Artery Research (Mar 2012)

Vascular characteristics in patients with resistant hypertension and type-II-diabetes mellitus

  • Trine Koustrup Soender,
  • Jacob Eifer Møller,
  • Brian Bridal Løgstrup,
  • Jess Lambrechtsen,
  • Jørgen Hangaard,
  • Kenneth Egstrup

DOI
https://doi.org/10.1016/j.artres.2012.02.002
Journal volume & issue
Vol. 6, no. 2

Abstract

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Background: Resistant hypertension is presumed to be common in patients with type-II-diabetes mellitus (type-II-DM) and arterial stiffness has been proposed to play a major role in the development hereof. Our objective with this study was to examine differences in vascular characteristics in patients with controlled (CH), uncontrolled (UH) and resistant hypertension (RH) and type-II-DM and to assess whether increased arterial stiffness could explain the prevalence of resistant hypertension. Methods and results: Vascular characteristics were examined using ambulatory blood pressure measurements, applanation tonometry and cardiac ultrasound. We estimated carotid-to-femoral pulse wave velocity using Sphygmocor. Characteristic impedance, arterial resistance, arterial compliance and augmentation index was estimated from analysis of pressure- and flow-curves. Finally ambulatory arterial stiffness index was estimated using ambulatory blood pressure measurements. We included 114 patients in the study of whom 39 had RH. When compared to patients with CH, patients with RH had increased pulse wave velocity (10.8 m/s [8.78; 12.23] versus 8.55 m/s [7.55; 10.6], P = 0.002) and reduced total arterial compliance (0.81 ml/mmHg [0.55; 0.95] versus 0.93 ml/mmHg [0.68; 1.36], P = 0.03) however differences were non-significant when adjusted for blood pressure (P = 0.2 and P = 0.2) Following statistical adjustment patients with UH had increased total arterial resistance though as compared to patients with CH (1.63 mmHg/ml*s−1 [1.37; 1.92] versus 1.38 mmHg/ml*s−1 [1.2; 1.71]) (P = 0.03). Conclusion: In the present study patients with RH and type-II-DM do not have increased intrinsic arterial stiffness when compared to patients with CH, thus we conclude that increased intrinsic arterial stiffness is not the cause of resistant hypertension in the present study.

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