis. Am Heart J. 2014;167:160–168.e1.

    Article  PubMed  Google Scholar 

  18. • Jiménez MC, Rexrode KM, Kotler G, Everett BM, Glynn RJ, Lee I-M, et al. Association between markers of inflammation and total stroke by hypertensive status among women. Am J Hypertens. 2016;29:1117–24. A prospective trial studying the interactions of inflammatory markers and HTN and risk of stroke in a groups of 27,330 women from the Women’s Health Study.

    Article  PubMed  PubMed Central  Google Scholar 

  19. • Wilson PWF, D’Agostino RB, Sullivan L, Parise H, Kannel WB. Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Arch Intern Med. 2002;162:1867. A study based on the Framingham cohort that associated risk of hypertension and cardiovascular diseases with overweight status.

    Article  PubMed  Google Scholar 

  20. Gelber R, Gaziano J, Manson J, Buring J, Sesso H. A prospective study of body mass index and the risk of developing hypertension in men. Am J Hypertens. 2007;20(4):370–7. https://doi.org/10.1016/j.amjhyper.2006.10.011.

    Article  PubMed  PubMed Central  Google Scholar 

  21. Brion MA, Ness AR, Davey Smith G, Leary SD. Association between body composition and blood pressure in a contemporary cohort of 9-year-old children. J Hum Hypertens [Internet]. 2007 [cited 2016 Dec 13];Available from: http://www.nature.com/doifinder/10.1038/sj.jhh.1002152.

  22. Moore LL, Visioni AJ, Qureshi MM, Bradlee ML, Ellison RC, D’Agostino R. Weight loss in overweight adults and the long-term risk of hypertension: the Framingham study. Arch Intern Med. 2005;165(11):1298–303. https://doi.org/10.1001/archinte.165.11.1298.

    Article  PubMed  Google Scholar 

  23. •• The SPRINT Research Group. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373:2103–16. Randomized control trial that found a mortality advantage with intensive blood pressure control compared to standard blood pressure control in a healthy population with risk factors for CHD.

    Article  PubMed Central  Google Scholar 

  24. • Bell BB, Rahmouni K. Leptin as a mediator of obesity-induced hypertension. Curr Obes Rep. 2016;5:397–404. A review of the mechanisms associating obesity, leptin, and the development of HTN.

    Article  PubMed  PubMed Central  Google Scholar 

  25. Alpert MA, Omran J, Mehra A, Ardhanari S. Impact of obesity and weight loss on cardiac performance and morphology in adults. Prog Cardiovasc Dis. 2014;56:391–400.

    Article  PubMed  Google Scholar 

  26. Taddei S, Virdis A, Mattei P, Favilla S, Salvetti A. Angiotensin II and Sympathetic activity in sodium-restricted essential hypertension. Hypertension. 1995;25(4):595–601. https://doi.org/10.1161/01.HYP.25.4.595.

    Article  CAS  PubMed  Google Scholar 

  27. Stepniakowski KT, Goodfriend TL, Egan BM. Fatty acids enhance vascular alpha-adrenergic sensitivity. Hypertens Dallas Tex 1979. 1995;25:774–8.

    CAS  Google Scholar 

  28. Hall JE, Hildebrandt DA, Kuo J. Obesity hypertension: role of leptin and sympathetic nervous system. Am J Hypertens. 2001;14(11):103S–15S. https://doi.org/10.1016/S0895-7061(01)02077-5.

    Article  CAS  PubMed  Google Scholar 

  29. • Oishi K, Zheng B, Kuo JF. Inhibition of Na, K-ATPase and sodium pump by protein kinase C regulators sphingosine, lysophosphatidylcholine, and oleic acid. J Biol Chem. 1990;265:70–5. Original research describing the relationship between Na, K-ATPase, and free fatty acids associated with obesity.

    CAS  PubMed  Google Scholar 

  30. Haynes WG. Interaction between leptin and sympathetic nervous system in hypertension. Curr Hypertens Rep. 2000;2(3):311–8. https://doi.org/10.1007/s11906-000-0015-1.

    Article  CAS  PubMed  Google Scholar 

  31. Cassaglia PA, Hermes SM, Aicher SA, Brooks VL. Insulin acts in the arcuate nucleus to increase lumbar sympathetic nerve activity and baroreflex function in rats. J Physiol. 2011;589(7):1643–62. https://doi.org/10.1113/jphysiol.2011.205575.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Esler M, Rumantir M, Wiesner G, Kaye D, Hastings J, Lambert G. Sympathetic nervous system and insulin resistance: from obesity to diabetes. Am J Hypertens. 2001;14:304s–9s.

    Article  CAS  PubMed  Google Scholar 

  33. • Kalupahana NS, Moustaid-Moussa N. The adipose tissue renin-angiotensin system and metabolic disorders: a review of molecular mechanisms. Crit Rev Biochem Mol Biol. 2012;47:379–90. A review discussing RAAS in adipose tissue and how it contributes to metabolic disorders.

    Article  CAS  PubMed  Google Scholar 

  34. Hall JE. Pathophysiology of obesity hypertension. Curr Hypertens Rep. 2000;2(2):139–47. https://doi.org/10.1007/s11906-000-0073-4.

    Article  CAS  PubMed  Google Scholar 

  35. McArdle MA, Finucane OM, Connaughton RM, McMorrow AM, Roche HM. Mechanisms of obesity-induced inflammation and insulin resistance: insights into the emerging role of nutritional strategies. Front Endocrinol [Internet]. 2013 [cited 2017 Sep 30];4. Available from: http://journal.frontiersin.org/article/10.3389/fendo.2013.00052/abstract.

  36. •• Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005;352:1685–95. A review article that discusses the evidence that atherosclerosis is a collection of immune mechanisms that interact with metabolic risk factors to initiate, propagate, and activate lesions in the arterial tree.

    Article  CAS  PubMed  Google Scholar 

  37. Zhang H, Zhang C. Regulation of microvascular function by adipose tissue in obesity and type 2 diabetes: evidence of an adipose-vascular loop. Am J Biomed Sci. 2009;1:133.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  38. Samuel VT, Shulman GI. The pathogenesis of insulin resistance: integrating signaling pathways and substrate flux. J Clin Invest. 2016;126(1):12–22. https://doi.org/10.1172/JCI77812.

    Article  PubMed  PubMed Central  Google Scholar 

  39. Caballero AE. Endothelial dysfunction in obesity and insulin resistance: a road to diabetes and heart disease. Obes Res. 2003;11(11):1278–89. https://doi.org/10.1038/oby.2003.174.

    Article  CAS  PubMed  Google Scholar 

  40. • Yang J, Park Y, Zhang H, Gao X, Wilson E, Zimmer W, et al. Role of MCP-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice. Am J Physiol Heart Circ Physiol. 2009;297:H1208–16. Basic science research demonstrating the interaction between diabetes-associated TNF-α and the evolution of vascular inflammation and endothelial dysfunction mediated by chemoattractant protein-1 (MCP-1).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Tsao PS, Aoki N, Lefer DJ, Johnson G, Lefer AM. Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat. Circulation. 1990;82(4):1402–12. https://doi.org/10.1161/01.CIR.82.4.1402.

    Article  CAS  PubMed  Google Scholar 

  42. • Schächinger V, Britten MB, Zeiher AM. Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease. Circulation. 2000;101:1899–906. Clinical cohort trial linking impaired coronary vasoreactivity to increased cardiovascular event rates.

    Article  PubMed  Google Scholar 

  43. Pepine CJ, Nichols WW. The pathophysiology of chronic ischemic heart disease. Clin Cardiol. 2007;30(S1):I4–9. https://doi.org/10.1002/clc.20048.

    Article  PubMed  Google Scholar 

  44. Davignon J, Ganz P. Role of endothelial dysfunction in atherosclerosis. Circulation. 2004;109(23 Suppl 1):III27–32. https://doi.org/10.1161/01.CIR.0000131515.03336.f8.

    PubMed  Google Scholar 

  45. Lee S, Park Y, Zuidema MY, Hannink M, Zhang C. Effects of interventions on oxidative stress and inflammation of cardiovascular diseases. World J Cardiol. 2011;3(1):18–24. https://doi.org/10.4330/wjc.v3.i1.18.

    Article  PubMed  PubMed Central  Google Scholar 

  46. Lee S, Park Y, Dellsperger KC, Zhang C. Exercise training improves endothelial function via adiponectin-dependent and independent pathways in type 2 diabetic mice. Am J Physiol Heart Circ Physiol. 2011;301(2):H306–14. https://doi.org/10.1152/ajpheart.01306.2010.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  47. Karasu C. Glycoxidative stress and cardiovascular complications in experimentally-induced diabetes: effects of antioxidant treatment. Open Cardiovasc Med J. 2010;4(1):240–56. https://doi.org/10.2174/1874192401004010240.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  48. Lakshmi SVV, Padmaja G, Kuppusamy P, Kutala VK. Oxidative stress in cardiovascular disease. Indian J Biochem Biophys. 2009;46(6):421–40.

    CAS  PubMed  Google Scholar 

  49. Visser M. Elevated C-reactive protein levels in overweight and obese adults. JAMA. 1999;282(22):2131–5. https://doi.org/10.1001/jama.282.22.2131.

    Article  CAS  PubMed  Google Scholar 

  50. • Van de Voorde J, Pauwels B, Boydens C, Decaluwé K. Adipocytokines in relation to cardiovascular disease. Metabolism. 2013;62:1513–21. A review that discusses adipocytokines, the concept of adiposopathy, and the role of adipocytokines in endothelial dysfunction, hypertension, atherosclerosis, and cardiovascular disease.

    Article  PubMed  Google Scholar 

  51. Hernandez-Pando R, Bornstein QL, Aguilar Leon D, Orozco EH, Madrigal VK, Martinez Cordero E. Inflammatory cytokine production by immunological and foreign body multinucleated giant cells. Immunology. 2000;100(3):352–8. https://doi.org/10.1046/j.1365-2567.2000.00025.x.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  52. Libby P, Ridker PM, Hansson GK. Inflammation in atherosclerosis. J Am Coll Cardiol. 2009;54(23):2129–38. https://doi.org/10.1016/j.jacc.2009.09.009.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  53. Lumeng CN, Bodzin JL, Saltiel AR. Obesity induces a phenotypic switch in adipose tissue macrophage polarization. J Clin Invest. 2007;117(1):175–84. https://doi.org/10.1172/JCI29881.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  54. Li P, Wang L, Liu C. Overweightness, obesity and arterial stiffness in healthy subjects: a systematic review and meta-analysis of literature studies. Postgrad Med [Internet]. 2016 [cited 2016 Dec 8];Available from: https://www.tandfonline.com/doi/full/10.1080/00325481.2017.1268903.

  55. Despres JP, Krauss RM. Obesity and lipoprotein metabolism. In: Handbook of obesity: etiology and pathophysiology. New York: Marcel Dekker; 2004. p. 845–871.

  56. Song G, Wu X, Zhang P, Yu Y, Yang M, Jiao P, et al. High-density lipoprotein inhibits ox-LDL-induced adipokine secretion by upregulating SR-BI expression and suppressing ER stress pathway. Sci Rep. 2016;6(1):30889. https://doi.org/10.1038/srep30889.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  57. Tabas I, Williams KJ, Boren J. Subendothelial lipoprotein retention as the initiating process in atherosclerosis: update and therapeutic implications. Circulation. 2007;116(16):1832–44. https://doi.org/10.1161/CIRCULATIONAHA.106.676890.

    Article  CAS  PubMed  Google Scholar 

  58. Norris AL, Steinberger J, Steffen LM, Metzig AM, Schwarzenberg SJ, Kelly AS. Circulating oxidized LDL and inflammation in extreme pediatric obesity. Obesity. 2011;19(7):1415–9. https://doi.org/10.1038/oby.2011.21.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  59. • Holvoet P, Kritchevsky SB, Tracy RP, Mertens A, Rubin SM, Butler J, et al. The metabolic syndrome, circulating oxidized LDL, and risk of myocardial infarction in well-functioning elderly people in the health, aging, and body composition cohort. Diabetes. 2004;53:1068–73. A cohort study analyzing the association of oxidized LDL and the risk of CHD in a population of 3,033 elderly patients in the Health, Aging and Body Composition study.

    Article  CAS  PubMed  Google Scholar 

  60. • Holvoet P, Mertens A, Verhamme P, Bogaerts K, Beyens G, Verhaeghe R, et al. Circulating oxidized LDL is a useful marker for identifying patients with coronary artery disease. Arterioscler Thromb Vasc Biol. 2001;21:844–8. A randomized control trial involving 304 patients that found a significant association between oxidized LDL, a high Global Risk Assessment Score, and the presence of CVD.

    Article  CAS  PubMed  Google Scholar 

  61. • Du Y, Li S, Cui C-J, Zhang Y, Yang S-H, Li J-J. Leptin decreases the expression of low-density lipoprotein receptor via PCSK9 pathway: linking dyslipidemia with obesity. J Transl Med [Internet]. 2016 [cited 2016 Dec 8];14. Available from: http://translational-medicine.biomedcentral.com/articles/10.1186/s12967-016-1032-4. A molecular biology study that linked to PCSK-9-induced downregulation of LDL-R to increased levels of leptin.

  62. Gropler RJ. The road connecting obesity and coronary vasomotor function: straight line or U-turn? JACC Cardiovasc Imaging. 2012;5(8):816–8. https://doi.org/10.1016/j.jcmg.2012.07.001.

    Article  PubMed  PubMed Central  Google Scholar 

  63. •• Galassi A, Reynolds K, He J. Metabolic syndrome and risk of cardiovascular disease: a meta-analysis. Am J Med. 2006;119:812–9. A meta-analysis of 21 prospective studies that linked MetS to CVD, CVD mortality, and all-cause mortality.

    Article  CAS  PubMed  Google Scholar 

  64. Lee S, Park Y, Zhang C. Exercise training prevents coronary endothelial dysfunction in type 2 diabetic mice. Am J Biomed Sci. 2011;3(4):241–52. https://doi.org/10.5099/aj110400241.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  65. Bastien M, Poirier P, Lemieux I, Després J-P. Overview of epidemiology and contribution of obesity to cardiovascular disease. Prog Cardiovasc Dis. 2014;56(4):369–81. https://doi.org/10.1016/j.pcad.2013.10.016.

    Article  PubMed  Google Scholar 

  66. •• Gami AS, Witt BJ, Howard DE, Erwin PJ, Gami LA, Somers VK, et al. Metabolic syndrome and risk of incident cardiovascular events and death. J Am Coll Cardiol. 2007;49:403–14. A meta-analysis of 37 studies that focused on MetS and its associated cardiovascular events and mortality. Finding that MetS is an independent risk factor for CVD and mortality.

    Article  CAS  PubMed  Google Scholar 

  67. • Solymoss BC, Bourassa MG, Marcil M, Levesque S, Varga S, Campeau L. Long-term rates of cardiovascular events in patients with the metabolic syndrome according to severity of coronary-angiographic alterations. Coron Artery Dis. 2009;20:1–8. A cohort study that followed 1,080 patients divided into groups based on presence or absence of significant CVD and presence or absence of MetS over the course of approximately 12 years, to determine the impact of CVD and MetS on the long-term risk of mortality and cardiovascular events.

    Article  PubMed  Google Scholar 

  68. • Bozkurt B, Aguilar D, Deswal A, Dunbar SB, Francis GS, Horwich T, et al. Contributory risk and management of comorbidities of hypertension, obesity, diabetes mellitus, hyperlipidemia, and metabolic syndrome in chronic heart failure: a scientific statement from the American Heart Association. Circulation. 2016;134:e535–78. A scientific statement that reviewed the various metabolic risk factors that contribute to the risk of developing HF.

    Article  PubMed  Google Scholar 

  69. • Huang Y, Wang S, Cai X, Mai W, Hu Y, Tang H, Xu D. Prehypertension and incidence of cardiovascular disease: a meta-analysis. BMC Med [Internet]. 2013 [cited 2017 Aug 16];11. Available from: http://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-177. A meta-analysis that reviewed 18 prospective cohort studies with 468,561 participants for associations between pHTN and CVD, finding that pHTN elevates risk for CVD.

  70. Ku CS, Lin SL, Wang DJ, Chang SK, Lee WJ. Left ventricular filling in young normotensive obese adults. Am J Cardiol. 1994;73:613–5.

    Article  CAS  PubMed  Google Scholar 

  71. • Kachur S, Lavie CJ, de Schutter A, Milani RV, Ventura HO. Obesity and cardiovascular diseases. Minerva Med. 2017;108:212–28. A review that looks at the impact of obesity on the risk of developing cardiovascular disease, as well as the paradoxical effect of obesity on survival.

    PubMed  Google Scholar 

  72. • Fuentes de las L, Brown AL, Mathews SJ, Waggoner AD, Soto PF, Gropler RJ, et al. Metabolic syndrome is associated with abnormal left ventricular diastolic function independent of left ventricular mass. Eur Heart J. 2007;28:553–9. A cohort study that followed 607 patients with normal LV function, assessing the effect of MetS on LV function; finding that MetS is an independent risk factor for diastolic.

    Article  Google Scholar 

  73. Guo X, Zhang X, Zheng L, Guo L, Li Z, Yu S, et al. Not associated with all-cause mortality: a systematic review and meta-analysis of prospective studies. PLoS One. 2013;8:e61796.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  74. Vasan RS, Larson MG, Leip EP, Evans JC, O’Donnell CJ, Kannel WB, et al. Impact of high-normal blood pressure on the risk of cardiovascular disease. N Engl J Med. 2001;345(18):1291–7. https://doi.org/10.1056/NEJMoa003417.

    Article  CAS  PubMed  Google Scholar 

  75. Isomaa B, Almgren P, Tuomi T, Forsén B, Lahti K, Nissén M, et al. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care. 2001;24(4):683–9. https://doi.org/10.2337/diacare.24.4.683.

    Article  CAS  PubMed  Google Scholar 

  76. Romero-Corral A, Montori VM, Somers VK, Korinek J, Thomas RJ, Allison TG, et al. Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies. Lancet. 2006;368(9536):666–78. https://doi.org/10.1016/S0140-6736(06)69251-9.

    Article  PubMed  Google Scholar 

  77. Doehner W, Clark A, Anker SD. The obesity paradox: weighing the benefit. Eur Heart J. 2010;31(2):146–8. https://doi.org/10.1093/eurheartj/ehp339.

    Article  PubMed  Google Scholar 

  78. • Ortega FB, Lavie CJ, Blair SN. Obesity and cardiovascular disease. Circ Res. 2016;118:1752–70. A review that discusses and proposes a mechanism for the increased survival seen in the obesity paradox.

    Article  CAS  PubMed  Google Scholar 

  79. • Ahmad FS, Ning H, Rich JD, Yancy CW, Lloyd-Jones DM, Wilkins JT. Hypertension, obesity, diabetes, and heart failure-free survival: the Cardiovascular Disease Lifetime Risk Pooling Project. JACC Heart Fail. 2016;4:911–9. A pooled cohort study involving four cohorts that assessed the impact of obesity on heart failure, finding that prevention of hypertension, obesity, and diabetes by ages 45 and 55 years may substantially prolong heart failure-free survival, decrease heart failure-related morbidity, and reduce the public health impact of heart failure.

    Article  PubMed  PubMed Central  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Graduate Medical Education, Ocala Regional Medical Center, 1431 SW 1st Ave., Ocala, FL, 34471, USA

    Sergey Kachur & Rebecca Morera

  2. New York University School of Medicine, New York, NY, USA

    Alban De Schutter

  3. Department of Cardiovascular Diseases, John Ochsner Heart and Vascular Institute, Ochsner Clinic School-the University of Queensland School of Medicine, New Orleans, LA, USA

    Carl J. Lavie

Authors
  1. Sergey Kachur
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Rebecca Morera
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Alban De Schutter
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Carl J. Lavie
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Sergey Kachur.

Ethics declarations

Conflict of Interest

The authors declare no conflicts of interest relevant to this manuscript.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

Additional information

This article is part of the Topical Collection on Hypertension and the Kidney

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Kachur, S., Morera, R., De Schutter, A. et al. Cardiovascular Risk in Patients with Prehypertension and the Metabolic Syndrome. Curr Hypertens Rep 20, 15 (2018). https://doi.org/10.1007/s11906-018-0801-2

Download citation

  • Published:

  • DOI: https://doi.org/10.1007/s11906-018-0801-2

Keywords

Search

Navigation