(Circulation. 1996;94:1733-1740.)
© 1996 American Heart Association, Inc.
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the Division of Cardiology and the Cardiovascular Intervention Research Center, Department of Medicine and the Department of Pathology, Cedars-Sinai Medical Center, the Cedars-Sinai Research Institute and the UCLA School of Medicine, Los Angeles, Calif.
Correspondence to Neal Eigler, MD, Cardiovascular Intervention Center, Cedars-Sinai Medical Center, 8700 Beverly Blvd, #6560, Los Angeles, CA 90048.
Background Our objectives were to quantify the thrombogenicity and extent of vascular injury created by slotted-tube geometry stainless steel and nitinol coronary stents in a rabbit carotid artery model.
Methods and Results Stents were implanted in rabbit right carotid arteries without antiplatelet therapy. Stainless steel stents were implanted for 4 days while nitinol stents were placed for 4 and 14 days (n=8, 8, and 6, respectively). Stent thrombosis was assessed by thrombus weight, grading thrombus encroachment of the lumen, and by blood flow in the stented and contralateral arteries. Stainless steel stents at 4 days contained more thrombus than 4- and 14-day nitinol stents (20.0±5.9 versus 2.5±0.6 and 2.7±0.3 mg, respectively; P<.000001). Stainless steel stents were more often occluded by thrombus (6 of 8) or contained more subocclusive thrombus (2 of 8) than nitinol stents (0 of 14, P<.002). Resting blood flow was reduced in arteries with stainless steel stents compared with 4- and 14-day nitinol stents (1.5±2.8 versus 24.0±2.0 and 25.5±1.9 mL/min, respectively, P<.000001). Stainless steel stents were less uniformly expanded, had deeper strut penetration into the vascular wall, and were associated with more extensive medial smooth muscle cell necrosis. There were strong correlations (r=.77 to .95) between variables of thrombosis extent (thrombus weight and grade) and histologically determined vascular injury (strut penetration and medial necrosis).
Conclusions Slotted-tube stainless steel stents were more thrombogenic and created more extensive vascular injury than nitinol stents in a rabbit carotid artery model. The mechanisms underlying these differences probably are related to metallurgic and design geometry properties of the two stent types.
Key Words: prosthesis angioplasty coronary artery disease revascularization stents thrombosis
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