Why CMS should still not extend reimbursement indications for carotid stenting or other carotid ‘revascularization’ procedures

This commentary—authored by Anne Abbott, PhD, MBBS, Lawrence Schott, MD, Lan Gao, MMed, PhD, Hrvoje Budincevic, MD, PhD, Rishad Faruqi, MD, Tatjana Rundek, MD, PhD, Jean-Baptiste Ricco, MD, PhD, Saeid Shahidi, MD, and Gert J. de Borst, MD, PhD—consists of a multinational, multispecialty, multidisciplinary updated evidence review and policy advice, which was published on the U.S. Centers for Medicare & Medicaid Services (CMS) website on Aug. 8, 2023. This review and policy advice was prompted by CMS’ proposed decision to fund “free-for-all” carotid artery “stenting” procedures in any American aged at least 65 years, on certain disability benefits and/or with end-stage renal failure who is determined as having at least “50” or “70%” carotid stenosis (despite no accurate and reproducible method of classifying degree of carotid stenosis). This manuscript is based on a longer group submission posted on the CMS website in February 2023. 

We classify the types of misinformation being used to errantly push U.S. Medicare to expand reimbursement indications for carotid artery stenting (CAS) and a new hybrid procedure known as transcarotid arterial revascularization (TCAR). This is already an environment with too many unnecessary carotid procedures done in the name of stroke risk reduction. Founding members of the Faculty Advocating Collaborative and Thoughtful Carotid Artery Treatments (FACTCATS) explained in 2012 why reimbursement indications for CAS should not be expanded.^1,2 The fundamental reasons were higher risks with CAS (stroke, death and myocardial infarction) compared to carotid endarterectomy (CEA) and declining carotid procedural indications due to greatly improved non-invasive stroke risk reduction methods. The situation has not changed, except that the excessive hazards with stenting are clearer, non-invasive medical intervention for stroke risk reduction has improved further and the safety and efficacy of TCAR remain unproven. Once again, we advise that expanding reimbursement indications for carotid procedures “would have serious negative health and economic repercussions for the USA and any other country that may follow such inappropriate action.”¹

Introduction 

Since 2005, CMS has limited carotid stenting (CAS) reimbursement indications to individuals considered at high-risk from carotid surgery (carotid endarterectomy, CEA) who are symptomatic with >70% carotid stenosis and to other high-CEA-risk patients if used in appropriate studies (those with 50-70% stenosis if symptomatic or >80% stenosis if asymptomatic).³ High-CEA-risk is defined by CMS as having major comorbidities and/or anatomic risk factors (including current life-threatening cardiac conditions).³ The definition is open to interpretation. CMS also created minimum standards upon which CAS coverage (reimbursement) is dependent.³

As per the January 2023 online CMS announcement,⁴ a “multispecialty alliance” (the “Alliance”) asked that CMS:

• Expand CAS reimbursement indications to all individuals with >70% asymptomatic carotid stenosis and any symptomatic person with >50% stenosis (including those not considered high-CEA-risk)
• Eliminate the minimal standards for facility requirements
• Leave coverage for any CAS procedure (including TCAR) not described by the CMS National Coverage Determination (NCD) to the discretion of the local Medicare Administrative Contractors

Founding members of FACTCATS published evidence reviews and advice to U.S. Medicare in 2012 and 2013 outlining why reimbursement indications for CAS should not be expanded.^1,2 The main reasoning then was the higher risk of stroke and death with CAS compared to CEA, as well as declining carotid procedural indications due to greatly improved non-invasive stroke risk reduction methods (risk factor identification and amelioration using lifestyle interventions and medication). The situation has not changed, except that the excessive hazards with CAS are clearer, non-invasive medical intervention for stroke risk reduction has improved further and the safety and efficacy of TCAR remain unproven.^5–10

CMS reimbursement indications were not expanded following the 2012 Medicare Evidence Development & Coverage Advisory Committee (MEDCAC) meeting.⁵ The results have been greatly limited access to procedural “carotid revascularization” by non-surgically trained practitioners, the saving of up to several million older Americans from unnecessary, excessively dangerous carotid procedures, the saving of up to at least 60 billion American healthcare dollars and an excellent global health policy example.^5,11 This analysis is a cut-down version of our updated evidence review and policy advice for CMS that was publicly posted Feb. 10, 2023, with 71 co-signatories.

The Alliance used an online letter to CMS and a 2022 review article as the case for ‘new evidence’ supporting expansion of reimbursement indications for CAS, TCAR and any other procedure they may consider under the umbrella of CAS in the future.^4,12,13 However, the case for expansion consists of misinformation favoring procedural over-use and lacks a cost-effectiveness analysis. We have classified the most important forms of misinformation encouraging procedural overuse into four types: factual errors (untrue statements), fact distortion (a fact is conveyed then misconstrued), omitted information (omission of information relevant to clinical decision making) and speculation. We would like to emphasize that we are not targeting individuals, rather we are addressing misinformation. Further, this misinformation is common in the medical literature.

Factual errors

1. CAS is not equivalent, or noninferior, to CEA as claimed^12,13

CAS is more dangerous for patients than CEA. In every adequately powered randomized trial comparison, CAS (when used for primary or secondary stroke risk reduction) was associated with approximately 1.5–2 times as many peri-procedural strokes or deaths as CEA.⁵ Several individual randomized trials of symptomatic patients showed a statistically significant higher periprocedural rate of stroke or death from CAS compared to CEA (including the International Carotid Stenting Study [ICSS], the Carotid Revascularization Endarterectomy vs. Stenting Trial [CREST-1], and the Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis [EVA-3-S] trial).⁵ Registries and administrative databases have also consistently shown higher periprocedural rates of stroke or death with CAS compared to CEA.^2,5,14

By contrast, no individual randomized trial of CAS versus CEA in patients with asymptomatic (or recently asymptomatic) carotid stenosis has been sufficiently powered for this comparison because of low event rates and, hence, the requirement for larger study samples.^5,15,16 Underpowered trials involving asymptomatic patients include the 2^nd Asymptomatic Carotid Surgery Trial (ACST-2), published in 2021.^17,18 However, all individual randomized trials of asymptomatic, or recently asymptomatic patients, with more than 200 subjects have shown trends towards more periprocedural stroke or death with CAS than CEA. For example, in ACST-2, the odds ratio (OR) for 30-day peri-procedural death or stroke with CAS versus CEA was 1.35 (95% confidence interval [CI] 0.91–2.03). The comparison reached statistical significance in a 2019 meta-analysis of randomized trials (eight trials and 3,467 patients: OR 1.64, 95% CI 1.02–2.64)¹⁵ and borderline significance in a 2020 meta-analysis of randomized trials (seven trials and 3,378 patients: OR 1.72, 95% CI 1.00–2.97).¹⁶

In randomized trials, myocardial infarction was generally less common with CAS than CEA. However, where published, in randomized trials of CAS versus CEA involving symptomatic and/or asymptomatic patients, peri-procedural stroke (mostly caused by CAS) was overall 4.6 times more common than clinically defined myocardial infarction.¹⁹ Further, periprocedural death was 34% higher with CAS and periprocedural stroke, death, and clinically defined myocardial infarction were 1.6 times more common after CAS than CEA.^5,19 The difference in this latter, triple-composite outcome measure reached statistical significance in meta-analyses involving symptomatic patients.^5,15,16

There are still insufficient randomized trial data to adequately power this triple-composite comparison for asymptomatic patients.^5,15,16 However, randomized trial results indicate that it is highly likely that if CAS is rolled out into routine practice (involving many more asymptomatic patients than in trials with/or without lower procedural standards) it would cause significantly more strokes, deaths and myocardial infarctions than CEA. That would be clinically and economically highly significant.⁵

Further, in adequately powered randomized trial comparisons, rates of periprocedural stroke or death and later ipsilateral stroke have been higher with CAS compared to CEA for as long as patients have been followed up.⁵ Rates of new ipsilateral stroke beyond the periprocedural period were generally similar with each procedure. This indicates that patients who have a periprocedural stroke tend to live long-term with their stroke. Meanwhile, those that die in the periprocedural period do not recover. Therefore, compared to CEA, the harm from CAS is durable.⁵ Differing results have been reported with respect to ‘protection devices’ for lowering the CAS-associated risk of stroke or death.⁵ Further, severe carotid re-stenosis is more common after CAS than CEA and CAS tends to cost more.^20,21 Complications (apart from stroke and death) that are more likely with, or particular to, CAS compared to CEA include hemodynamic instability (severe hypotension or bradycardia, including the need for a permanent pacemaker) and retroperitoneal haemorrhage.⁵

2. Age is not the only risk factor for harm from CAS as claimed^12,13

In randomized trials, CAS has not been shown to be more beneficial than CEA or non-invasive medical intervention alone in any subgroup of patients. Particularly vulnerable to stroke from CAS compared to CEA are:

• The most senior patients (aged >70 years). Randomized trial comparisons in younger patients have been underpowered, probably because of lower event rates and less representation⁵
• Those who are most recently symptomatic (especially within the previous 7–14 days, which is when best practice CEA is most likely to be beneficial)^5,22
• Women. However, men are also at higher risk of stroke or death from CAS compared to CEA⁵
• Those with certain carotid anatomical features, such as longer, angulated, or tandem lesions⁵
• Those who have CAS in low volume centers or outside trials⁵
• Regression of carotid plaque has been seen from non-invasive medical intervention alone, in contrast to what was claimed^12,13

Studies have shown that statin and ezetimibe therapy can cause carotid plaque regression and content stabilization.^23-28 Moreover, statins, ezetimibe and PCSK9 inhibitors reduce the risk of stroke and other arterial disease morbidity and mortality whether or not individuals undergo a carotid artery procedure.^29–31

Fact distortion

1. Inappropriate dismissal of ‘minor’ or ‘nondisabling’ strokes in attempt to justify CAS^12,13

The most severe or fatal periprocedural strokes are usually defined as being associated with a modified Rankin score of >3.⁵ Fortunately, severe strokes are less common than milder strokes. A well-recognized method of falsely claiming equivalence between CAS and CEA is to ignore milder strokes.¹⁹ However, this distorts the facts in two ways. Firstly, so-called ‘minor’ strokes may impose significant disability and reduced quality of life and should not be discounted.^32,33 Secondly, past randomized trials of CAS versus CEA were underpowered to compare the peri-procedural rate of the most severe strokes. Therefore, it is incorrect to claim that CAS and CEA are similar with respect to causing severe strokes.⁵

2. Inappropriate use of periprocedural myocardial infarction to justify CAS^12,13

As explained above, in all adequately powered randomized trial comparisons, CAS was associated with significantly more periprocedural stroke, death and clinically defined myocardial infarction than CEA.^15,16,19 However, because myocardial infarction was often more frequent with CAS than CEA in randomized trials, including it in a primary outcome measure with stroke and death means the adverse outcomes are more evenly distributed between CEA and CAS. Therefore, larger sample sizes are required to show statistically significant procedural differences. As explained above, this has been achieved in meta-analyses of randomized symptomatic patients.^15,16 Underpowered triple-composite outcome comparisons camouflage the statistically significant higher periprocedural rate of stroke or death with CAS compared to CEA. “No statistically significant difference” is often due to underpowering, and this is demonstrated with meta-analyses involving larger subject numbers.^5,15,16,19

3. Inappropriately using the SAPPHIRE trial to justify CAS in high-CEA-risk patients^12,13

The Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial was inappropriate to determine a role for carotid artery procedures in individuals considered at high-CEA-risk because it lacked a non-invasive-treatment-only option.³⁴ Performing randomized trials of only procedures and concluding that a procedure is best, or indicated, constitutes procedural bias.^19,35 Outcomes with non-invasive treatment alone have not been measured in these patients. Further, high-surgical-risk medical comorbidities (such as unstable angina, congestive cardiac failure and advanced age) identify individuals with high rates of procedural complications and not likely to live long enough to benefit from a carotid artery procedure.^36-40 Interestingly, patients deemed high-CEA-risk using CMS criteria do not appear better off with CAS compared to CEA.⁴¹

The SAPPHIRE trial had other major limitations for applicability in clinical practice. It included myocardial infarction in the primary outcome measure (the pitfalls of this are described above). Further, myocardial infarction was unusually defined as a “creatinine kinase level >2 times the upper limit of normal with a positive myocardial band (MB) fraction.”³⁴ However, elevated cardiac enzymes are not necessarily indicative of significant heart damage, are not rare after non-cardiac surgery, and are perhaps more common after CEA than CAS.^42-44 Further, the SAPPHIRE sample size was very small (334, 70% asymptomatic) with only 17 total 30-day periprocedural strokes or deaths (OR for CAS versus CEA: 0.9, 95% CI 0.3–2.3) and 55 total strokes or deaths by one year (OR for CAS versus CEA: 0.6, 95% CI 0.3–1.1). The trial was underpowered, particularly with respect to analysis of asymptomatic and symptomatic patients separately. As far as we know, the SAPPHIRE trial is the only randomized procedural trial of high-CEA-risk patients.^12,13 SAPPHIRE’s limitations, and unknown outcomes with current best practice non-invasive treatment alone, underscore the lack of evidence supporting a procedural approach in “high-surgical-risk” individuals and an outstanding over-reliance on SAPPHIRE in health policy and guidelines.⁴⁵

4. Inappropriately using outdated and overreaching guidelines to justify CAS^12,13

It is inappropriate to cite outdated procedural standards (such as a 30-day periprocedural stroke or death rate <2–3% for asymptomatic carotid stenosis patients or <6% for stroke or TIA patients with carotid stenosis) to encourage ongoing routine use of carotid artery procedures, let alone reimbursement expansion. The randomized trials upon which such guidelines and standards are based are long outdated due to ongoing advances in non-invasive stroke prevention.^5,45 Further, prevailing guidelines encourage carotid artery procedures for many more patient subgroups than have ever been shown to benefit (see below).^5,45

5. Patient choice in treatment decisions^12,13

The Alliance repeatedly referred to patient choice, or preference, as a reason to expand reimbursement indications. Patient preference, and informed consent, are prerequisites for any medical intervention.⁴⁶ This is usually the last “bastion” in protecting patients.⁴⁶ However, patient preference strongly depends on the way information is presented (or omitted). This has already been demonstrated with decision-making in asymptomatic carotid stenosis patients.⁴⁷ This demonstrates the importance of how physicians talk to patients. Meanwhile, “shared decision-making” could be a way of making patients take responsibility for treatment that, rather than help, is more likely to harm them.

Omitted information

1. Implications of improved non-invasive risk reduction^12,13

The efficacy of any carotid procedure in stroke risk reduction can only be established using sufficiently powered comparisons against current best practice non-invasive medical intervention alone (healthy lifestyle habits and appropriate medication). This point was consistently missed by the Alliance. Mention was made in the 2022 review of very low (approximately 1%) annual stroke rates in asymptomatic carotid stenosis patients leading to new trials (CREST-2 and the 2nd European Carotid Surgical Trial [ECST-2]) comparing procedures to non-invasive treatment alone.¹³ In the Alliance letter of request, “expanded” non-invasive medical intervention was deemed “experimental,” instead of the gold standard against which all procedures should be compared.^5,12

The ‘Alliance’ advocating for expansion of CAS reimbursement neglected to explain an evidence base showing that stroke rates have dropped by >50-65% with non-invasive care alone in asymptomatic and symptomatic individuals with carotid stenosis, and other cerebrovascular disease populations, since all past randomized trials of CEA versus non-invasive treatment alone.^{5,7,8,48–53} The Alliance did not mention that these outstanding achievements with non-invasive care mean that there is no current evidence of patient benefit from any carotid procedure. However, there are ongoing reported rates of periprocedural stroke or death of >1–6%.¹⁴ Even if procedural stroke and death rates of consistently zero were possible, this is insufficient to justify carotid procedures in the absence of a clinically significant benefit compared to current best-practice non-invasive care alone.^5,54

2. Degree of 50–99% asymptomatic carotid stenosis does not justify a procedure^12,13

The Alliance cited a recent Oxford Vascular Study publication describing how patients with 80–99%, compared to 50–79%, asymptomatic carotid stenosis had a higher ipsilateral stroke rate.^12,13,55 However, they did not explain that the highest average annual ipsilateral stroke rate seen in that study approximated only 3%, not high enough to ensure a procedural benefit if Asymptomatic Carotid Atherosclerosis Study (ACAS) results are used as an indicator.^51,54,56 Furthermore, they neglected to explain that the non-invasive stroke prevention treatment used in that study (and particularly in the associated meta-analysis studies) was suboptimal. Therefore, it is highly likely that the 3% average annual ipsilateral stroke rate is higher than that achievable with current best practice non-invasive care alone.⁵⁴

3. TCAR has not been shown to be as safe as CEA or more effective than non-invasive care^12,13

Even with large numbers of registry patients, there is no clear evidence that TCAR is as safe as CEA in terms of the risk of stroke or death, at least in standard-surgical-risk patients.^32,57–61 TCAR (like CEA) appears to be safer than CAS in the Vascular Quality Initiative (VQI) registry ^57–59 However, definitive interpretation of TCAR studies is impossible because of underpowering, lack of randomization, mismatch in patient comorbidity loads, combined patient symptomatic status, predominance of asymptomatic patients, retrospective interrogation and lack of comparison with current best practice non-invasive care.^9,10,61,62 CEA remains the safest carotid revascularization procedure and should still be considered in selected symptomatic patients.^5,10 However, patients and their carers need to understand that the evidence for an overall CEA benefit compared to non-invasive care alone was collected decades ago and needs re-evaluation.^5,63

4. Differentiating ‘asymptomatic’ and ‘symptomatic’ and those shown to benefit^12,13

The Alliance request expansion of reimbursement in “selected candidates.” However, no details are provided about how to select patients. Definitions are not given for asymptomatic or symptomatic patients or for categorizing degree of carotid stenosis.^12,13Further, the Alliance omitted to explain the patient subgroups ever shown to have an overall benefit from a procedure (only CEA) compared to non-invasive treatment alone in randomized trials.^48–51,64 The overall CEA benefit was small (approximately 1%/year for asymptomatic/recently asymptomatic carotid stenosis patients and up to approximately 3.2%/year for symptomatic patients with ipsilateral carotid stenosis).⁵ Further, patients had to satisfy all trial selection criteria, have a life expectancy of at least 3–5 years and fit into one of the four following groups:⁵

• Men aged <75–80 years with 60–99% asymptomatic (or recently asymptomatic) carotid stenosis (defined using conventional intra-arterial angiography or ultrasound and North American Symptomatic Carotid Endarterectomy Trial [NASCET] criteria)^51,64
• Symptomatic Women with 70–99% stenosis (defined using conventional intra-arterial angiography and NASCET criteria and without near occlusion) having CEA within 2–3 weeks of their last same-sided non-severe stroke or TIA)⁶⁵
• Symptomatic Men with 50–69% stenosis (defined using conventional intra-arterial angiography and NASCET criteria) having CEA within 2–3 weeks of their last same-sided non-severe stroke or TIA⁶⁵
• Symptomatic Men with 70–99% stenosis (defined using conventional intra-arterial angiography and NASCET criteria and without near occlusion) having CEA within 3 months of their last same-sided non-severe stroke or TIA. However, the CEA benefit fell rapidly over this time and was highest within the first 2–3 weeks⁶⁵

There has never been evidence of procedural efficacy for any other subpopulation of carotid stenosis patients. Further, evidence for the groups defined above is outdated. A “lean to” approach with respect to procedural reimbursement (or “access”) in other subpopulations is inappropriate, given the large numbers of additional implicated patients, and especially when there is evidence of net harm.⁵ Prevailing policy should be reevaluated with appreciation of the health and economic importance of appropriate “exnovation” and independent monitoring of outcomes with all treatment modalities (procedural and nonprocedural).^5,66 Further, it needs to be recognized that a randomized trial is not always needed to answer clinical question. For example, if ipsilateral stroke rates associated with carotid arterial disease are clearly sufficiently close to zero with non-invasive care alone, then randomized procedural trials are not required.⁵

5. Categorizing degree of stenosis (and risk) has changed, and is fraught with error^12,13

The dominant method of measuring carotid stenosis in previous randomized trials was catheter-based digital subtraction angiography and the NASCET criteria for stenosis.⁶⁷ Ultrasound was used to some extent in ACAS and was used in ACST-1 (the 1^st Asymptomatic Carotid Surgery Trial).^51,64 However, most arterial imaging is now non-invasive. Furthermore, there is inherent error with each imaging modality and correlation is far from perfect.^5,68,69 Concerningly, angiography using magnetic resonance imaging and computed tomography, and “real world” operators, tend to overestimate carotid stenosis severity, encouraging procedural overuse.^70–72 Changes in imaging methodology for categorizing degree of carotid stenosis and measuring risk, along with major advances in noninvasive care and the lack of enforcement of procedural standards outside trials, are major reasons why the original randomized trials of CEA versus non-invasive intervention alone are outdated and/or non-applicable, and the Alliance requests are inappropriate.^5,73–75

Speculation

It is speculation that outcomes with CAS may improve.^12,13 This speculation is not relevant to funding decisions currently under discussion. In fact, the evidence base indicates that CAS (at least by the transaortic route) should be avoided.

Conclusions

In summary, rather than expansion, the evidence base clearly demonstrates that it is time for exnovation when it comes to reimbursement indications for carotid artery procedures.⁶⁶ There are many reasons, and any reason alone could lead to net patient harm:⁵

1. Prevailing guidelines advocate for carotid procedures on many more subgroups than have ever been shown to benefit.
2. CAS is more dangerous than CEA, and TCAR has not been shown to be as safe as CEA.
3. Procedural complication rates, when measured, are usually higher in practice than in trials.
4. There is no current randomized trial evidence of carotid procedural benefit for any patient subgroup compared to current best practice non-invasive care alone. Further, all patients should receive current best practice non-invasive care. Plus, randomized trials are not required to answer every clinical question. For example, if ipsilateral stroke rates are clearly sufficiently close to zero with non-invasive care alone, then randomized procedural trials in such patients are unnecessary and may be unethical.
5. Methods of categorizing carotid stenosis have changed and lack reproducibility.
6. Routine procedural reimbursement blocks new, critically needed research (such as CREST-2 and the Stent-Protected Angioplasty in Asymptomatic Carotid Artery Stenosis vs. Endarterectomy [SPACE-2] trial) to assess carotid procedural efficacy against non-invasive care alone.^5,76
7. Healthcare system sustainability in the U.S. (and elsewhere) is threatened by rising costs, including from poor quality care.^77,78

CMS, and other payers of health services, are key in protecting patients and healthcare resources. This is particularly pertinent in an environment already compromised by misinformation and self-serving practices.^35,79,80 Overuse of carotid artery procedures is a global problem driven by entrenched misdirected incentives.^5,81,82 It can be overcome by redirecting wasted resources to effective interventions, new research, and establishing outcomes-based, rather than activity-based, medicine.^5,83 Patient welfare focused medicine requires putting aside pressure from those likely to gain directly or indirectly, in terms of funds and/or popularity, and objectively sorting the scientific facts. Further, it means insisting on independently maintained clinical standards which ensure healthcare excellence, free from conflict of interest, and which protect patients from harmful or unproven treatment.

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Anne Abbott is a neurologist in the Department of Neuroscience at Central Clinical School, Monash University, in Melbourne, Australia. She has received several grants for independent research on the topic of stroke prevention. However, she was not academically funded at the time of creating this manuscript. She is also the founding member of FACTCAT. All authors, and most co-signatories, are FACTCAT members. The views of particular FACTCATs do not necessarily reflect the views of others. Lawrence Schott, MD, is a retired neuroradiologist, in Ireland and was the medical officer (2000–2013) for the Coverage and Analysis Group (CAG), Office of Clinical Standards and Quality (OCSQ), at CMS, and the lead medical officer, Medicare Evidence Development & Coverage Advisory Committee (MEDCAC), Management of Carotid Atherosclerosis, Jan. 25, 2012. Lan Gao, MMed, PhD, is a senior lecturer in health economics at the Institute for Health Transformation, School of Health & Social Development, Deakin University, in Melbourne, Australia. Hrvoje Budincevic, MD, PhD, is head of the Stroke and Intensive Care Unit and deputy dead of the Department of Neurology at Sveti Duh University Hospital, in Zagreb, Croatia. Rishad Faruqi, MD, is clinical associate professor of surgery (affiliate) at Stanford University and clinical associate professor of surgery (affiliate) at University of California, San Francisco (UCSF). Tatjana Rundek, MD, PhD, is professor of neurology in the Department of Neurology at Miller School of Medicine in Miami, Florida. She holds National Institutes of Health (NIH) grants that are unrelated to this manuscript. Jean-Baptiste Ricco, MD, PhD, is a vascular surgeon in the Department of Vascular Surgery at the University Hospital of Toulouse and University of Poitiers in France. Saeid Shahidi, MD, is a senior consultant in vascular surgery, chief consultant in supra aortic disease, research chief physician in vascular surgery, and associate professor at the University of Copenhagen and Zealand, Department of Cardiology and Vascular Surgery at Zealand University Hospital in Roskilde, Denmark. Gert J. de Borst, MD, PhD, is head of the Department of Vascular Surgery at University Medical Centre of Utrecht, the Netherlands. 

Co-signatories: Anne Abbott (Neurologist, Australia); Mohamad AbdalKader (interventional neuroradiologist, U.S.); Yogesh Acharya (vascular surgeon, Ireland); Nishath Altaf (vascular surgeon, Australia); Pier Luigi Antignani (angiologist, Italy); Omar Ayoub (neurologist, Saudi Arabia); Hernan Bazan (vascular surgeon, U.S.); Peter Bell (vascular surgeon, United Kingdom); Ruth Benson (vascular surgeon, New Zealand); Aleš Blinc (cardiologist/vascular physician, Slovenia); Alejandro Brunser (neurologist, Chile); Hrvoje Budincevic (neurologist, Croatia); Jonathan Cardella (vascular surgeon, U.S.); Robert Chang (vascular surgeon, U.S.); Alun Davies (vascular surgeon, United Kingdom); Gert J. de Borst (vascular surgeon, the Netherlands); Rishad Faruqi (vascular surgeon, U.S.); Aaron Gaekwad (neurologist physician trainee, Australia); Lan Gao (health economist, Australia); Hannah Gardener (epidemiologist, U.S.); Richard Genova (registered vascular technologist, U.S.); George Geroulakos (vascular surgeon, Greece/United Kingdom); Athanasios Giannoukas (vascular surgeon, Greece); Harry Gibbs (general & vascular medicine physician, Australia); Peter Gloviczki, (vascular surgeon, U.S.); Anders Gottsäter (vascular physician, Sweden); Guillaume Goudot (vascular physician, France); Jose Gutierrez (neurologist, U.S.); Vassilis Hadjianastassiou (vascular surgeon, United Kingdom); Kimberley Hammar (PhD candidate & resident [emergency medicine], Sweden); Robert Harbaugh (neurosurgeon, U.S.); Eitan Heldenberg (vascular surgeon, Israel); Caitlin Hicks (vascular surgeon, U.S.); Michal Juszynski (vascular surgeon, Poland); Stavros Kakkos (vascular surgeon, Greece); Anthony Kam (neuroradiologist, Australia); Zubair Kareem (neurologist, U.S.); Tien Khoo (internist [general & acute] medicine, Australia); Stefan Kiechl (neurologist, Austria); Timothy Kleinig (neurologist, Australia); Michael Knoflach (neurologist, Austria); Simona Lattanzi (neurologist, Italy); Kaitlyn Lillemoe (neurologist, U.S.); Ian Loftus (vascular surgeon, United Kingdom); Fedor Lurie (vascular surgeon, U.S.); Jonas Malmstedt (vascular surgeon, Sweden); Devender Mittapalli (vascular surgeon, United Kingdom); Wesley Moore (vascular surgeon, U.S.); Bibombe Patrice Mwipatayi (vascular surgeon, Australia); Achim Neufang (vascular surgeon, Germany); Branimir Nevajda (neurologist and stroke specialist, United Kingdom); Alexander Oberhuber (vascular surgeon/endovascular specialist, Germany); Jean Panneton (vascular surgeon, U.S.); Malay Patel (vascular surgeon, India); David Pelz (neuroradiologist, Canada); Fernando Picazo Pineda (vascular surgeon, Australia); Bartlomiej Piechowski-Jozwiak (neurologist, United Arab Emirates); Holger Poppert (neurologist, Germany); Alkoredi Fatai Radji (neurologist, France); Jean-Baptiste Ricco (vascular surgeon, France); Peter Ringleb (neurologist, Germany); Jenni Robertson (consumer representative & stroke survivor, United Kingdom); David Robinson (vascular surgeon, Australia); Sara Rostanski (vascular neurologist, U.S.); Tatjana Rundek (neurologist, U.S.); David Saloner (arterial/biomedical imaging specialist, U.S.); Felix Schlachetzki (neurologist, Germany); Lawrence Schott (neuroradiologist, Ireland); Saeid Shahidi (vascular surgeon, Denmark); Joseph Shalhoub (vascular surgeon, United Kingdom); Francesco Spinelli (vascular surgeon, Italy); Daniel Staub (angiologist, Switzerland); Francesco Stilo (vascular surgeon, Italy); Tim Stokes (consumer representative & survivor of stroke misdiagnosis, Australia); Sherif Sultan (vascular surgeon, Ireland); Costas Thomopoulos (cardiologist, Greece); Raffi Topakian (Neurologist, Austria); Francesco Torella (vascular surgeon, United Kingdom); Olise Uyagu (general medical practitioner, Australia); Claude Vaislic (vascular surgeon, France); Fred Weaver (vascular surgeon, U.S.); Martin Veller (vascular surgeon, South Africa); Maarit Venermo (vascular surgeon, Finland); Alex Vesey (vascular surgeon, United Kingdom); Tissa Wijeratne (neurologist, Australia); Joshua Willey (neurologist, U.S.); Mary-Ann Williams (consumer representative & stroke survivor, Australia); Roz Williamson (allied health, Australia); Kim Wootton (consumer representative & stroke survivor, Australia); and Wei Zhou (vascular surgeon, U.S.).