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Carotid artery stenting: where are we up to with evidence‐based practice?

Interventions for carotid artery stenosis are among the most analysed in the history of surgery. Since the advent of endovascular technology and its application to carotid artery angioplasty and stenting (CAS) there have been many randomized trials comparing CAS with carotid endarterectomy (CEA), and numerous interpretations of the data; with contemporary studies utilizing techniques of rapid exchange technology for angioplasty and stenting, with or without the use of cerebral protection devices (CPD). Some new facet of information was gleaned from each of these trials, which requires careful consideration and analysis in order to incorporate such knowledge into our overall strategy for stroke prevention. In this commentary, we seek to assess and evaluate the evidence for the role of CAS in contemporary practice. In the Endarterectomy versus Angioplasty in patients with Severe Symptomatic Carotid Stenosis (EVA-3S) trial at 4 years, the overall probability of peri-procedural stroke/death, or non-procedural ipsilateral stroke was 11.1% for the CAS patients versus 6.2% for CEA. There was also no requirement to use embolic CPD in this trial as this was left to the discretion of the proceduralist, but in the EVA-3S, there was also a significantly lower risk of stroke or death in the CAS group, for those treated using CPD (7.9 versus 25%). This study was mainly criticized for the loose credentialing of specialists as CAS proceduralists, compared with CEA surgeons, but was also unique in that the most experienced CAS interventionalists (>50 carotid stent procedure) had the highest rate of procedural stroke (12.2%). In the Stent-protected Angioplasty versus CEA in symptomatic patients study (SPACE), the authors concluded that the trial failed to prove non-inferiority of CAS compared with CEA for the periprocedural complication rate. SPACE also concluded that restenosis was more common with CAS, which may be symptomatic. In a post-hoc analysis, the 30-day rate of ipsilateral stroke and death in patients undergoing CAS was lower in patients <68 years of age, compared with those >68 years; conversely, for CEA the 30-day rate of ipsilateral stroke and death was lower in older patients. In the International Carotid Stenting Study (ICSS), the 30 days risk of stroke, death or myocardial infarction (MI) was 7.4% CAS versus 4.0% CEA (P < 0.003), at 3 months this was 8.5 versus 5.2% (P < 0.006). The ICSS also included a magnetic resonance imaging (MRI) sub-study on 231 patients (124 CAS, 107 CEA) before and after treatment, new diffusion-weighted imaging (DWI) white matter lesions were noted in CAS patients who had a fivefold increased risk (hazard ratio (HR) 5.2 (95% confidence interval (CI) 2.8–9.8; P < 0.0001) ). Little is known about the prognostic implications of new ischaemic lesions (silent brain infarcts) after CAS or CEA. It is unknown whether these subclinical MRI lesions will produce structural damage to the brain or cause neuropsychological deterioration. The most likely cause of such lesions is embolization of atherosclerotic plaque material to the cerebral circulation in the ipsilateral hemisphere, perhaps as a result of manipulation of, dissection or use of shunt in CEA; and use of guidewires, sheaths, filters and stents in the ipsilateral carotid artery, and also in the aortic arch for contralateral new lesions in CAS. In a systematic review of cognitive performance, De Rango and colleagues found that there are no data indicating a cognitive change after CAS or CEA in patients who do not experience stroke complications, even if new silent embolic lesions, especially after CAS, were detected on cerebral imaging. However, Vemeer and colleagues in a longitudinal study (mean 3.6 years follow-up) found that the presence of silent brain infarcts on MRI at baseline in the general population doubled the risk of dementia, and that people with silent infarcts had a steeper decline in cognitive function than those without silent infarcts, but this decline was confined to people who had additional silent brain infarcts after baseline. They also demonstrated that the relation between infarcts and cognitive decline was stronger for multiple infarcts than for single infarcts and may also be reflected in a stepwise deterioration. Silent infarcts in the thalamus are associated with a greater decline in memory performance, whereas infarcts located elsewhere resulted in a greater decline in psychomotor speed. White matter lesions also predicted fall-related fractures and hospitalization, with an HR of 6.8 (95% CI: 1.5–30, P = 0.013). In the Carotid Revascularization, Endarterectomy versus Stent Trial (CREST), overall, the combined periprocedural risk (including symptomatic, and asymptomatic patients) of any death, stroke, or MI (also including asymptomatic ‘biochemical MI’) was not significantly different between CAS versus CEA (5.2 versus 4.5%, HR:1.18, P < 0.38). However, in symptomatic patients this was 6.0% CAS versus 3.2% CEA, stroke/death, HR 1.9 (95% CI: 1.1–3.2), and 2.5% CAS versus 1.4% CEA, HR 1.9 (95% CI: 0.8–4.4) for asymptomatic patients; an almost doubling of the risk of stroke and death from CAS. When MI was included, stroke/death and MI occurred in CAS (6.7%) versus CEA (5.4%) (HR 1.3 (95% CI: 0.8–2.0) for symptomatic patients, and CAS (3.5%) versus CEA (3.6%) (HR 1.0 (95% CI: 0.6–1.9) for asymptomatic patients. But what does a biochemical MI mean, and does biochemical MI confer a significantly worse prognosis for patients? In vascular surgery patients, elevated levels of troponin I (Tn I) in the early post-operative period was found to be associated with a sixfold increase in mortality at 6 months. In a similar project involving 447 vascular surgery patients, an elevated creatine kinase-MB fraction in the postoperative period was associated with a fourfold increase in late mortality, while elevated Tn I was associated with a twofold increase in late mortality. And, higher-quartile levels of Tn I were associated with higher mortality rates during follow-up. After emergency orthopaedic surgery, a high incidence of Tn I increases were noted and found to correlate to significantly worse mortality and cardiac events at 1 year. Troponin increases were asymptomatic, and there was no evidence that intervention improved outcome. In the Carotid Stenting Trialist Collaboration (CSTC; using pooled individual patient data from EVA-3S, SPACE, ICSS), with 486 Perspectives