Intensifying medical therapy would obviate the need for carotid revascularization in all but 4% of patients with asymptomatic carotid stenosis.
Intensifying medical therapy would obviate the need for carotid revascularization in all but 4% of patients with asymptomatic carotid stenosis, contends J. David Spence, MD, professor of neurology and clinical pharmacology, and director of the Stroke Prevention and Atherosclerosis Research Centre, University of Western Ontario, London, Ontario, Canada.
In the United States, about 60% of carotid stenting and endarterectomy procedures are performed for asymptomatic carotid stenoses. Dr. Spence’s study, which included patients with asymptomatic carotid stenosis at 2 Canadian clinics, showed that the risk of asymptomatic stenosis in those on medical therapy is less than the risk of stenting or endarterectomy. Based on the findings, it appears that less than 5% of patients with asymptomatic carotid stenosis may benefit from stenting or endarterectomy due to the availability of more intensive medical therapy.
Dr. Spence documented a regression of carotid plaque and a reduction in the incidence of microemboli on transcranial Doppler ultrasonography since the implementation of a new treatment paradigm at the 2 Canadian clinics in 2003. The new treatment paradigm bases the intensity of medical therapy on measurement of carotid plaque instead of risk factors; thus, even patients who are already at goals for lipid and blood pressure levels will have their treatment intensified if the total plaque area progresses.
The incidence of microemboli and the number of clinical events (stroke, death, or carotid endarterectomy) were tabulated for 468 patients with asymptomatic carotid stenosis, 199 of whom presented before the change in treatment paradigm in 2003, and 269 of whom presented after January 1, 2003.
Previously, Dr. Spence reported that patients in the top quartile of carotid total plaque area had more than triple the risk of stroke, death, or myocardial infarction (MI) than patients in the lowest quartile, after adjusting for potential confounding variables. Patients with progression of plaque had approximately twice the adjusted risk of stroke than those with stable plaque or regression of plaque.
Before 2003, 12.6% of patients had microemboli detected on transcranial Doppler, compared with only 3.7% after 2003 (P <.0001). The stroke risk for patients with microemboli was 10.3% at 1 year and 21.6% at 2 years. The corresponding stroke risk for patients without microemboli was 1.4% at 1 year and 2.3% at 2 years.
The annual rate of plaque progression was increasing before 2002, but has decreased markedly since 2003, and since 2005, “we have seen regression of plaque in 50% of patients, and regression on average in the entire clinic population,” said Dr. Spence. The composite of stroke, death, MI, or carotid endarterectomy in the first 2 years decreased from 17.6% to 5.2% (P <.0001) since the treatment paradigm changed. In addition, since 2003, treatment intensification has resulted in significant decreases in plasma cholesterol, triglycerides, and lowdensity lipoprotein cholesterol, and a significant increase in high-density lipoprotein cholesterol.
“The benefit of endarterectomy shown in the past was based on less intensive medical therapy than now exists,” said Dr. Spence. Only those patients with microemboli despite intense medical therapy, which represents only 3.7% of the patients with asymptomatic carotid stenosis, should be considered for endarterectomy or stenting, he noted.