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Rivista di Angiologia

Official Journal of the International Union of Angiology, the International Union of Phlebology and the Central European Vascular Forum
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
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International Angiology 2012 February;31(1):10-5


lingua: Inglese

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

Husmann M. 1, Thalhammer C. 1, Spring S. 1, Meier T. 1, Roffi M. 2, Schwarz U. R. S. 3, Rousson V. 4, Amann-Vesti B. R. 1

1 Clinic for Angiology, University Hospital Zurich, Zurich, Switzerland; 2 Division of Cardiology, University Hospital Geneva, Geneva, Switzerland; 3 Clinic for Neurology, University Hospital Zurich, Zurich, Switzerland; 4 Department of Biostatistics, ISPM, University of Zurich, Zurich, Switzerland


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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