Is Carotid Angiography Necessary? Editors Disagree
The crux of the question addressed by our protagonists is whether the benefits of carotid angiography (CAA) outweigh the potential risks of the procedure compared with the noninvasive but less precise use of carotid Doppler ultrasound (DU) and lack of information about the intracranial circulation. The interpretation of the existing data can be, in part, philosophical: as Rothwell outlined, the net increase in risk for angiography is about 1 stroke for every 200 cases studied. Does this outweigh the benefits of intracranial vascular imaging provided by CAA? The downside of DU as the sole investigation prior to endarterectomy is the possibility that inappropriate surgery is undertaken due to a spurious result, failure to detect tandem lesions or intracranial aneurysms.
One of us (S.M.D.) is swayed by the arguments that the decisions for endarterectomy are based on NASCET angiographic criteria for stenosis, that tandem lesions and incidental intracranial aneurysms are not uncommon and may influence clinical management decisions. Intracranial disease is even more important in Asian patients, where it is the predominant type of cerebral atherosclerosis.1 Patients with intracranial disease have a worse prognosis and arguably medical therapy may need to be more intensive.2 At our institution, CAA is routinely performed before surgery and DU is used only as a screening test. However, CAA is becoming replaced by magnetic resonance angiography (MRA) and computed tomographic angiography (CTA), and its main role is likely to be restricted to patients requiring endovascular interventions such as angioplasty and stenting. In most cases, a combination of DU and high-resolution MRA would provide sufficient information about the surgical extracranial plaque and relevant intracranial arterial pathology.3
The other (G.A.D.) is less convinced. The risk of 1 stroke for every 200 cases is clinically meaningful and may be significantly greater, as highlighted by Moore. For example, aspirin is routinely given after acute ischemic stroke to save approximately 1 stroke for every 100 treated.4 It would seem illogical to be employing a procedure with almost the same magnitude of risk as the benefit accrued for a standard therapy. Further, the risk of surgery is not increased by the presence of tandem intracranial stenotic lesions (NASCET)5 nor small intracranial aneurysms,6 and the benefits are not dissimilar. Our practice is to perform CEA based on ultrasound evidence alone but with the caveat that DU results from other institutions are cross-checked with a repeat study from our own laboratory.
Where to from here? Imaging technology and interventional strategies are evolving so rapidly that this argument is likely to recede into the pages of history over the next decade. Again, science advances, patients benefit!
Leung SY, Ng THK, Yuen ST, Lauder IJ, Ho FCS. Pattern of cerebral atherosclerosis in Hong Kong Chinese: severity in intracranial and extracranial vessels. Stroke. 1993; 24: 779–786.
Benesch CG, Chimowitz MI. Best treatment for intracranial arterial stenosis? 50 years of uncertainty: the WASID Investigators. Neurology. 2000; 55: 465–466.
Ackerman RH, Morelia RC. Identifying clinically relevant carotid disease. Stroke. 1994; 25: 1–3.
Kappelle LJ, Eliasziw M, Fox AJ, Sharpe BL, Barnett HJ. Importance of intracranial atherosclerotic disease in patients with symptomatic stenosis of the internal carotid artery: the North American Symptomatic Carotid Endarterectomy Trial. Stroke. 1999; 30: 282–286.
Kappelle LJ, Eliasziw M, Fox AJ, Barnett HJ. Small, unruptured intracranial aneurysms and management of symptomatic carotid artery stenosis: North American Symptomatic Carotid Endarterectomy Trial Group. Neurology. 2000; 55: 307–309.