We read the meta-analysis of Kern et al. on carotid artery stenting (CAS) with great interest.1 The introduction of percutaneous angioplasty for stenosed or occluded arteries by Andreas Gruentzig in 1977 revolutionized the practice of cardiovascular medicine.2 Similarly, the introduction of stents has improved the effectiveness of percutaneous interventions by preventing elastic recoil and restenosis, thereby leading to improved patency rates for revascularized arteries.3 The 'unblocking' of obstructed arteries seems a logical approach when the obstruction of flow resulting from the stenotic atherosclerotic plaque underlies the clinical, atherosclerosis-related event. The clinical success of coronary angioplasty and stenting has demonstrated that this is a sound concept. When the atherosclerotic complications are related to events involving atherothrombotic emboli rather than limited blood flow, however, angioplasty and stenting might not be suitable treatment modalities. Cerebrovascular events relating to carotid artery plaques are mostly linked to atherothrombotic emboli from the carotid plaque that cause occlusion—often temporary—of downstream intracranial arteries. The extracranial arteries supplying the brain are generally interconnected with extensive collateral networks. In view of this rich collateral circulation, restoration of blood flow in a stenosed carotid artery is often unnecessary. The proven benefits of carotid endarterectomy might therefore be attributable to removal of a source of potential atherothrombotic emboli. Indeed, complete carotid occlusions do not warrant any revascularization procedures.
The majority of atherosclerotic plaques consist of a fibrous cap overlying a lipid–necrotic core isolating the highly thrombogenic necrotic plaque content from the circulation (American Heart Association [AHA] type IV and V atherosclerotic plaques). Balloon angioplasty and stenting result in surface disruption, intimal dissections and fragmentation of the plaque, thereby restoring normal lumen size. This procedure, however, exposes thrombogenic plaque content to the blood, and almost invariably results in thrombus deposition at the angioplasty site.4 In the case of carotid artery angioplasty and stenting, this could have severe adverse consequences. Indeed, among 162 patients undergoing CAS, mostly for symptomatic disease, 28 patients (17%) developed 58 new (mostly asymptomatic ) ischemic lesions detected on diffusion-weighted MRI of the brain.5 Bosiers et al. have shown that post-interventional transient ischemic attacks and strokes are related to carotid stent free cell area, which relates to the area of uncovered fragmented plaque matter. This was shown to be true especially for patients treated for symptomatic, as opposed to asymptomatic, carotid lesions.6 In addition, the data from the EVA-3S trial might also underscore the clinical significance of the above-described vascular biological scenario, as stenting of symptomatic carotid plaques resulted in a prohibitively high incidence of post-procedural neurological events.7
Minimizing free cell area or even completely covering the fragmented plaque with a covered stent might represent a way to increase the safety of carotid percutaneous interventions. Furthermore, it is conceivable that only certain types of plaques such as calcified (AHA type VII) or fibrotic (AHA type VIII) plaques are suitable for carotid stenting. Hence, identification of plaque morphology suitable for carotid stenting, using pre-procedural ultrasound or other noninvasive scanning methods, such as MRI, becomes mandatory.
Acknowledging the importance of atherothrombotic embolization in the development of clinical events relating to carotid artery disease and stenting might help in the development of new strategies that will improve the efficacy and safety of CAS for patients with carotid artery disease.
Kern R et al. (2007) Stenting for carotid artery stenosis. Nat Clin Pract Neurol 3: 212–220
Gruentzig A et al. (1979) Nonoperative dilatation of coronary-artery stenosis: percutaneous transluminal coronary angioplasty. N Engl J Med 301: 61–68
Sigwart U et al. (1987) Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty. N Engl J Med 316: 701–706
Bauters C et al. (1996) Morphological changes after percutaneous transluminal coronary angioplasty of unstable plaques. Insights from serial angioscopic follow-up. Eur Heart J 17: 1554–1559
Pinero P et al. (2006) Silent ischemia after neuroprotected percutaneous carotid stenting: a diffusion-weighted MRI study. AJNR Am J Neuroradiol 27: 1338–1345
Bosiers M et al. (2007) Does free cell area influence the outcome in carotid artery stenting? Eur J Vasc Endovasc Surg 33: 135–141
Mas JL et al. (2006) Endarterectomy versus stenting in patients with symptomatic severe carotid stenosis. N Engl J Med 355: 1660–1671
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Vainas, T., Sayed, S., Cuypers, P. et al. Carotid stenting: looking beyond the degree of carotid stenosis. Nat Rev Neurol 3, E1 (2007). https://doi.org/10.1038/ncpneuro0561