Blood Pressure Management

There is strong evidence that even a modest reduction of systemic hypertension can substantially reduce the risk of secondary stroke. For instance, in the PROGRESS (Perindopril pROtection aGainst REcurrent Stroke Study) trial, a combination of an angiotensin-converting enzyme (ACE) inhibitor with a thiazide diuretic resulted in a decrease in the average blood pressure by 12/5 and reduced the risk of recurrent stroke by 43%.7

Patients with acute stroke often present with hypertension that slowly resolves over the first 24 to 48 hours. Castillo et al8 observed that the average blood pressure during the first 24 hours of stroke has a U-shaped effect on outcome, with the best outcomes associated with a systolic blood pressure of 180 mm Hg. Patients with blood pressures 20 mm Hg higher or lower than 180 mm Hg had substantially larger stoke volumes and worse neurologic outcomes. Based on these observations, acutely lowering the systolic blood pressure below 180 mm Hg is not recommended during the first 24 hours after a stroke. However, it is important to consider lowering systolic blood pressure below 180 mm Hg in patients receiving intravenous thrombolytics, as blood pressures over 185/110 mm Hg have been associated with a significant in crease in cerebral hemorrhage.9

Statins

There are two large trials that suggest that the use of a statin can reduce the risk of both primary and secondary stroke. In the Heart Protection Study (HPS), 20,536 patients with stroke risk factors such as hypertension, vascular disease, and diabetes were randomly assigned to receive 40 mg of simvastatin or placebo. At the end of the 5-year follow-up period, the risk of primary stroke was 25% lower in the treatment group. In the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial,10 patients with a history of stroke or TIA within 6 months were randomly assigned to treatment with either 80 mg of atorvastatin or placebo. In the 5-year follow-up period there was an 18% relative reduction in the risk of secondary stroke in patients treated with atorvastatin. Interestingly, there was an increase in the relative risk of hemorrhagic stroke among statin users that was not observed in the HPS trial.

Based on the data from these two studies, statins should be used in all patients with risk factors for ischemic stroke including VAOS. Statins, in addition to lowering total body cholesterol, may help stabilize plaque, halt or reverse atherosclerosis, and improve arterial endothelial function. In addition, statins significantly lower the risk of cardiac events in patients with vascular risk factors, a major source of morbidity and mortality in this patient population.

Surgical Revascularization

In experienced hands, VA revascularization can be done with acceptable risk.11 Perioperative mortality and stroke during revascularization is uncommon (<2%).11 Nevertheless, surgical morbidity from these procedures is common. In a recent series of 29 patients who underwent proximal VA revascularization either by transposition or endarterectomy, 48% of patients sustained some sort of surgical approach morbidity such as Horner’s syndrome, recurrent laryngeal nerve injury, or chylothorax.12 Despite its high morbidity rate, surgical revascularization is still a reasonable option in patients who fail medical management and who are poor candidates for an endovascular approach. It is also notable that surgical revascularization carries an 80% 5-year patency rate,11 considerably better than what has been reported in most endovascular series to date.

Patient Preparation

Vertebral artery origin atherosclerosis, like carotid artery disease, is often a marker of systemic vascular disease. Not surprisingly, the cause of death in most VAOS patients, even symptomatic ones, is cardiac disease. A careful history and physical examination often uncover other health issues such as congestive heart failure or angina that may require additional workup, optimization, and planning prior to an invasive procedure. Palpation of the femoral and peripheral pulses, including an Allen test, helps to identify potential problems with percutaneous access. Physiologic testing of heart function is often important in preoperative preparation before a stent is placed.

Imaging

Antiplatelet Agents

All patients being prepared for VA stent placement require dual antiplatelet therapy, usually with aspirin and clopidogrel. In patients undergoing elective procedures the patient is started on 75 mg of clopidogrel and 325 mg of aspirin 1 week prior to the procedure. Based on the American College of Surgery (ACS) literature, patients who require more urgent treatment should be loaded with 300 mg of clopidogrel at least 8 hours prior to stenting. Alternatively, 600 mg of clopidogrel at least 3 hours prior to the procedure is effective.15 Platelet aggregation studies may be useful in identifying patients who may be nonresponders to aspirin or clopidogrel, although they are not routinely available in all centers and their utility remains controversial.

Anesthesia

Vertebral artery origin stenting can often be performed with the patient under moderate conscious sedation. Although most patients tolerate VA-origin angioplasty and stenting under conscious sedation, it is not the best choice in all patients. General anesthesia should be considered for patients with congestive heart failure (CHF), dementia, or even severe lumbar spine disease who cannot lie flat comfortably for at least 1 hour. General anesthesia with neurophysiologic monitoring may also be a good choice for patients with poor collateral flow who may not tolerate temporary occlusion of the VA during angioplasty. If general anesthesia is selected, then somatosensory evoked potentials (SSEPs), motor evoked potentials (MEPs), and electroencephalogram (EEG) monitoring are an option to assess the presence of ischemia. A blood pressure cuff should be placed on the ipsilateral arm, so that it can be inflated during the subclavian injections to improve visualization of the VA if necessary.

Puncture

The most convenient access point is generally the common femoral artery, although radial or brachial access can be used if femoral access is impossible or the VA anatomy is not favorable for a femoral approach. Often, patients with VA stenosis have other manifestations of peripheral vascular disease (Fig. 33.1). A 6-French (F), 10- or 25-cm groin sheath is usually sufficient for access if a guide catheter will be used. In patients with very tortuous anatomy an 80-cm Raabe guide sheath (Cook Medical, Bloomington, IN) parked just proximal to the VA origin in the subclavian artery provides additional support.

Intravenous heparin (usually 70 units/kg) is given to all patients after arterial access is secured. The activated clotting time (ACT) is measured with a Hemochron ACT analyzer (ITC Nexus Dx, Edison, NJ) 15 minutes after heparin administration. Patients are re-bolused with intravenous heparin hourly as needed to maintain the ACT between 250 and 300 seconds.16

Guide Catheter Placement

A 6F guide catheter (or guide sheath) on a continuous heparinized saline flush is navigated into the subclavian artery just proximal to the VA origin. A preprocedure angiogram of the entire length of the VA should be performed to verify balloon and stent measurements as well as to identify more distal disease. Cerebral angiography should also be performed to assess blood flow and define the baseline anatomy should an embolus occur.

On occasion, aortic arch anatomy may not provide adequate support for the guide catheter in the proximal subclavian artery. If this occurs, a “buddy wire” can provide additional support. In this technique an 0.018- or 0.014-inch wire is passed through the guide sheath and into the brachial artery. The wire is then left in place throughout the procedure to help prevent the guide catheter from slipping back into the arch (Fig. 33.2). A guide catheter can also be passed through a guide sheath in a coaxial arrangement to improve stability if necessary.