|
|||||||
|
|
|
|||||
|
|
|||||||
( Geriatrics )
Of the half-million strokes that occur each year in the United States, 20 to 30% can be directly linked to carotid occlusive disease. The degree of stenosis involving the carotid bifurcation is an important predictor of stroke risk. Asymptomatic disease may be diagnosed on routine physical exam or screening of the carotid bifurcation in patients with risk factors for ischemic strokes. Symptomatic disease includes transient ischemic attacks, stroke in evolution, and complete stroke.
Duplex ultrasound scanning is the standard test for the initial evaluation of carotid artery disease. Patients undergoing surgery should also have magnetic resonance angiography or an angiogram of the carotid vessels. Stroke prevention includes lifestyle modification such as cessation of smoking, strict dietary and medical management of hyperlipidemia, diabetes, and hypertension. Antiplatelet, anticoagulant, and thrombolytic therapy can be used where indicated.
Eugene JR, Abdallah M, Miglietta M, Vernenkar VV, Pascual R,
Briones R, Barnes T, Hager J. Carotid occlusive disease: Primary care of patients with or without symptoms. Geriatrics 1999; 54(May):24-41.
A half-million strokes occur each year in the United States, and 20 to 30% can be directly linked to carotid occlusive disease.(FN1)
Carotid artery stenosis, sometimes described as carotid artery syndrome, is a clinical syndrome that can cause stroke secondary to acute arterial occlusion or embolization.
Primary care physicians familiar with the current diagnostic approach to and management of carotid occlusive disease can:
* help prevent new onset of stroke
* minimize the progressive deterioration of neurologic symptoms
* and diminish the rate of death associated with strokes.
In this article, we outline an evidence-based approach for the appropriate management of older patients suspected of having carotid occlusive disease.
CLINICAL RISK OF STROKE AND CAROTID STENOSIS
Stroke is the third most common cause of death in the United States. Common risk factors include age, hypertension, coronary artery disease, diabetes, hyperlipidemia, and tobacco use. The Framingham study demonstrated that age is the single most important risk factor for stroke.(FN2) The stroke rate more than doubles for each successive 10 years after age 55.(FN3)
Projecting from the Rochester study,(FN4) 80% of stroke patients will survive the initial neurologic insult. Among the survivors:
* 29% will have no residual neurologic deficit
* 71% will have continued neurologic deficit to various degrees. Of those with residual neurologic deficit, 18% will be disabled and 4% will require total custodial care.
Persons who have had a first stroke have a 10% chance of a recurrent stroke within 1 year, with mortality ranging from 16 to 55%.(FN5)
Differences in mortality rates can be attributed to different patient populations, variability in prehospital care, underlying health, and timing of treatment. Transient ischemic attacks (TIA) and ischemic stroke are associated with a variety of cardiogenic, vascular, and hematologic etiologies (table 1). For stroke associated with carotid disease, the 1-year risk of stroke increases with escalating degrees of carotid stenosis.(FN6,7)
Amid controversies, investigations in which patients were followed using serial noninvasive cerebrovascular studies have concluded that:
* 50% carotid artery stenosis carries a 4% per year risk of stroke and TIA.(FN8)
* Once the stenosis reaches 75%, the combined rate of stroke and TIA ranges from 10.5 to 18% per year, whereas the 1-year stroke rate alone ranges from 3.3 to 5%.(FN7,9)
* When the lumen of the artery is 80% stenosed, the risk of TIA or stroke increases to 35% at 6 months and 46% at 12 months.(FN10)
These findings were confirmed in the North American Symptomatic Carotid Endarterectomy Trial (NASCET), which found that even in medically treated patients stenosis of 70 to 89% carried an 11% risk of stroke at 1 year, as opposed to 35.1% for patients with 90 to 94% carotid stenosis.(FN11)
In addition to the degree of stenosis, the morphology of the plaque at the carotid bifurcation is an important predictor of stroke risk.(FN12-13) Soft heterogeneous plaque, as determined by B-mode ultrasonography, carries an increased risk of stroke independent of the degree of carotid stenosis.(FN14) In addition, a complex ulceration within a carotid plaque increases the risk of stroke in both asymptomatic and medically treated patients.(FN13, 15)
Nevertheless, the decision to operate is based on the degree of stenosis, because surgery has been found to be beneficial for patients with moderate to severe stenosis, regardless of plaque morphology.(FN13,16)
CLINICAL PRESENTATION
Carotid artery occlusive disease can be divided into two broad presentations: asymptomatic and symptomatic disease. It is important to note that symptomatic disease, as defined by the NASCET collaborators, does not include vague symptoms such as vertigo, dizziness, syncope, and blurred vision.(FN16) In general, ischemic symptoms fall into three categories: TIA, stroke in evolution, and complete stroke.
Asymptomatic. Asymptomatic carotid occlusive disease is diagnosed either on routine physical exam or screening of the carotid bifurcation by duplex ultrasonography in patients with associated risk factors for ischemic strokes (table 2). Typically, when the bell of the stethoscope is applied over the carotid artery, a bruit at the carotid bifurcation can be heard if a stenosis is present. For optimum accuracy, place the bell of the stethoscope about 2 cm below the angle of the mandible, at the medial border of the sternocleido-mastoid muscle, with the head turned to the contralateral side.
The presence of a bruit by no means is indicative of a severe stenosis, nor does its absence signify that carotid disease is not present. In fact, very tight stenosis and, certainly, total occlusion will fail to generate enough laminar flow to cause a bruit. In that case, a bruit that was present on initial evaluation but disappears a few months later may be indicative of impending occlusion or thrombosis. The presence of a bruit warrants further investigation (figure).
Symptomatic.
By definition, a TIA is an ischemic neurologic event that can last from several seconds to hours but no longer than 24 hours. Symptoms may range from a small loss of sensation to the contralateral hand to complete hemiparesis.
One type of TIA is the crescendo TIA, which is defined as a rapid recurrence of neurologic deficits with temporary improvement between embolic events. Another variant subset of TIA is amaurosis fugax, whereby the patient experiences temporary blindness on the ipsilateral side of the carotid lesion. This transient loss of vision, usually described as "a shade that comes down," is due to platelets or cholesterol embolization to the ophthalmic artery, causing monocular blindness. The most common source of these ophthalmic emboli, otherwise known as Hollenhorst plaques, is an ulcerated plaque at the bifurcation of the common carotid artery.
A stroke in evolution is a neurologic deficit that progresses or fluctuates without returning to normal. It can be difficult to differentiate from a TIA. With complete stroke, the neurologic deficit is stable without change in degree of manifestation and lasts more than 24 hours. At this point, the evidence of stroke usually can be seen as an infarct on MRI or CT of the brain.
Radiologic evaluation of the carotid vessels is indicated for the patient who presents with:
* risk factors for ischemic stroke
* or signs and symptoms of TIA. These studies can be invasive or noninvasive. In the past, the only method available was angiography.
More recently, however, duplex ultrasound has become the standard test for the initial evaluation of carotid artery disease.
Duplex ultrasound. At some institutions, carotid duplex ultrasound is the only test performed prior to surgical intervention. However, such practice is recommended only in centers with institutional validation and ongoing quality assurance.(FN17) Duplex ultrasound is particularly valuable in the evaluation of atypical or nonhemispheric symptoms and is highly superior to angiography for plaque characterization. Duplex scan can be very accurate when performed with B-mode two-dimensional imaging, color flow technology, and velocity-waveform analysis.
It is a simple, noninvasive test with 94% sensitivity for detecting high-grade stenosis or occlusion.(FN18)
On the other hand, duplex ultrasound has limitations. Its accuracy is operator-dependent, and it does not provide information about intrathoracic and intracranial vessels. Ultrasound also tends to overestimate the degree of stenosis of the internal carotid artery, which decreases the specificity of the test to 70 to 85%.(FN19-21) Therefore, standard angiography or magnetic resonance angiography (MRA) is needed for confirmation of the degree of stenosis.
Thus, duplex ultrasound is used as an initial evaluation or screening test to select patients in need of angiography. (FN20,22) In most clinical practices today, the need for carotid angiography is obviated in the presence of concordant MRA and duplex ultrasound.
MR Angiogram.
MRA is an emerging, noninvasive technology for the evaluation of arterial vessels. This test is less technician-dependent than duplex ultrasound and can provide accurate information about intracranial vessels. MRA, however, is not readily available in most hospitals, and it is expensive.
Although MRA can be very accurate in determining occlusive disease, motion by the patient can compromise clarity and resolution in 10 to 15% of studies. In 5 to 10% of cases, MRA examination is hindered because of patient intolerance secondary to claustrophobia and the presence of metallic devices in the body. In addition, it is very difficult with MRA to differentiate high-grade stenosis from occlusion or simply a kinked vessel.
For the combination of these reasons, MRA is not an effective screening test. Nevertheless, MRA combined with duplex ultrasound is 100% accurate in detecting various degrees of carotid stenosis when their findings correlate.(FN19,22)
Today, MRA is used routinely as a preoperative evaluation to confirm duplex ultrasound findings and delineate anatomy. This test is particularly recommended in patients who are allergic to contrast dye or have renal insufficiency. MRA is also useful in patients who have recently been exposed to a large load of contrast dye during investigative tests such as cardiac catheterization.
Angiography.
Angiography remains the gold standard for the evaluation of occlusive artery disease, and carotid artery stenosis is no exception.(FN23) The value of angiography has clearly been demonstrated in the NASCET trial, which recommends conventional angiography as an essential investigative study for defining the risk of stroke as well as deciding appropriate treatment for extracranial carotid artery stenosis.(FN24)
More recently, a review of guidelines and multidisciplinary consensus from the National Stroke Association still supports the NASCET recommendations. These guidelines also underline the controversies surrounding the use of noninvasive blood-flow measures to supplant angiography. In accordance with the NASCET recommendation, angiography is still performed in addition to duplex ultrasound when a decision has been made for operative intervention, unless the patient:
* is allergic to contrast dye
* has renal insufficiency
* desires a noninvasive test
* has been exposed to a large quantity of contrast dye, as in concurrent cardiac catheterization.
Angiography should also be obtained if there is no correlation between findings on an MRA and an initial duplex scan. Furthermore, information about the morphology of a plaque (ulceration, homogeneity) can be obtained, especially with digital manipulation of contrast angiography.
On the other hand, angiography, is not without disadvantages. It is an invasive procedure with associated risk (albeit low) of stroke, arterial dissection, pseudoaneurysm formation, and infection. This is why MRA is becoming more popular in some institutions and has essentially replaced angiography in some centers in the United States.
Additional work-up.
Carotid stenosis is only one of many causes of strokes. For example, the heart can be an important source of emboli and must be excluded with ancillary testing such as echocardiography if no other source is suspected or found. A complete history and physical exam are of paramount importance. Documentation of extremity pulses is essential to rule out or monitor the progression of associated peripheral vascular disease.
MEDICAL TREATMENT
Medical treatment for the prevention of atherothrombotic stroke in the patient with carotid occlusive disease encompasses antiplatelets (aspirin, ticlopidine HCl [Ticlid], and clopidogrel [Plavix]) and anticoagulants (heparin and warfarin).(FN25-27)
Antiplatelets.
For the patient in whom a carotid stenosis has been identified, the recommended approach includes:
* a strict, low-fat diet
* aggressive medical management of hyperlipidemia
* and antiplatelet therapymainly with aspirin, ticlopidine, or clopidogrel. These antiplatelets decrease platelet aggregation and thereby reduce the risk of stroke. Aspirin, 325 mg/d, is typically used for carotid stenosis <60%, unless there is a history of allergic reaction to aspirin. With aspirin allergy, ticlopidine, 250 mg bid, is an appropriate alternative. After a complete stroke, there is evidence that ticlopidine is more effective than aspirin for secondary prevention of stroke.(FN26) More recently, the efficacy and safety of clopidogrel as a substitute for aspirin was established in the Clopidogrel versus Aspirin in Patients at Risk for Ischemic Events (CAPRIE) trial. Clopidogrel was found to be more effective and safer than aspirin in reducing adverse cardiovascular events in patients with atherosclerosis.(FN28)
Anticoagulants.
Warfarin (Coumadin) and heparin are two anticoagulants used extensively to prevent TIA and imminent stroke. There is also evidence that these drugs halt the progression of thrombolytic stroke.(FN29) Immediate administration of heparin is particularly critical when a patient presents with clinical and radiologic evidence (MRA or ultrasound) of carotid artery occlusion from thrombosis or dissection. Low-molecular-weight heparin given subcutaneously within the first 48 hours of symptoms has also been shown to improve stroke outcome.(FN29) Warfarin, which is instituted while heparin therapy is being maintained, can be used alone from the beginning if TIAs occur less than once every few days.(FN29)
Thrombolytic therapy.
Tissue plasminogen activator (t-PA) is a thrombolytic agent approved by the FDA and endorsed by the American Heart Association and the American Academy of Neurology for use in patients with acute ischemic stroke (<3 hours old) and no contraindications as evidenced by CT of the brain.(FN29,30) It is important to point out that t-PA should not be given concurrently with anticoagulants or antiplatelets for at least 24 hours after the thrombolytic has been administered.(FN31)
SURGICAL TREATMENT
Surgical management with carotid endarterectomy was found to be more effective than aspirin in reducing the risk of stroke when internal carotid artery stenosis was:
* >60% in the Asymptomatic Carotid Atherosclerosis Study (ACAS) group(FN32)
* 70 to 99% in the NASCET study.(FN33)
Endarterectomy was safe and effective in reducing strokes in patients who were asymptomatic, resulting in an absolute risk reduction for stroke and death rate of 5.9% over 5 years as opposed to 11% for medically treated patients.(FN34) This potential benefit is based on ACAS's low perioperative morbidity and mortality of 1.1%. Therefore, the most recent guidelines published are reluctant to endorse carotid endarterectomy for asymptomatic patients because of concern about the reproducibility of the ACAS low perioperative results.(FN35)
Severe stenosis.
Patients with severe carotid stenosis (70 to 99%) derive a substantial benefit from carotid endarterectomy, with a 17% absolute reduction in the risk of ipsilateral stroke at 2 years. More important, these benefits persist for 5 years or more. Therefore, the role of surgery in patients with severe stenosis is well established.(FN16)
Mild to moderate stenosis.
The NASCET study has recently concluded its trial for patients with mild to moderate stenosis.(FN16) It was found that patients with moderate carotid stenosis (50 to 69%) gain only a moderate reduction in the risk of stroke following endarterectomy. Thus they should undergo surgery only if they are at good medical risk and the surgeon possess "exceptional skills," as evidenced by a perioperative risk of disabling stroke and death no greater than 2%.
Otherwise, these patients lose the small benefits provided by carotid endarterectomy. If none of the criteria mentioned above can be met, symptomatic patients with moderate disease or stenosis should be treated medically or referred to centers where patients have a low rate of perioperative complications.
Patients with less than 50% stenosis do not benefit from endarterectomy, and therefore medical management is recommended.(FN16)
Contralateral occlusion.
Fifteen percent of patients with carotid disease can be expected to have complete occlusion of one of the carotid vessels.(FN36) The NASCET trial has shown that surgical treatment of severe (>70%) symptomatic carotid stenosis in the face of contralateral carotid stenosis or occlusion provides better long-term outcome than medical treatment in terms of risk reduction of ipsilateral stroke.(FN37) Although initial perioperative morbidity is higher, no significant difference in mortality and stroke morbidity exist after 30 days when compared with patients with unilateral disease.(FN35,38-39)
An earlier study had addressed the management of moderate (50 to 69%) stenosis in the face of contralateral severe stenosis or occlusion. It was found that carotid endarterectomy provides better stroke prevention for this subset of patients.(FN40) However, adherence to NASCET recommendations for moderate unilateral carotid stenosis should still be followed. That is, unless one can ensure a combined risk of disabling stroke and death rate of <2%, surgery for mild to moderate stenosis should not be performed.
Other options. Thromboendarterectomy of the occluded vessels has been abandoned by most surgeons and is discouraged because the perioperative mortality and stroke morbidity is unacceptably high. On the other hand, the NASCET study found carotid endarterectomy to be beneficial for patients with near total occlusion (90 to 94%).(FN41)
AGE AND PERIOPERATIVE RISK
Although considered a landmark study by many experts, NASCET does not provide recommendations applicable to patients older than age 80. For this population, earlier community-based studies may be used to address the appropriateness of the NASCET recommendations in regard to carotid endarterectomy.(FN42) However, the results of these community-based studies have been conflicting.
Some studies report that advancing age has a negative impact on the outcome of carotid endarterectomy. Specifically, a higher perioperative combined stroke and death rate was found among octogenarians when compared with younger age groups.(FN26,43) This finding was also echoed in other pre-NASCET studies.(FN44,45) The risk of perioperative stroke and death was found to be increased significantly with advancing age. For instance, patients age 75 to 79 were found to have a mortality risk three times higher than patients younger than age 70. Patients age 80 and older experienced a mortality rate four times higher following carotid endarterectomy when compared with patients in their 60s.(FN20)
Conversely, other studies have consistently documented excellent results for patients age 75 or older who had undergone carotidsurgery.(FN46,47) In addition, although octogenarians may often have greater and more complex medical comorbidity, a recent study found carotid endarterectomy to be safe and beneficial in reducing the incidence of stroke.(FN48)
In view of these findings, careful selection of symptomatic patients age 75 and older is recommended. Medical management with antiplatelet agents or warfarin anticoagulation must be considered for octogenarians with serious comorbidity.(FN26) Once the safety profiles of stent angioplasty of the carotid artery are established, it may emerge as an alternate treatment for high-risk older patients.
SUMMARY
Carotid occlusive disease can result in neurologic deficit that is devastating for both the patient and family. We hope the diagnostic approach we have outlined will enable physicians to properly investigate and treat patients suspected of having carotid occlusive disease. The timely diagnosis of carotid stenosis can prevent new-onset stroke or worsening of acute cerebral infarction.
ADDED MATERIAL
JEAN-RENOIR EUGENE, DO, MPH MOHAMMED ABDALLAH, DO MAURIZIO MIGLIETTA,
DO VIC V. VERNENKAR, DO RUDOLFO PASCUAL, MD RENATO BRIONES, MD
THOMAS BARNES, MD JEFFREY HAGER, DO
Dr. Eugene and Dr. Vernenkar are chief surgical residents and
Dr. Miglietta is a senior surgical resident, St. Barnabas Hospital,
Bronx, NY. Dr. Abdallah is an attending vascular surgeon, Atlantic City Medical Center, Atlantic City, NJ. Dr. Pascual is chairman, department of vascular surgery, Deborah Heart and Lung Center, Browns Mills, NJ. Dr. Briones and Dr. Barnes are attending vascular surgeons, Deborah Heart and Lung Center. Dr. Hager is director, vascular fellowship program, Deborah Heart and Lung Center, and assistant professor of surgery, Philadelphia College of Osteopathic Medicine.
The authors wish to thank Neil Weintraub, MD, attending vascular surgeon at St. Barnabas Hospital, Bronx, NY, for his thorough review of the manuscript. His insightful comments were of tremendous benefit and improved the content of the article.
TABLE 1 Selected etiologies of TIAs and ischemic stroke
CARDIOGENIC VASCULAR
Atrial fibrillation Carotid stenosis
Atrial flutter Arterial dissection
Sick sinus syndrome Fibromuscular dysplasia
Ventricular aneurysm Intracranial arterial stenosis
Valvular surgery
Mitral valve prolapse HEMATOLOGIC
Patent foramen ovale
Infectious endocarditis Protein C+S deficiency
Sickle-cell disease
TTP
Hypercoagulable state
TTP: Thrombotic thrombocytopenic purpura
Source: Prepared for GERIATRICS by Jean Renoir Eugene, DO, MPH; Mohammed Abdallah, DO; Maurizio Miglietta, DO; Vic V. Vernenkar, DO; Rudolfo Pascual, MD; Renato Briones, MD; Thomas Barnes, MD; and Jeffrey Hager, DO.
The degree of stenosis and morphology of the plaque at the carotid bifurcation are important predictors of ischemic stroke risk in the older patient. Illustration for GERIATRICS by Andrew Grivas
Figure. Algorithm for clinical management of carotid artery disease
FOOTNOTES
1. Eton D, Weaver FA (eds). Vascular disease: A multi-specialty
approach to diagnosis and management. Austin: Landes Bioscience, 1998:27.
2. Kannel WB. Current status of the epidemiology of brain infarction associated with occlusive arterial disease. Stroke 1971; 2:295-318.
3. Moore WS (ed). Surgery for cerebrovascular disease. New York: Churchill Livingstone, 1987:85.
4. Matsumoto N, Whisnant JP, Kurland LT, Okazaki H. Natural history of stroke in Rochester Minnesota, 1955 through 1969: An extension of a previous study, 1945 through 1954. Stroke 1973; 4(1):20-9.
5. Meyer FB, Sundt TM Jr., Piepgras DG, et al. Emergency carotid endarterectomy for patients with acute carotid occlusion and profound neurological deficits. Ann Surg 1986; 203:82-9.
6. Sacco RL, Benjamin EJ, Broderick JP, et al. American Heart Association Prevention Conference, IV: Prevention and rehabilitation of stroke risk factors. Stroke 1997; 28:1507-17.
7. Norris JW, Zhu CZ, Bornstein NM, Chambers BR. Vascular risks of asymptomatic carotid stenosis. Stroke 1991; 22(12):1485-90.
8. Moore WS (ed). Vascular surgery: A comprehensive review. Philadelphia: WB Saunders, 1998:558.
9. Chambers RB, Norris JW. Outcome in patients with asymptomatic neck bruits. N Engl J Med 1986; 315:860-5.
10. Roederer GO, Laglois YE, Jager Y, et al. The natural history of carotid arterial disease in asymptomatic patients with cervical bruits. Stroke 1984; 15(4):605-13.
11. Morganstein LB, Fox AJ, Sharpe BL, et al. The risk and benefits of carotid endarterectomy in patients with near occlusion of the carotid artery. North American Symptomatic Carotid Endarterectomy Trial (NASCET) Group. Neurology 1997; 48(4):911-15.
12. Park AK, McCarthy WJ, Pearce WH, Matsumura JS, Yao JS. Carotid plaque morphology correlates with presenting symptomatology. J Vasc Surg 1998; 27(5):872-8.
13. Eliasziw M, Streifler JY, Fox AJ, Hachinski VC, Ferguson GG, Barnett HJ. Significance of plaque ulceration in symptomatic patients with high grade stenosis. North American Symptomatic Carotid Endarterectomy Trial. Stroke 1994; 25(2):304-8.
14. Langsfeld M, Gray-Weale AC, Lusbey RJ. The role of plaque morphology and diameter reduction in the development of new symptoms in asymptomatic carotid arteries. J Vasc Surg 1989; 9:548-57.
15. Harward TRS, Kroener JM, Wickbom IG, Bernstein EF. Natural history of asymptomatic ulcerative plaques of the carotid bifiurcation. Am J Surg 1983; 146(2):208-12.
16. Barnett HJM, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 1998; 339(20):1415-25.
17. Curley PJ, Norrie L, Nicholson A, Galloway JM, Wilkinson AR. Accuracy of carotid duplex is laboratory specific and must be determined by internal audit. Eur J Vasc Endovasc Surg 1998; 15(6):511-14.
18. Turnipseed WD, Kennel TW, Turski, Acher CW, Hoch JR. Combined use of duplex imaging and magnetic resonance angiography for evaluation of patients with symptomatic ipsilateral high grade stenosis, J Vasc Surg 1993; 17(5):832-9.
19. Jackson MR, Chang AS, Robles HA, et al. Determination of 60% or greater carotid stenosis: a prospective comparison of magnetic resonance angiography and duplex ultrasound with conventional angiography. Ann Vasc Surg 1998; 12(3):236-43.
20. Mittl RL, Broderick M, Carpenter JP, Goldberg HI. Blinded-reader comparison of magnetic resonance angiography and duplex ultrasonography for carotid artery bifurcation stenosis. Stroke 1994; 25(1):4-10.
21. Dipel DW, de Kinkelder A, Bakker SL, Van Kootemn F, van Overhagen H, Koudstaal PJ. The diagnostic value of colour duplex ultrasound for symptomatic carotid stenosis in clinical practice. Neuroradiology 1999; 41(1):1-8.
22. Nicholas GG, Osborn MA, Jaffe JW, Reed JF III. Carotid artery stenosis: Preoperative noninvasive evaluation in a community hospital. J Vasc Surg 1995; 22(1):9-16.
23. Worthy SA, Henderson J, Griffiths PD, Oates CP, Gholkar A. The role of duplex sonography and angiography in the investigation of carotid artery disease. Neuroradiology 1997; 39(2):122-6.
24. Eliasziw M, Rankin RN, Fox AJ, Haynes RB, Barnett HJ. Accuracy and prognostic consequences of ultrasonography in identifying severe carotid artery stenosis. North American Symptomatic Carotid Endarterectomy Trial (NASCET) Group. Stroke 1995; 26(10):1747-52.
25. Grata JC, Norris TW, Kamm B, and the TASS Baseline and Angiographic Data Subgroup. Prevention of stroke with ticlopidine: Who benefits most? Neurology 1992; 42:111.
26. Hass WY, Easton JD, Adams HP, et al. A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high risk patients. N Engl J Med 1989; 321:501-50.
27. Dyken ML. Antiplatelet agents and stroke prevention. Semin Neurol 1998; 18(4):441-50.
28. Creager MA. Results of CAPRIE trial: Efficacy and safety of clopidogrel versus aspirin in patients at risk of ischemic events. Vasc Med 1998; 3(3):257-60.
29. Adams DR, Victor M, Ropper HA (eds). Cerebrovascular accident In: Principles Of Neurology (6th ed). New York: McGraw-Hill, 1997:777-873.
30. Caplan LR, Mohr JP, Kistler JP, Koroshetz W. Should thrombolytic therapy be the first line of treatment for acute ischemic stroke? N Engl J Med 1997; 337(18):1309-10.
31. Kelly RE. Stroke prevention and intervention. New option for improved outcomes. Postgrad Med 1998; 103(2):43-58.
32. The Asymptomatic Carotid Atherosclerosis Study Group: Study design for randomized prospective trial of carotid endarterectomy for asymptomatic atherosclerosis. Stroke 1989; 20(7):8849.
33. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991; 325(7):445-53.
34. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995; 273:1421-8.
35. Gorelick PB, Sacco RL, Smith DB, et al. Prevention of first stroke: A review of guidelines and a multidisciplinary consensus statement from the National Stroke Association. JAMA 1999; 281(12):1112-20.
36. da Silva AF, McCollum P, Szymanska T, de Cossart L. Prospective study of carotid endarterectomy and contralateral carotid occlusion. Br J Surg 1996; 83(10):1370-2.
37. Gasecki AP, Eliasziw M, Ferguson GG, Hachinski V, for the North American Symptomatic Carotid Endarterectomy Trial. Long-term prognosis and effect of endarterectomy in patients with symptomatic severe carotid stenosis and contralateral carotid stenosis or occlusion. J Neurosurg 1995; 83(5):778-82.
38. Coyle KA Smith RB III; Salm AA, Dodson TF, Chaikof EL, Lumsden AB. Carotid endartercetomy with contralateral carotid occlusion: Review of 10-years experience. Vardiovasc Surg 1996; 4(1);71-5.
39. Mackey WC, O'Donnell TF, Callow AD. Carotid endarterectomy contralateral to an occluded carotid artery: Perioperative risk and late results. J Vasc Surg 1990; 11:778-85.
40. Hetzer NR, Flanagan RA, O'Hare PJ, Beven KG. Surgical versus nonoperative treatment of symptomatic carotid stenosis. Ann Surg 1986; 204:154-62.
41. Morganstein LB, Fox AJ, Sharpe BL, et al. North American Symptomatic Carotid Endarterectomy Trial (NASCET) Group. The risk and benefits of carotid endarterectomy in patients with near occlusion of the carotid artery. Neurology 1997; 48(4):911-15.
42. Hallett JW, Pietropaoli JA, Ilstrup DM, et al. Comparison of North American Symptomatic Carotid Endarterectomy Trial and population based outcomes for carotid endarterectomy. J Vasc Surg 1998; 27:845-51.
43. Hsia DC, Krushat WM, Moscoe LM. Epidemiology of carotid endarterectomies among Medicare beneficiaries. J Vasc Surg 1992; 16:201-8.
44. Meyer FB, Meissner I, Fode NC, Losasso TJ. Carotid endarterectomy in elderly patients. Mayo Clin Proc 1991; 66:464-9.
45. Fisher ES, Malenka DJ, Solomon NA, et al. Risk of carotid endarterectomy in the elderly. Am J Public Health 1989; 79:1617-20.
46. Perler BA. The impact of advanced age on the results of carotid endarterectomy: An outcome analysis. J Am Coll Surg 1996; 183:559- 64.
47. Perler BA. The impact of advanced age on the results of carotid endarterectomy in the elderly. Is it worthwhile? Surgery 1994;116:479-83.
48. Perler BA Dardick A, Burleyson GP, Gordon TA, Williams GM. Influence of age and hospital volume on the results of carotid endarterectomy: A statewide analysis of 9918 cases. J Vasc Surg1998; 27:25-33.
TABLE 2 RISK FACTORS ASSOCIATED WITH ISCHEMIC STROKE
Hypertension Cigarette smoking Hyperlipidemia
Diabetes mellitus Obesity Sedentary lifestyle
Alcoholism Oral contraceptive use Hypercoagulable state
Source: Prepared for GERIATRICS by Jean Renoir Eugene, DO, MPH: Mohammed Abdallah, DO; Maurizio Miglietta, DO; Vic V. Vernenkar, DO; Rudolfo Pascual, MD; Renato Briones, MD; Thomas Barnes, MD; and Jeffrey Hager, DO.
HAGER, Carotid occlusive disease: Primary care of patients with or without symptoms. Vol. 54, Geriatrics, 05-01-1999.