gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Effects of Irbesartan versus Atenolol on Vascular Stiffness and Aortic Blood Pressure in Essential Hypertension

Meeting Abstract

  • R.E. Schmieder - Universitätsklinikum Erlangen-Nürnberg (Erlangen, D)
  • C. Ott - Universitätsklinikum Erlangen-Nürnberg (Erlangen, D)
  • M.P. Schneider - Universitätsklinikum Erlangen-Nürnberg (Erlangen, D)
  • M. Ludwig - University of Bonn (Bonn, D)
  • K.O. Stumpe - University of Bonn (Bonn, D)
  • R.E. Kolloch - Gilead Medical Center, Bielefeld (Bielefeld, D)
  • M. Krekler - Bristol-Myers Squibb, München (München, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP160

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2005/05hoch160.shtml

Veröffentlicht: 8. August 2006

© 2006 Schmieder et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

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Background: In the LIFE trial treatment with an angiotensin receptor blocker (ARB) lead to greater reduction of cardiovascular mortality than betablocker treatment, even though brachial blood pressure was reduced similarly. We hypothesized as a pathogenetic mechanism that vascular stiffness and aortic blood pressure may be affected differently by ARBs and betablockers.

Methods: In the Cardiovascular Irbesartan Project subjects with essential hypertension were treated for 18 months with either irbesartan or atenolol. In 156 subjects aortic augmentation index (AI) and aortic blood pressure were determined by pulse wave analysis (SphygmocorÔ) at both the radial and carotid artery after 6 and 18 months of treatment.

Results: AI was reduced by irbesartan but not by atenolol (DAI derived from the carotid artery: -12.3±22.0 vs +6.0±23.0%; p<0.001 after 6 months and -8.7±24.1 vs +0.9±24.2% after 18 months; p=0.051). Aortic and brachial systolic blood pressure were reduced similarly by irbesartan (-12±17 vs -12±18 after 6 months and -13±19 vs -14±21 mmHg after 18 months; both n.s.) whereas atenolol lead to smaller reductions of aortic than brachial blood pressure (-9±17 vs -13±18 after 6 months and -11±18 vs -14±18 mmHg after 18 months, both p<0.001).

Conclusions: Vascular stiffness was reduced only with irbesartan. Furthermore, irbesartan reduced aortic and brachial blood pressure similarly, whereas atenolol reduced aortic blood pressure less than brachial blood pressure. These differences in central hemodynamics may contribute to the superior effect of ARBs compared to betablockers on cardiovascular mortality, despite similar brachial blood pressure reductions.