全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

In-Stent Ulceration: An Unusual Pathology

DOI: 10.1155/2014/893143

Full-Text   Cite this paper   Add to My Lib

Abstract:

In-stent restenosis occurs in 10–60% of cases undergoing interventional therapy. Many mechanisms explain the reason for in-stent restenosis, but restenosis due to an ulcerated plaque is very rare and has not been well reported in the literature. We report an interesting case of 72-year-old man presenting with neurological symptoms secondary to in-stent restenosis of the carotid artery caused by an ulcerated plaque. We also explain the different mechanisms for restenosis along with the treatment options. 1. Introduction Interventional therapy has been highly impacted by the number of lesions treated with stents, which exceeds 50% of all interventional procedures. Although stents have been successful in reducing the restenosis compared to balloon angioplasty, in-stent restenosis (ISR) occurs in 10–60% of cases [1–4]. ISR can be explained by many mechanisms, but restenosis due to an ulcerated plaque is very rare and has not been reported in the literature. We report a case where a patient presented with neurological symptoms secondary to an ulcerated ISR of the carotid artery. 2. Case Report A 72-year-old Caucasian man with past medical history of diabetes mellitus, hypertension, smoking, bilateral carotid endarterectomy, and a left carotid artery stent (14 months ago) presented with symptoms of blurred vision and dizziness. He experienced very similar symptoms prior to the past carotid endarterectomy. A subsequent carotid ultrasound showed a 60–79% stenosis of his left internal carotid artery and no significant stenosis of the right internal carotid artery. Carotid angiography showed an eccentric stenosis in the left internal carotid artery at the stent site with a crater/ulcer within the restenosis tissue inside the stent (Figure 1(a)). An Accunet 6.5 filter (Abbott Vascular, Santa Clara, CA) was deployed distal to the stent in the left internal carotid artery. Later, an Acculink (Abbott Vascular) ?mm self-expanding stent was deployed successfully. Postdeployment angiograms revealed brisk flow with no evidence of embolization into the filter, but the ulcerative nature of the crater continued to be present. Balloon dilatation was performed in the mid-portion of the stent after which residual stenosis was approximately 10% with minimal visualization of the crater-like lesion (Figure 1(b)). After successfully retrieving the filter device, final angiograms of cervical and cerebral arteries revealed brisk flow with no evidence of distal embolization maintaining patency of the middle cerebral and anterior cerebral circulation. At the 3-, 6-, 12-, and 24-month

References

[1]  P. W. Serruys, P. De Jaegere, F. Kiemeneij et al., “A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease,” The New England Journal of Medicine, vol. 331, no. 8, pp. 489–495, 1994.
[2]  D. L. Fischman, M. B. Leon, D. S. Baim et al., “A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease,” The New England Journal of Medicine, vol. 331, no. 8, pp. 496–501, 1994.
[3]  F. V. Till, D. Aliabadi, J. W. Kinn, B. M. Kaplan, K. H. Benzuly, and R. D. Safian, “Real life stenting: a comparison of target vessel revascularization in Benestent-Stress lesions to non Benestent-Stress lesions,” Circulation, vol. 94, supplement 1, pp. 1–332, 1996.
[4]  S. H. Fenton, D. L. Fischman, M. P. Savage et al., “Long-term angiographic and clinical outcome implantation of balloon-expandable stents in aortocoronary saphenous vein grafts,” American Journal of Cardiology, vol. 74, no. 12, pp. 1187–1191, 1994.
[5]  P. S. Teirstein, V. Massullo, S. Jani et al., “Catheter-based radiotherapy to inhibit restenosis after coronary stenting,” The New England Journal of Medicine, vol. 336, no. 24, pp. 1697–1703, 1997.
[6]  A. K. Mitra and D. K. Agrawal, “In stent restenosis: bane of the stent era,” Journal of Clinical Pathology, vol. 59, no. 3, pp. 232–239, 2006.
[7]  P. Libby and D. I. Simon, “Inflammation and thrombosis: the clot thickens,” Circulation, vol. 103, no. 13, pp. 1718–1720, 2001.
[8]  F. Cipollone, M. Marini, M. Fazia et al., “Elevated circulating levels of monocyte chemoattractant protein-1 in patients with restenosis after coronary angioplasty,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 21, no. 3, pp. 327–334, 2001.
[9]  B. J. Rollins, “Chemokines,” Blood, vol. 90, no. 3, pp. 909–928, 1997.
[10]  C. Setacci, G. de Donato, F. Setacci et al., “Safety and feasibility of intravascular optical coherence tomography using a nonocclusive technique to evaluate carotid plaques before and after stent deployment,” Journal of Endovascular Therapy, vol. 19, pp. 303–311, 2012.
[11]  N. Tamakawa, H. Sakai, and Y. Nishimura, “Evaluation of carotid artery plaque using IVUS virtual histology,” Interventional Neuroradiology, vol. 13, no. 1, pp. 100–105, 2007.
[12]  E. Eeckhout, J.-J. Goy, J.-C. Stauffer, P. Vogt, and L. Kappenberger, “Endoluminal stenting of narrowed saphenous vein grafts: long-term clinical and angiographic follow-up,” Catheterization and Cardiovascular Diagnosis, vol. 32, no. 2, pp. 139–146, 1994.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133