Appropriate management of asymptomatic carotid stenosis

Abstract

With modern intensive medical therapy, the annual risk of ipsilateral stroke in patients with asymptomatic carotid stenosis (ACS) is now down to ∼0.5%. Despite this, there is a widespread practice of routine intervention in ACS with carotid endarterectomy (CEA) and stenting (CAS). This is being justified on the basis of much higher risks with medical therapy in trials conducted decades ago, compared with lower risks of intervention in recent trials with no medical arm. Such extrapolations are invalid. Although recent trials have shown that after subtracting periprocedural risks the outcomes with CEA and CAS are now comparable to medical therapy, the periprocedural risks still far outweigh the risks with medical therapy. In the asymptomatic carotid trial (ACT) 1 trial, the 30-day risk of stroke or death was 2.9% with CAS and 1.7% with CEA. In the CREST trial, the 30-day risk of stroke or death among asymptomatic patients was 2.5% for stenting and 1.4% for endarterectomy. Thus, intensive medical therapy is much safer than either CAS or CEA. The only patients with ACS who should receive intervention are those who can be identified as being at high risk. The best validated method is transcranial Doppler embolus detection. Other approaches in development for identifying vulnerable plaques include intraplaque haemorrhage on MRI, ulceration and plaque lucency on ultrasound, and plaque inflammation on positron emission tomography/CT. Intensive medical therapy for ACS includes smoking cessation, a Mediterranean diet, effective blood pressure control, antiplatelet therapy, intensive lipid-lowering therapy and treatment with B vitamins (with methylcobalamin instead of cyanocobalamin), particularly in patients with metabolic B₁₂ deficiency. A new strategy called 'treating arteries instead of risk factors', based on measurement of carotid plaque volume, is promising but requires validation in randomised trials.

Keywords: Endarterectomy; Medical therapy; Stenting; Transcranial Doppler; carotid stenosis.

Figure 1

Effects of statins (hydroxymethylglutarate (HMG) coenzyme A reductase inhibitors) on synthesis of ubiquinone (coenzyme Q10, CoQ10). Between the inhibition of HMG coenzyme A reductase and cholesterol are many intermediate metabolites. By the same action that lowers levels of low-density lipoprotein cholesterol, statins also lower levels of CoQ10; this may lead to mitochondrial dysfunction contributing to myopathy and insulin resistance/diabetes (reproduced by permission of Vanderbilt University Press from: Spence).

Figure 2

Detection of microemboli by transcranial Doppler identifies high-risk asymptomatic carotid stenosis. The white arrow in the upper channel shows the M-mode image of a microembolus in the middle cerebral artery ipsilateral to an asymptomatic carotid stenosis; the high-intensity transit signal is seen (white arrow) in the Doppler channel below (reproduced by permission of Wolters Kluver from: Spence JD et al).

Figure 3

Microemboli during deployment of a carotid stent. Microemboli during carotid stenting. Showers of emboli commonly (even usually) occur during carotid stenting. Panel A shows microemboli in both middle cerebral arteries while crossing the aortic arch during stenting of a common carotid; panel B shows microemboli in the middle cerebral artery during stenting of the ipsilateral internal carotid artery (courtesy of Dr Claudio Muñoz. Reproduced by permission of Springer to reproduce from: Spence et al).

Figure 4

Decline in the risk of carotid occlusion with more intensive medical therapy. Among 3681 patients in the database, the percentage of patients who progressed to occlusion was much higher before 2002; the frequency decreased markedly after implementation in 2002–2003 of more intensive therapy based on plaque measurements. Error bars indicate 95% CI (reproduced by permission of the American Medical Association from: Yang et al).