PURPOSE: To report a retrospective study that sought to identify clinical factors contributing to the development of in-stent restenosis in the carotid arteries, to profile the patients at greatest risk, and to review the treatment modalities evolved from our experience. METHODS: Between December 2000 and April 2003, 195 carotid angioplasty/stenting (CAS) procedures (12 bilateral) were performed in 183 patients (131 men; median age 65.9 years, interquartile range 55.2-72.7). Stenting for de novo stenoses was performed in 119 (61%) carotid arteries; 76 (39%) vessels were treated for postsurgical restenosis. Nearly two thirds of the patients (117, 64%) were symptomatic. Patients were evaluated at 3 and 6 months and at 6-month intervals thereafter with duplex ultrasonography. Angiography was used to confirm any recurrent lesion detected on the ultrasound scan. RESULTS: Overall perioperative neurological complications included 4 (2.2%) minor strokes, 1 (0.5%) intracranial hemorrhage, and 1 (0.5%) major stroke; both patients with major neurological complications died at 5 and 12 days, respectively, after the procedure. During the 12.5-month follow-up (range 0-27.2), 3 non-procedure-related late deaths and another 9 (4.9%) neurological events occurred (2 strokes and 7 transient ischemic attacks). In-stent restenosis after CAS was present in 10 (5.2%) of 193 carotid arteries (9/181 patients) in follow-up; all but 1 artery had been treated for postsurgical restenosis. All lesions were treated secondarily with endovascular procedures. Statistical analysis demonstrated that postsurgical restenosis was the only predictive factor for the development of in-stent restenosis (OR 15.5, 95% CI 2.05 to 125.6, p=0.001) in this cohort. CONCLUSIONS: The present study, far from being exhaustive on the subject, indicates that patients who develop restenosis after carotid endarterectomy are also prone to develop restenosis after CAS; moreover, although strongly recommended for postsurgical restenosis, CAS carries a greater risk of in-stent restenosis in this subgroup, thus reducing the benefits of this procedure.

Setacci, F., Pula, G., Baldi, I., DE DONATO, G., Setacci, C., Cappelli, A., et al. (2003). Determinants of in-stent restenosis after carotid angioplasty: a case-control study. JOURNAL OF ENDOVASCULAR THERAPY, 10(6), 1031-1038 [10.1583/1545-1550(2003)010<1031:DOIRAC>2.0.CO;2].

Determinants of in-stent restenosis after carotid angioplasty: a case-control study.

SETACCI, FRANCESCO;DE DONATO, GIANMARCO;SETACCI, CARLO;CAPPELLI, ALESSANDRO;
2003-01-01

Abstract

PURPOSE: To report a retrospective study that sought to identify clinical factors contributing to the development of in-stent restenosis in the carotid arteries, to profile the patients at greatest risk, and to review the treatment modalities evolved from our experience. METHODS: Between December 2000 and April 2003, 195 carotid angioplasty/stenting (CAS) procedures (12 bilateral) were performed in 183 patients (131 men; median age 65.9 years, interquartile range 55.2-72.7). Stenting for de novo stenoses was performed in 119 (61%) carotid arteries; 76 (39%) vessels were treated for postsurgical restenosis. Nearly two thirds of the patients (117, 64%) were symptomatic. Patients were evaluated at 3 and 6 months and at 6-month intervals thereafter with duplex ultrasonography. Angiography was used to confirm any recurrent lesion detected on the ultrasound scan. RESULTS: Overall perioperative neurological complications included 4 (2.2%) minor strokes, 1 (0.5%) intracranial hemorrhage, and 1 (0.5%) major stroke; both patients with major neurological complications died at 5 and 12 days, respectively, after the procedure. During the 12.5-month follow-up (range 0-27.2), 3 non-procedure-related late deaths and another 9 (4.9%) neurological events occurred (2 strokes and 7 transient ischemic attacks). In-stent restenosis after CAS was present in 10 (5.2%) of 193 carotid arteries (9/181 patients) in follow-up; all but 1 artery had been treated for postsurgical restenosis. All lesions were treated secondarily with endovascular procedures. Statistical analysis demonstrated that postsurgical restenosis was the only predictive factor for the development of in-stent restenosis (OR 15.5, 95% CI 2.05 to 125.6, p=0.001) in this cohort. CONCLUSIONS: The present study, far from being exhaustive on the subject, indicates that patients who develop restenosis after carotid endarterectomy are also prone to develop restenosis after CAS; moreover, although strongly recommended for postsurgical restenosis, CAS carries a greater risk of in-stent restenosis in this subgroup, thus reducing the benefits of this procedure.
Setacci, F., Pula, G., Baldi, I., DE DONATO, G., Setacci, C., Cappelli, A., et al. (2003). Determinants of in-stent restenosis after carotid angioplasty: a case-control study. JOURNAL OF ENDOVASCULAR THERAPY, 10(6), 1031-1038 [10.1583/1545-1550(2003)010<1031:DOIRAC>2.0.CO;2].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/2545
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