Vessel wall damage caused by cerebral protection devices: ex vivo evaluation in porcine carotid arteries.
OBJECTIVE
To determine the extent of vessel wall damage caused by cerebral protection devices designed for carotid angioplasty by using ex vivo porcine carotid arteries.


METHODS
The local animal experimentation committee did not require its approval for this study. With a benchtop vascular model (flow rate, 470 mL/min; dicrotic pulsatile flow, 76 pulses per minute; pressure, 115/67 mm Hg [mean pressure, 91 mm Hg]) into which 85 porcine internal carotid arteries (ICAs) were inserted, five different protection devices (Angioguard [Cordis/Johnson & Johnson, Miami, Fla], Filterwire EX [Boston Scientific, Natick, Mass], Trap [Microvena, White Bear Lake, Minn], Neuroshield [Abbott Laboratories, Redwood City, Calif], and Percusurge [Abbott Laboratories]) were evaluated. Adverse movement (1 cm up, 2 cm down, and 1 cm up again) of the activated devices (deployed filters or inflated balloons [Percusurge only]) was simulated, and the device was retrieved. For each of these steps (deployment, movement, retrieval) the amount of debris from the vessel wall in the effluent of the ICA was determined by using a 100-microm filter. The Mann-Whitney test was used to test for differences, and a correction for multiple comparisons was made. P < .05 was considered to indicate a significant difference. The authors attempted to determine whether there was a notable association between the total amount of debris captured and the classification of damage at microscopy. Carotid arteries were analyzed histologically with light and scanning electron microscopy.


RESULTS
All examined protection devices caused dislodged debris, which was captured in the effluent filter. There were significant differences among the devices in terms of the total amount of debris captured in the filters (lowest amounts of debris, 4.75 mg [Angioguard] and 5.02 mg [Filterwire EX]; highest amount, 7.51 mg [Trap]; P < or = .001 for all). All devices caused histologically visible wall damage, with the degree of intimal denudation correlating with the mass of the debris. The Trap device caused the most severe intimal and subintimal wall damage. Adverse movement resulted in no increased debris dislodgment as compared with the debris dislodged during deployment and retrieval of the devices.


CONCLUSIONS
On the basis of the data obtained, cerebral protection devices themselves have a potential influence on embolization rates by causing debris to be dislodged during carotid stent placement.
Müller-Hülsbeck
Stefan
S
Department of Radiology, University Hospital Schleswig-Holstein-Campus Kiel, Arnold-Heller-Strasse 9, 24105 Kiel, Germany. muehue@rad.uni-kiel.de
Stolzmann
Paul
P
Liess
Carsten
C
Hedderich
Jürgen
J
Paulsen
Friedrich
F
Jahnke
Thomas
T
Heller
Martin
M
D000800:Angioplasty, Balloon / Q000009:adverse effects / Q000295:instrumentation*; D000818:Animals; D020212:Carotid Artery Injuries / Q000473:pathology*; D002343:Carotid Artery, Internal / Q000473:pathology*; D016893:Carotid Stenosis / Q000473:pathology*; D004730:Endothelium, Vascular / Q000293:injuries* / Q000473:pathology; D004867:Equipment Design; D005374:Filtration / Q000295:instrumentation*; D020766:Intracranial Embolism / Q000473:pathology / Q000517:prevention & control*; D008855:Microscopy, Electron, Scanning; D008955:Models, Cardiovascular; D009131:Muscle, Smooth, Vascular / Q000293:injuries* / Q000473:pathology; D015607:Stents / Q000009:adverse effects*; D013552:Swine