Influence of plaque volume on hemodynamic response and stress hormone release in patients undergoing carotid artery

M Husmann1, C Thalhammer, S Spring

  • 1Clinic for Angiology, University Hospital Zurich, Raemistrasse 100, Zurich, Switzerland.

Insights

Carotid artery stenting (CAS) can cause bradycardia related to plaque size. This study found no significant stress hormone release during CAS, suggesting the procedure isn't a major stressor.

Area of Science:

  • Cardiovascular Medicine
  • Interventional Cardiology
  • Neurosurgery

Background:

  • Carotid artery stenting (CAS) can induce bradycardia and hypotension via barostimulation.
  • The influence of periprocedural hypotension on CAS outcomes is debated.
  • The relationship between carotid plaque characteristics, stress hormone release, and hemodynamic changes during CAS is not well understood.

Purpose of the Study:

  • To investigate if carotid artery plaque characteristics predict stress hormone release.
  • To determine if plaque characteristics predict postprocedural hemodynamic instability.
  • To assess the association between plaque volume, morphology, and hemodynamic responses during CAS.

Main Methods:

  • Prospective study of 26 patients undergoing CAS.
  • Carotid plaque volume and morphology assessed using 2D/3D Duplex sonography.
  • Plasma catecholamines (adrenaline, noradrenaline) and renin measured pre- and post-stent placement; ECG, heart rate, and blood pressure monitored.

Main Results:

  • Increasing carotid plaque volume correlated with the degree of bradycardia post-stent deployment (r=0.57; P=0.01).
  • Plaque size did not predict postprocedural hypotension.
  • Plaque echogenicity showed no correlation with changes in blood pressure, heart rate, or catecholamine levels.

Conclusions:

  • CAS-induced bradycardia is associated with carotid plaque size.
  • The procedure did not significantly increase catecholamine release, indicating a lack of a substantial stress response.
  • Carotid plaque characteristics may influence hemodynamic responses during CAS, specifically bradycardia.
Abstract

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