Journal of the American Heart Association · 2026
High-Shear Environment Promotes Acute Carotid Stent Thrombosis in Patients With Tandem Lesions.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Kern Axelle Y, Kreinin Yevgeniy, Charle Lise, Robert Camille, Epshtein Mark, Lucchetti Agnese, Emonts Caroline, Bolle Tim, Gries Thomas, Chakfé Nabil, Pop Raoul, Korin Netanel, Mangin Pierre H
Аннотация
BACKGROUND: Stent thrombosis is a serious complication of angioplasty with stenting, as evidenced by the associated morbidity and mortality events. Its incidence is particularly elevated after emergent carotid stenting in patients with acute ischemic stroke, reaching 20%. A better understanding of the mechanisms driving stent thrombosis will open up new avenues to limit this alarming complication. Its 2 main determinants are the ruptured atherosclerotic plaque and the stent itself, whose particular role in the process remains unknown.
METHODS: Using a new macrofluidic model mimicking the geometry of the human carotid artery, the intrinsic thrombogenicity of carotid stents was evaluated.
RESULTS: Real-time video microscopy combined with scanning electron microscopy revealed that the Casper and the Wallstent, 2 widely used commercial stents, are thrombogenic and promote the formation of a massive thrombus in the carotid bifurcation (Casper: median, 9 [interquartile range, 6.4-24.4]×105 μm2; Wallstent: median, 9.5 [interquartile range, 1.5-20.8]×105 μm2). This result was consistent with a retrospective clinical study in stented patients with tandem lesions, in which 21.1% presented stent thrombosis, and 38.7% of these cases occurred at the bifurcation. Moreover, a stent lying in the carotid bifurcation of the macrofluidic model generated a prothrombotic high-shear environment, triggering thrombosis, which was prevented in the presence of aspirin or abciximab. Finally, stents with a new design could avoid the formation of large thrombi in the carotid bifurcation (full stent: median, 8.9 [interquartile range, 7.8-17.2]×105 μm2; stent with an opening at the bifurcation: median, 2.1 [interquartile range, 1.1-3]×105 μm2), opening up the perspective of new ways to prevent carotid stent thrombosis.
CONCLUSIONS: Stents placed inside the carotid bifurcation are responsible for a massive thrombus formation that could lead to stent thrombosis. The absence of mesh prevents its formation.
METHODS: Using a new macrofluidic model mimicking the geometry of the human carotid artery, the intrinsic thrombogenicity of carotid stents was evaluated.
RESULTS: Real-time video microscopy combined with scanning electron microscopy revealed that the Casper and the Wallstent, 2 widely used commercial stents, are thrombogenic and promote the formation of a massive thrombus in the carotid bifurcation (Casper: median, 9 [interquartile range, 6.4-24.4]×105 μm2; Wallstent: median, 9.5 [interquartile range, 1.5-20.8]×105 μm2). This result was consistent with a retrospective clinical study in stented patients with tandem lesions, in which 21.1% presented stent thrombosis, and 38.7% of these cases occurred at the bifurcation. Moreover, a stent lying in the carotid bifurcation of the macrofluidic model generated a prothrombotic high-shear environment, triggering thrombosis, which was prevented in the presence of aspirin or abciximab. Finally, stents with a new design could avoid the formation of large thrombi in the carotid bifurcation (full stent: median, 8.9 [interquartile range, 7.8-17.2]×105 μm2; stent with an opening at the bifurcation: median, 2.1 [interquartile range, 1.1-3]×105 μm2), opening up the perspective of new ways to prevent carotid stent thrombosis.
CONCLUSIONS: Stents placed inside the carotid bifurcation are responsible for a massive thrombus formation that could lead to stent thrombosis. The absence of mesh prevents its formation.