| Carotid Endarterectomy (CEA) |
| Overview of Carotid artery disease |
 | Stroke risk for patient who had
 | TIA: approximate 7 % / year |
| CVA: 5% to 20% / year |
| Amaurosis fugax may have lower risk of stroke than those with hemispheric
symptoms. (Oxfordshire Community Stroke Project). |
| Recurrent hemispheric events carry a greater stroke risk than a single
event (28% versus 12% at 2 years). |
|
| Two mechanisms of stroke from carotid artery disease
| Emboli to branches of anterior and middle cerebral arteries |
| Flow-related "watershed" infarct associated with coexistent
intracranial cerebrovascular disease. |
|
| Posterior cerebral artery (PCA)
| In 20% to 25% of patients, one PCA is supplied by carotid artery while
the other arises from the basilar artery. |
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| North American Symptomatic CEA Trial (NASCET) |
| 659 symptomatic patients with carotid stenosis of 70 - 99% |
| Degree of stenosis: determined by comparing the most narrow linear
diameter of the vessel with the normal internal carotid artery beyond the carotid bulb. |
| Randomization was halted in Feb 1991: analysis showed a highly
significant benefit from CEA. |
| The cumulative risk of ipsilateral stroke at 2 years: |
| Treatment group |
Surgical |
Medical |
| # of patients |
328 |
331 |
| Risk of ipsilateral stroke |
9% |
26% |
| Risk of major / fatal ipsilateral stroke |
2.5% |
13.1% |
| An absolute risk reduction of 17% (± 3.5%) |
| An absolute risk reduction of 10.6% (± 2.6%) for major or fatal
ipsilateral stroke |
|
| The European Carotid Surgery Trial (ECST) |
| 778 patients with severe stenosis, randomized |
| Method for determining stenosis from Angio was different from NASCET.
| Degree of stenosis is greater with ECST criteria. |
|
| Greater operative stroke and death rate, may account for the difference
in the risk reduction. |
| Treatment group |
Surgical |
Medical |
| # of patients |
455 |
323 |
| 3 year risk of any death or stroke |
12.3% |
21.9% |
| 3 year risk of disabling or fatal stroke or surgical death |
6% |
11% |
| An absolute risk reduction of 5%. The operative risk of stroke or death
was 7.5%. |
| 374 patients with mild stenosis (0%-29%) was randomized, no statistical
difference between patients treated medically and surgically.
| Only 2 of 155 patients followed medically for 3 years had an ipsilateral
ischemic stroke lasting > 7 days. |
|
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| CEA in patients with recent strokes |
| Joint Study of Extracranial Arterial Occlusion 1969:
| 50 patients with severe strokes: treated with CEA < 2 weeks: 34%
improved, mortality was 42%. |
| CEA > 2 weeks after stroke in 18 patients: improvement in 72%,
mortality rate 17% |
| 187 patients treated nonoperatively: 53% improvement and 20%
mortality |
|
| Generally accepted therapy for carotid stenosis after infarction: a
delayed endarterectomy 4 to 6 weeks after the event. |
| Giordano et al in 1985: 49 CEA performed on patients with neurologic
deficits > 24 hours: Postoperative strokes occurred in 18.5% of 27 patients
operated within 5 weeks, and no strokes occurred in 22 patients who received surgery after
5 weeks. |
| Whittemore et al: 28 patients with "small fixed neurologic
deficits," 15 received CEA for stenosis > 75% within 1 week without neurologic
complications. |
| In a subset analysis of NASCET reported by Gasecki et al, 100
patients with a "nondisabling" stroke with carotid stenosis of 70% to 99%
received endarterectomy from 3 to 30 days after stroke, with a stroke rate of 4.8%. |
| To identify lower-risk candidates for early CEA with acute neurologic
deficits: CT scans at 1 and 5 days after presentation.
| Dosick et al: excellent results by stratifying patients based on the
presence of infarction on CT.
 | Negative CT: CEA at 5 -14 days |
| Positive scans: CEA delayed to 4 - 6 weeks |
|
| Other reports have not supported the use of CT scans to define a subset
of patients that may safely undergo early CEA. |
|
| Patients with less ischemic damage, by clinical presentation or CT
scan, may have less postoperative hemorrhagic conversion.
| Other theories: improve control of perioperative anticoagulation and
hypertension. |
|
| Evaluating the use of anticoagulants in the treatment of stroke,
Ramirez-Lassepas and Quinones found intracranial hemorrhage to occur with embolic stroke,
large cerebral infarcts, markedly elevated blood pressure, excessive anticoagulation, and
heparin induced thrombocytopenia. |
| Risk of waiting before surgery.
| Dosick and colleagues: Incidence of recurrent stroke during this waiting
period 9.5%. |
| The incidence of recurrent neurologic symptoms within 1 month in the VA
Cooperative Studies with carotid stenosis greater than 50% was 6%. |
|
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| CEA in Acute Carotid Occlusion |
| Symptoms range from asymptomatic occlusion to frank stroke. |
| Symptomatic acute occlusion of less than 6 hours may be an indication for
emergent CEA. |
| Most such emergent operations occur in the setting of a postoperative
neurologic change from thrombosis after CEA. |
| Other rare circumstances include carotid thrombosis after cerebral
angiography or a patient with known carotid stenosis presenting with a neurologic deficit.
|
| In a small series of CEA patients with neurologic deficits in the early
postoperative period, 76% experienced neurologic improvement (13 of 22) with emergent
surgery, 20% improved when managed nonoperatively. |
|
| Crescendo TIA |
| Transient neurologic deficits occurring with increasing frequency,
greater duration, or greater severity is believed to be at very high risk for stroke. |
| Most of these pateints are aggressively treated, and natural history data
for large numbers of patients are lacking. |
| Mentzer et al: 12 patients with crescendo TIAs and high-grade carotid
stenosis.
| 5 patients managed nonoperatively and four suffered strokes, 1 died of
cerebral infarction. |
| 7 patients had CEA, with complete recovery in each case. |
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| References & further reading |
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