Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Original Article
  • Published:

Persistent elevation of central pulse pressure during postural stress in patients with type 2 diabetes mellitus

Abstract

An abnormal increase or decrease in blood pressure (BP) in response to postural stress is associated with increased risk of developing hypertension and stroke. However, the haemodynamic responses contributing to changes in central BP with postural stress are not well characterised. We aimed to determine this in controls compared to patients with type 2 diabetes mellitus (T2DM), whom we hypothesised would have an abnormal postural response. 41 participants (20 control, 21 T2DM) underwent measurement of brachial and central BP (by radial tonometry), with simultaneous bioimpedance cardiography (to determine stroke volume (SV) and cardiac output (CO)) and heart rate variability in seated and standing postures. Systemic vascular resistance (SVR; mean arterial pressure/CO), and arterial elastance (EA; end systolic pressure/SV) were calculated. Postural changes were defined as seated minus standing values. Central pulse pressure (PP) was higher in patients with T2DM and did not change from seated-to-standing positions, whereas there was a significant decrease upon standing in controls (P<0.05). The change in central systolic BP (SBP) correlated with change in SVR and EA in controls (r=0.67 and 0.68, P<0.05, respectively), but not in patients with T2DM (r=−0.05 and r=0.03, P>0.05, respectively). SV was the only significant correlate of change in central SBP in T2DM patients (r=0.62, P<0.05) and this was not observed in controls (r=−0.08 P>0.05). We conclude that central haemodynamic responses to postural stress are altered in patients with T2DM and result in persistent elevation of central PP while standing. This may contribute to increased cardiovascular risk associated with T2DM.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Figure 1
Figure 2
Figure 3

Similar content being viewed by others

References

  1. Thomas RJ, Liu K, Jacobs DR, Bild DE, Kiefe CI, Hulley SB . Positional change in blood pressure and 8-year risk of hypertension: the CARDIA Study. Mayo Clin Proc 2003; 78 (8): 951–958.

    Article  Google Scholar 

  2. Rose KM, Holme I, Light KC, Sharrett AR, Tyroler HA, Heiss G . Association between the blood pressure response to a change in posture and the 6-year incidence of hypertension: prospective findings from the ARIC study. J Hum Hypertens 2002; 16 (11): 771–777.

    Article  CAS  Google Scholar 

  3. Yatsuya H, Folsom AR, Alonso A, Gottesman RF, Rose KM . Postural changes in blood pressure and incidence of ischemic stroke subtypes: the ARIC study. Hypertension 2011; 57 (2): 167–173.

    Article  CAS  PubMed  Google Scholar 

  4. Vlachopoulos C, Aznaouridis K, O'Rourke MF, Safar ME, Baou K, Stefanadis C . Prediction of cardiovascular events and all-cause mortality with central haemodynamics: a systematic review and meta-analysis. Eur Heart J 2010; 31 (15): 1865–1871.

    Article  Google Scholar 

  5. Nichols WW, O'Rourke MF . McDonald's blood flow in arteries: Theoretical, Experimental and Clinical Principles. Hodder Arnold: London, 2005.

    Google Scholar 

  6. Davis SC, Westerhof BE, van den Bogaard B, Bogert LW, Truijen J, Kim YS et al. Active standing reduces wave reflection in the presence of increased peripheral resistance in young and old healthy individuals. J Hypertens 2011; 29 (4): 682–689.

    Article  CAS  Google Scholar 

  7. Sharman JE, Davies JE, Jenkins C, Marwick TH . Augmentation index, left ventricular contractility, and wave reflection. Hypertension 2009; 54 (5): 1099–1105.

    Article  CAS  Google Scholar 

  8. Wilkinson IB, MacCallum H, Flint L, Cockcroft JR, Newby DE, Webb DJ . The influence of heart rate on augmentation index and central arterial pressure in humans. J Physiol 2000; 525: 263–270.

    Article  CAS  PubMed  Google Scholar 

  9. Gilroy D, Wright L, Stowasser M, Sharman JE . Brachial and central blood pressure respond differently to postural changes in patients with treated hypertension (abstract). Hypertension 2011; 58 (1): 121.

    Google Scholar 

  10. Mattace-Raso F, Hofman A, Verwoert G, Wittemana J, Wilkinson I, Cockcroft J . Determinants of pulse wave velocity in healthy people and in the presence of cardiovascular risk factors: 'establishing normal and reference values'. Eur Heart J 2010; 31 (19): 2338–2350.

    Article  Google Scholar 

  11. Williams SB, Cusco JA, Roddy MA, Johnstone MT, Creager MA . Impaired nitric oxide-mediated vasodilation in patients with non-insulin-dependent diabetes mellitus. J Am Coll Cardiol 1996; 27 (3): 567–574.

    Article  CAS  Google Scholar 

  12. Stamler J, Vaccaro O, Neaton JD, Wentworth D . Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. Diabetes Care 1993; 16 (2): 434–444.

    Article  CAS  Google Scholar 

  13. Kannel WB, Wilson PW, Zhang TJ . The epidemiology of impaired glucose tolerance and hypertension. Am Heart J 1991; 121 (4 Pt 2): 1268–1273.

    Article  CAS  Google Scholar 

  14. El Assaad MA, Topouchian JA, Darne BM, Asmar RG . Validation of the Omron HEM-907 device for blood pressure measurement. Blood Press Monit 2002; 7 (4): 237–241.

    Article  PubMed  Google Scholar 

  15. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42 (6): 1206–1252.

    Article  CAS  PubMed  Google Scholar 

  16. Sharman JE, Lim R, Qasem AM, Coombes JS, Burgess MI, Franco J et al. Validation of a generalized transfer function to noninvasively derive central blood pressure during exercise. Hypertension 2006; 47 (6): 1203–1208.

    Article  CAS  Google Scholar 

  17. Chen CH, Nevo E, Fetics B, Pak PH, Yin FC, Maughan WL et al. Estimation of central aortic pressure waveform by mathematical transformation of radial tonometry pressure. Validation of generalized transfer function. Circulation 1997; 95 (7): 1827–1836.

    Article  CAS  Google Scholar 

  18. Holland DJ, Sacre JW, McFarlane SJ, Coombes JS, Sharman JE . Pulse wave analysis is a reproducible technique for measuring central blood pressure during hemodynamic perturbations induced by exercise. Am J Hypertens 2008; 21 (10): 1100–1106.

    Article  Google Scholar 

  19. Charloux A, Lonsdorfer-Wolf E, Richard R, Lampert E, Oswald-Mammosser M, Mettauer B et al. A new impedance cardiograph device for the non-invasive evaluation of cardiac output at rest and during exercise: comparison with the "direct" Fick method. Eur J Appl Physiol 2000; 82 (4): 313–320.

    Article  CAS  Google Scholar 

  20. Chantler PD, Lakatta EG, Najjar SS . Arterial-ventricular coupling: mechanistic insights into cardiovascular performance at rest and during exercise. J Appl Physiol 2008; 105 (4): 1342–1351.

    Article  PubMed  Google Scholar 

  21. Roman MJ, Devereux RB, Kizer JR, Okin PM, Lee ET, Wang W et al. High central pulse pressure is independently associated with adverse cardiovascular outcome the strong heart study. J Am Coll Cardiol 2009; 54 (18): 1730–1734.

    Article  PubMed  Google Scholar 

  22. Jacobsen TN, Morgan BJ, Scherrer U, Vissing SF, Lange RA, Johnson N et al. Relative contributions of cardiopulmonary and sinoaortic baroreflexes in causing sympathetic activation in the human skeletal muscle circulation during orthostatic stress. Circ Res 1993; 73 (2): 367–378.

    Article  CAS  Google Scholar 

  23. Sprangers RL, Wesseling KH, Imholz AL, Imholz BP, Wieling W . Initial blood pressure fall on stand up and exercise explained by changes in total peripheral resistance. J Appl Physiol 1991; 70 (2): 523–530.

    Article  CAS  Google Scholar 

  24. Tanaka H, Sjoberg BJ, Thulesius O . Cardiac output and blood pressure during active and passive standing. Clin Physiol 1996; 16 (2): 157–170.

    Article  CAS  Google Scholar 

  25. Klabunde R . Cardiovascular physiolgy concepts. Lippincott Williams & Wilkins: Philadelphia, 2005.

    Google Scholar 

  26. Tomsin K, Mesens T, Molenberghs G, Gyselaers W . Diurnal and position-induced variability of impedance cardiography measurements in healthy subjects. Clin Physiol Funct Imaging 2011; 31 (2): 145–150.

    Google Scholar 

  27. Davies JE, Hadjiloizou N, Leibovich D, Malaweera A, Alastruey-Arimon J, Whinnett ZI et al. Importance of the aortic reservoir in determining the shape of the arterial pressure waveform—The forgotten lessons of Frank. Artery Res 2007; 1 (2): 40–45.

    Article  Google Scholar 

  28. Benvenuto LJ, Krakoff LR . Morbidity and mortality of orthostatic hypotension: implications for management of cardiovascular disease. Am J Hypertens 2011; 24 (2): 135–144.

    Article  Google Scholar 

  29. Velagaleti RS, Gona P, Chuang ML, Salton CJ, Fox CS, Blease SJ et al. Relations of insulin resistance and glycemic abnormalities to cardiovascular magnetic resonance measures of cardiac structure and function: the Framingham Heart Study. Circ Cardiovasc Imaging 2010; 3 (3): 257–263.

    Article  PubMed  Google Scholar 

  30. Liao D, Carnethon M, Evans GW, Cascio WE, Heiss G . Lower heart rate variability is associated with the development of coronary heart disease in individuals with diabetes: the atherosclerosis risk in communities (ARIC) study. Diabetes 2002; 51 (12): 3524–3531.

    Article  CAS  Google Scholar 

  31. Sztajzel J . Heart rate variability: a noninvasive electrocardiographic method to measure the autonomic nervous system. Swiss Med Wkly 2004; 134 (35-36): 514–522.

    Google Scholar 

  32. Cruickshank K, Riste L, Anderson SG, Wright JS, Dunn G, Gosling RG . Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an integrated index of vascular function? Circulation 2002; 106 (16): 2085–2090.

    Article  Google Scholar 

  33. Sengstock D, Vaitkevicius PV, Supiano MA . Does increased arterial stiffness increase the risk for postural hypotension? Am J Geriatr Cardiol 2005; 14 (5): 224–229.

    Article  Google Scholar 

  34. Mitchell GF, Vita JA, Larson MG, Parise H, Keyes MJ, Warner E et al. Cross-sectional relations of peripheral microvascular function, cardiovascular disease risk factors, and aortic stiffness: the Framingham Heart Study. Circulation 2005; 112 (24): 3722–3728.

    Article  PubMed  Google Scholar 

  35. Ryan SM, Waack BJ, Weno BL, Heistad DD . Increases in pulse pressure impair acetylcholine-induced vascular relaxation. Am J Physiol 1995; 268 (1 Pt 2): H359–H363.

    CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to J E Sharman.

Ethics declarations

Competing interests

Dr Sharman has research collaborations with AtCor medical.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Schultz, M., Climie, R., Nikolic, S. et al. Persistent elevation of central pulse pressure during postural stress in patients with type 2 diabetes mellitus. J Hum Hypertens 27, 437–444 (2013). https://doi.org/10.1038/jhh.2012.60

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/jhh.2012.60

Keywords

This article is cited by

Search

Quick links