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.
Aim:
Carotid artery stenting (CAS) may cause bradycardia and hypotension due to barostimulation. The impact of periprocedural hypotension on CAS outcome remains controversial. The role of carotid plaque volume and catecholamine hormone release during CAS on hemodynamic changes has not been investigated so far. The aim of this prospective study was to evaluate if carotid artery plaque characteristics are predictive for stress hormone release or for postprocedural hemodynamic instability.
Methods:
In 26 patients undergoing CAS, carotid plaque volume and morphology were assessed by two- and three-dimensional (3D)-Duplex sonography prior to the procedure. Arterial plasma adrenaline, noradrenaline and renin concentrations were measured at the time of sheath insertion and 5 minutes after stent placement. ECG, heart rate, and invasive blood pressure were monitored throughout the procedure.
Results:
CAS caused no significant changes in hormone release, but increasing plaque volume was related to the degree of bradycardia following stent deployment (r=0.57; P=0.01). Plaque size was not associated with postprocedural hypotension. Plaque echogenicity (echolucent, heterogeneous or echogenic) did not correlate with changes in systolic blood pressure, heart rate or catecholamine hormone release.
Conclusion:
CAS caused bradycardia in relation to plaque size, but did not cause catecholamine release which may indicate that the endovascular procedure is not associated with a relevant stress reaction.
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