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The impact of third-generation beta-blocker antihypertensive treatment on endothelial function and the prothrombotic

Gregory P Vyssoulis1, Andreas G Marinakis, Konstantinos A Aznaouridis

  • 1First Cardiology Department of Athens University, Hippokration Hospital, Athens, Greece.

American Journal of Hypertension
|July 6, 2004
PubMed

Insights

Nebivolol significantly reduced prothrombotic markers in hypertensive smokers, unlike carvedilol. Smoking status is crucial for selecting antihypertensive treatments, with nebivolol showing benefits in smokers.

Area of Science:

  • Cardiovascular Pharmacology
  • Hypertension Management
  • Thrombosis Research

Background:

  • Beta-blockers are vital for cardiovascular disease treatment.
  • The impact of vasodilating beta-blockers on endothelial function and prothrombotic states remains under-investigated.

Purpose of the Study:

  • To investigate the effects of vasodilating beta-blockers (celiprolol, carvedilol, nebivolol) on prothrombotic markers in hypertensive patients.
  • To determine if smoking status influences the efficacy of these beta-blockers on prothrombotic markers.

Main Methods:

  • A study involving 550 hypertensive patients treated with monotherapy of celiprolol, carvedilol, or nebivolol.
  • Measurements of plasma fibrinogen, homocystine, and serum plasminogen activator inhibitor-1 (PAI-1) before and after 6 months of treatment.

Main Results:

  • Nebivolol, celiprolol, and carvedilol showed significant differences in reducing homocystine and fibrinogen levels.
  • In smokers, all three drugs differentially affected fibrinogen, PAI-1, and homocystine levels.
  • Nebivolol demonstrated a more pronounced reduction in these markers in smokers compared to nonsmokers.

Conclusions:

  • Nebivolol significantly decreased PAI-1, fibrinogen, and homocystine in hypertensive smokers.
  • Celiprolol showed a lesser but significant effect, while carvedilol had no significant favorable action on these markers in smokers.
  • Smoking status should guide the selection of antihypertensive therapy, particularly concerning prothrombotic risk.
Abstract

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