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| AuthorsMark O McCarron, MD, FRCPLarry B Goldstein, MDDavid B Matchar, MD | Section EditorsRobert H Fletcher, MD, MScScott E Kasner, MD | Deputy EditorH Nancy Sokol, MD |
Topic Outline
INTRODUCTION
Stroke is the second leading cause of death worldwide and the fourth leading cause of death in the United States (US), behind heart disease, cancer, and respiratory disease [1]. The prevalence of stroke has been rising gradually with the increasingly aging population, despite evidence of a decline in stroke incidence [2].
The impact of stroke is often devastating, with a 20 percent mortality from the acute event and 40 to 50 percent survival at five years [1,3]. Among survivors, data from the Framingham study reveal that 18 percent are unable to return to work, while up to 4 percent require total custodial care [4]. One-quarter of those over age 65 years require long-term institutional care after a first stroke [1]. Thrombolytic therapy can salvage brain tissue in some patients who present acutely with an ischemic stroke, but such patients represent only a small fraction of those suffering acute stroke. For the majority who go on to suffer a completed stroke, there is little that can be done to reverse the devastating effects of brain injury. For this reason, the greatest impact on this disease comes from prevention.
Patients who have had a stroke or transient ischemic attack (TIA) due to carotid stenosis are considered symptomatic and often benefit from early carotid revascularization [5]. Patients with carotid artery stenosis are considered to be symptomatic if they have had recent (within six months) transient or permanent focal neurologic symptoms related to the affected artery (eg, ipsilateral amaurosis fugax, contralateral weakness or numbness of an extremity or the face, dysarthria or aphasia). In contrast, nonspecific neurologic symptoms (eg, dizziness or syncope/near syncope) are not considered in the definition of symptomatic carotid stenosis [6]. (See "Management of symptomatic carotid atherosclerotic disease", section on 'Carotid endarterectomy'.)
Carotid stenosis may also be identified in asymptomatic patients. It should be noted that the cutoff used to define clinically significant carotid artery stenosis varies among studies, ranging from 50 to 70 percent stenosis [7-9].
Optimal management of patients with asymptomatic carotid stenosis to prevent stroke is not established. The therapeutic options, which are discussed in detail elsewhere, include medical management to address risk factors for atherosclerosis, focusing on control of hypertension, diabetes mellitus, smoking, and dyslipidemia; the administration of antiplatelet drugs to prevent platelet aggregation; and surgical revascularization by carotid endarterectomy (CEA) or carotid artery stenting (CAS). (See "Secondary prevention of stroke: Risk factor reduction" and "Management of asymptomatic carotid atherosclerotic disease".)
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