nitinol and Carotid-Artery-Thrombosis

Carotid stump syndrome is one of the recognised causes of recurrent ipsilateral cerebrovascular events after occlusion of the internal carotid artery. It is believed that microemboli arising from the stump of the occluded internal carotid artery or the ipsilateral external carotid artery can pass into the middle cerebral artery circulation as a result of patent external carotid-internal carotid anastomotic channels. Different pathophysiologic causes of this syndrome and endovascular options for treatment are discussed.

Topics: Aged; Alloys; Angiography, Digital Subtraction; Angioplasty; Carotid Artery Thrombosis; Carotid Artery, Common; Carotid Artery, External; Carotid Artery, Internal; Coated Materials, Biocompatible; Equipment Design; Female; Humans; Intracranial Embolism; Ischemic Attack, Transient; Magnetic Resonance Angiography; Male; Middle Aged; Stents; Syndrome; Ultrasonography, Doppler, Color

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.. 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).. 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.

Topics: Acute Disease; Alloys; Animals; Carotid Arteries; Carotid Artery Injuries; Carotid Artery Thrombosis; Equipment Design; Male; Microscopy, Electron, Scanning; Necrosis; Rabbits; Stainless Steel; Stents; Tunica Media; Wounds and Injuries

Coronary stenting is associated with two major complications: subacute thrombosis and neointimal proliferation resulting in restenosis. Our hypothesis is that the biocompatibility of metallic stents can be improved by coating with a polymer membrane that delivers agents that favorably modify the local arterial microenvironment. This study evaluates the kinetics, distribution, and bioactivity of the model drug forskolin delivered to the local arterial wall by a polyurethane-coated removable metallic stent.. Stents were used in rabbit carotid arteries (n = 20) for as long as 24 hours. The quantity of forskolin bound to the stent decreased exponentially with a half-life of 5.8 hours. Blood concentrations peaked at 140 +/- 39 pg/microL at 4 hours. The adjacent arterial media contained 60 +/- 39 ng/mg, which was 380- and 460-fold greater than the contralateral carotid media and the systemic blood, respectively (P < .0001). Media forskolin concentrations declined exponentially over time with a tissue half-life of 5.0 hours. Drug distributed throughout the vessel wall with decreasing gradients in the radial and axial dimensions consistent with a diffusion process. Removal of the stent was associated with a 100-fold decline in media forskolin concentration within 2 hours. Forskolin release was associated with a sustained 92% increase in carotid blood flow and a 60% decrease in local arterial resistance compared with coated control stents (P < .005). In another set of rabbits (n = 14) using a carotid crush injury, flow-reduction model, forskolin prolonged the time to flow variation and occlusion by 12-fold compared with the use of bare metal stents and 5-fold compared with the use of polyurethane-coated stents (P < .0001).. A polymer-coated metallic stent can deliver forskolin to the local arterial wall in high concentrations relative to the blood or other tissues. High local drug concentrations are dependent on maintaining stent-to-tissue gradients. The delivered drug is biologically active, demonstrating vasodilating and antiplatelet properties.

Topics: Alloys; Animals; Carotid Arteries; Carotid Artery Thrombosis; Cerebrovascular Circulation; Colforsin; Drug Delivery Systems; Equipment Design; Half-Life; Polyurethanes; Rabbits; Stents; Time Factors; Tissue Distribution; Vascular Resistance