Stroke remains a major cause of morbidity and mortality both in the United States and abroad. Worldwide, stroke is currently the second leading cause of death, after ischemic heart disease, accounting for 11.8% of total deaths.1 In the United States, stroke is the fifth leading cause of death and the leading cause of disability.2 Among stroke survivors, quality of life continues to decline for an average of 5 years following the event.3
Eighty-seven percent of strokes in the United States are ischemic, with the remainder related to intracerebral and subarachoid hemorrhage.4 Carotid atherosclerotic disease has been implicated as the cause of stroke (cerebral vascular accident [CVA]) via three major pathways:
Embolic: Unstable plaque embolization to the middle or anterior cerebral artery leads to transient ischemic attack (TIA) or stroke. This is the most common etiology of ischemic stroke secondary to carotid stenosis. High-risk plaques are soft and often radiolucent on cross-sectional imaging. They are fibrous ridges that have continuous penetration of lipids into the arterial wall. This results in an inflammatory cascade ultimately leading to lysis of proteolytic enzymes resulting in necrotic debris and an unstable plaque.5 Unstable plaques are rich with neovasculature that can rupture and lead to Intraplaque hemorrhage. This can increase the stenosis exponentially. Embolization occurs when the fibrous cap of the plaque ruptures. The underlying ulcer, which is exposed once the cap ruptures, serves as a nidus for platelet aggregation and puts the patient at risk for further embolic events.
Hypoperfusion: Less commonly, low flow state through a highly stenotic extracranial carotid artery can lead to hypoperfusion. In patients with poor collateralization, this can result in stroke.
In-situ-thrombosis: Acute thrombosis from dissection and/or atherosclerosis can lead to obstruction and stroke.
The carotid bifurcation is a high-risk location for atherosclerotic disease. The separation of flow between the high-resistance external carotid artery and the low-resistance internal-carotid artery leads to turbulent flow and plaque formation on the walls opposite the flow divider. Turbulent flow, coupled with an intimal injury, results in the inflammatory cascade leading to atherosclerotic plaque formation and eventual luminal narrowing. Luminal narrowing, in turn, leads to both increasing flow velocities and more turbulent flow. This resultant increased turbulence is a risk factor for embolic events.
Other risk factors for atherosclerotic carotid artery disease include hypertension, diabetes, hypercholesterolemia, obesity, genetics, and smoking.
Atherosclerotic carotid disease classically manifests symptoms as:
Transient ischemic attack (TIA): Although traditionally defined as acute onset neurologic events with symptoms lasting less than 24 hours, the most recent American Heart Association guidelines define TIAs as “brief episodes of neurological dysfunction resulting from focal cerebral ischemia not associated with permanent cerebral infarction.”6 This new definition dispenses of the somewhat arbitrary time-threshold which prior studies have found was too broad and resulted in 30% ...