Treating Carotid Plaques in the Dark

BY FRANK J.VEITH, M.D.

The vascular world today seems consumed with the issue of whether or not carotid stenting should replace carotid endarterectomy as the favored treatment for arteriosclerotic lesions of the carotid artery. Even without a definitive answer to this question, there is a great rush to train individuals from many specialties in the skills to perform carotid artery stenting (CAS). In addition, all sorts of unaudited registries exist purporting to evaluate CAS under a variety of conditions or with a variety of devices.

In addition, a number of randomized controlled trials comparing CAS with carotid endarterectomy (CEA) have been completed or are under way on both sides of the Atlantic Ocean.

Some of these trials, such as SAPPHIRE or EVA-3S, have been subjected to warm embrace or intense criticism depending upon whether one's bias lies in the "CAS is best" or "CEA is best" camp. Still the questions "which is best?" and "for whom?" remain unanswered and the subject of intense debate.

Underlying all these debates is the presumption that high-grade carotid bifurcation lesions should be treated. This is a flawed presumption which is based on landmark randomized controlled trials conducted over the last 2 decades.

These trials--the North American Symptomatic Carotid Endarterectomy Trial (NASCET), the European Carotid Surgery Trial (ECST), the Asymptomatic Carotid Atherosclerosis Study (ACAS), the Asymptomatic Carotid Surgery Trial (ACST), and others--compared CEA with best medical treatment in symptomatic and asymptomatic patients with high-grade carotid stenosis defined in various ways. In their day, these trials certainly provided level I evidence.

They no longer do. All these trials--landmark though they may have been--are now obsolete.

Best medical treatment has been transformed by the introduction of statins, ?-blockers, and better antiplatelet agents. Good level I evidence now exists showing that these drugs alone and in combination lower the incidence of stroke in patients at risk. The medical management controls from the 1990s and early 2000s no longer apply today.

Thus, the presumption that invasive treatment (CEA or CAS) prevents more strokes than does current best medical management is invalid. This is particularly true for patients with asymptomatic carotid stenosis, patients in whom the benefits of CEA were marginal even without 2007 medical treatment.

In view of this, the widely hyped question of which invasive treatment (CEA or CAS) is best is not the most important one related to carotid disease. Far more important is the question: Is invasive treatment of carotid bifurcation disease really justified in today's medical climate?. This is particularly true in asymptomatic patients who make up the majority of treated patients in practice, in registries, and in some randomized trials. This question can only be answered by randomized trials comparing CEA and/or CAS with current best medical treatment.

Only one such trial; the Transatlantic Asymptomatic Carotid Intervention Trial (TACIT), is on the drawing board, and funding is sufficiently in doubt that it may never be completed (see box). This would be most unfortunate since it could lead to hundreds of thousands of patients being treated without knowing if they really need it.

Only when (and if) trials such as TACIT are completed will we know that invasive treatment of any sort and its attendant risks and cost are truly worthwhile in patients with carotid stenosis.