Endovascular Treatment of Extracranial Occlusive Disease

Chapter 88 Endovascular Treatment of Extracranial Occlusive Disease



Stroke is currently the third leading cause of death in the United States.1 Carotid occlusive disease is the underlying pathology for 25% of the estimated 750,000 annual strokes.24 The prevalence of carotid stenosis is 0.5% after age 60 and increases to 10% in the population older than 80 years.57 There is a direct correlation between the degree of carotid artery stenosis and the risk of ipsilateral stroke.8 The majority of cases of carotid stenosis are asymptomatic; however, symptomatic stroke treatment and lost productivity due to stroke account for an estimated annual cost of $74 billion.9 The clinical and fiscal significance of stroke-related disabling morbidity has led to medical and surgical treatments for carotid occlusive disease, the goals of which lie in lowering the risk of stroke.


In the past, medical treatment for carotid occlusive disease was based on strategies stemming from studies directed at the treatment of general cardiovascular disease. However, more recently, prospective, randomized, controlled studies have proved a combination of surgical carotid revascularization by means of carotid endarterectomy (CEA) and medical management is highly successful in reducing the incidence of stroke among patients with moderate to severe symptomatic carotid stenosis10 and among those with severe asymptomatic carotid stenosis.3 CEA has been the standard of care for surgical revascularization for carotid occlusive disease; however, since the 1990s, carotid artery stenting (CAS) has evolved as an alternative treatment to CEA when dealing with patients deemed to be too high a surgical risk. High-risk patients account for up to one third of the patients undergoing CEA.11,12 CAS is an attractive alternative to CEA because it is less invasive, has less risk for cranial nerve damage, and has the ability to treat lesions that are anatomically out of reach or too difficult for CEA.12



Indications and Patient Selection


There is irrefutable evidence that for certain patient populations CEA offers an advantage over best medical treatment (BMT) alone. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) generated prospective, randomized data demonstrating symptomatic patients with carotid stenosis greater than 70% and a perioperative stroke or death rate below 6% are best treated by CEA over BMT alone.13,14 The Veterans Affairs Cooperative Studies Program (VACSP) also found a beneficial effect of CEA when compared to BMT.15 The Asymptomatic Carotid Atherosclerosis Study (ACAS) proved asymptomatic patients with carotid stenosis of greater than 60% could benefit from CEA with a reduction in 5-year ipsilateral stroke risk, provided that their perioperative stroke or death rate was less than 3% and their modifiable risk factors were aggressively treated.16 Based on the preceding results, the Stroke Council of the American Heart Association has published guidelines and indications for CEA.17 However, these key trials excluded patients deemed to be high risk for CEA. The initial indications for CAS were some of the key exclusion criteria from NASCET, VACSP, and ACAS, including restenosis after CEA, contralateral internal carotid artery (ICA) occlusion, previous neck irradiation, advanced age, renal failure, chronic obstructive pulmonary disease, and severe cardiopulmonary disease. The increasing use of CAS has led investigators to question whether either revascularization procedure is more beneficial over the other. Over the last 10 years, multiple studies have attempted to answer that question; however, variability in study design, technology used, and patient selection have made a comparison between CAS and CEA difficult.12,1822 It is beyond the scope of this chapter to detail individual study design flaws, results, and criticisms; however, several study trials have helped influence patient selection for CAS in my practice. The trial that led to U.S. Food and Drug Administration approval for CAS was the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE). The SAPPHIRE study led to a general sense that CAS was at least equivalent to CEA in high-risk patients. SAPPHIRE 30-day myocardial infarction (MI), stroke, and death rates were 4.8% in the CAS arm versus 9.8% in the CEA arm (P = 0.09).12 One-year MI, ipsilateral stroke, and death rates were 12.2% in CAS versus 20.1% in CEA (P = 0.048). The 3-year incidence of stroke was 7% for both CAS and CEA. The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) randomized 1326 symptomatic and 1196 asymptomatic patients to CAS or CEA with a median follow-up period of 2.5 years. This study recently concluded that among patients with symptomatic or asymptomatic carotid stenosis, the risk of the composite primary outcome of stroke, MI, or death did not differ significantly in the groups treated by CAS from those treated by CEA.18 This study did find a higher risk of periprocedural stroke with stenting (4.1% vs. 2.3%, P = 0.01) and periprocedural MI with endarterectomy (1.1% vs. 2.3%, P = 0.03). Further, quality-of-life analyses among survivors at 1 year indicated that stroke had a greater adverse effect than did MI on a range of health-status domains. It is the current practice of my colleagues and I to offer CAS to asymptomatic or symptomatic patients who would benefit from CEA but are deemed to be too high a surgical risk for CEA.



Preoperative Preparation


All patients in our surgical practice undergoing CAS are reported in ongoing clinical registries. Pretreatment patient evaluation consists of a noninvasive study suggesting carotid stenosis and a neurologic assessment performed by a neurologist or neurosurgeon. On the day of the procedure, the patient’s National Institutes of Health Stroke Scale is assessed and recorded. Preoperative laboratory results include hematocrit, hemoglobin, platelet count, white blood cell count, serum creatinine, prothrombin time, and activated partial prothrombin time obtained within a week of intervention. My colleagues and I also routinely obtain a baseline 12-lead electrocardiogram. Further cardiac or pulmonary evaluation is performed case by case as deemed medically necessary. MI is always a primary or secondary endpoint for clinical trials; thus, postprocedure creatine kinase, creatine kinase-MB, and troponin-I levels are routinely collected the morning after the procedure. All patients have a baseline brain computed tomography or magnetic resonance imaging to document preexisting infarctions.


In our practice, all patients considered for CAS are started on aspirin at a dosage of 325 mg daily at least 5 days prior to the procedure. My colleagues and I also start clopidogrel at least 24 hours prior to the procedure but preferably 3 to 5 days prior to intervention. Clopidogrel is loaded as a 300-mg dose the day before or 75 mg daily 5 days prior to intervention. Some evidence suggests the combination of aspirin and clopidogrel decreases restenosis by inhibiting myointimal proliferation.2325 In emergent cases in which patients are not pretreated, patients are loaded the day of surgery with aspirin at 325 mg and clopidogrel at 300 mg. After the angiogram is completed and the determination to proceed with CAS is made, 4000 U of heparin is administered intravenously and redosed at 1000 U every hour until completion of the stenting procedure. Although not a standard of care, many surgeons check activated coagulation times with the practice of anticoagulating to achieve the goal of doubling these times.




Procedure


Arterial access is gained through the femoral artery using the Seldinger technique to place a 6-French (Fr) sheath over a guidewire. Next, a 5-Fr diagnostic catheter is used to catheterize the common carotid artery (CCA). If needed, catheterization of the other vessels should be performed prior to the catheterization of the carotid artery needing treatment. Cervical carotid arteriography is performed to assess the degree of carotid stenosis. The intracranial circulation is also assessed at this point to characterize collateral flow, estimate delayed cranial perfusion secondary to stenosis, and identify any tandem lesions. Once measurements are performed and NASCET criteria are met for carotid stenting, a 0.035-inch exchange-length wire is passed under fluoroscopic road map guidance into the internal maxillary artery via the 5-Fr diagnostic catheter. The diagnostic catheter and femoral sheath are then removed over the exchange-length wire, and a 6-Fr, 90-cm sheath is passed under fluoroscopic guidance to a position 1 cm proximal to the cervical carotid bifurcation. If tortuous vessel anatomy does not allow the stiffer sheath to make the turn from the aortic arch into the right brachiocephalic or left CCA, a triaxial technique is used to advance the much stiffer sheath through this turn. This technique uses the 5-Fr diagnostic catheter over the exchange-length wire inside the 6-Fr sheath to give more support to the sheath through the turn. It is important on anteroposterior projections during positioning of the 90-cm sheath to visualize the projection over the chest. This ensures the sheath is taking a normal path through the turn from the aortic arch and not buckling.


The 0.035-inch exchange-length wire (and 5-Fr diagnostic catheter, if used) is removed, and more accurate measurements using a magnified cervical carotid arteriogram are performed using the 8-Fr outer diameter of the sheath as the measurement standard. The stenosis is determined according to NASCET criteria (Fig. 88-1A). The diameter of a straight portion of the ICA distal to the stenosis is determined to select the appropriate size of the distal protection device (DPD) and the appropriate diameter of the angioplasty balloon. The diameter of the CCA and the length of the stenosis are also determined to ensure selection of the appropriate length and diameter of the carotid stent. The carotid stent is sized so that it is 1 mm greater in diameter than the CCA.


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Jul 12, 2018 | Posted by in NEUROSURGERY | Comments Off on Endovascular Treatment of Extracranial Occlusive Disease

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