Michael Belkin

Embolism from vertebral artery origin occlusive disease

We report 10 patients with severe occlusive disease of the vertebral artery (VA) origin in the neck with intra-arterial embolism to the posterior circulation. The VA lesions in seven patients were complete occlusions, and three patients had severe atherostenosis. All patients had strokes in the vertebrobasilar territory. The most frequent recipient sites of intra-arterial embolism were the intracranial VA-posterior inferior cerebellar artery region (8), and the distal basilar artery (BA) and its superior cerebellar and posterior cerebral artery branches (7). Two patients had pontine infarction due to BA embolism. The most common clinical signs were due to cerebellar infarction. Atherosclerotic disease of the VA origin has features in common with disease of the internal carotid artery origin. Both have similar risk factors and demography, and each can cause strokes by intracranial intra-arterial embolism.

Brain edema after carotid surgery.

Article abstract-The postoperative hyperperfusion syndrome describes an abrupt increase in blood flow with loss of autoregulation in surgically reperfused brain. Reports described a spectrum of findings, including severe headache, transient ischemia, seizures, and intracerebral hemorrhage. Hypertension is common after carotid artery surgery and often plays a role in the pathophysiology. We now report five patients with severe white matter edema after carotid surgery, a finding not previously included in the hyperperfusion syndrome. Five to 8 days after carotid surgery and after hospital discharge, each patient developed hypertension, headache, hemiparesis, seizures, and aphasia or neglect due to severe white matter edema ipsilateral to the carotid surgery. One patient had a small hemorrhage within the edematous area. Hypertension was severe in four patients and moderate in one. The carotid artery was patent by ultrasound or angiography in each patient after surgery. Transcranial Doppler showed increased velocities ipsilateral to surgery in two patients and bilaterally in one. Computed tomographic abnormalities and neurologic signs resolved within 3 weeks in four of the five patients treated with antihypertensives and anticonvulsants. The fifth patient died from herniation secondary to massive edema. Brain edema with focal neurologic signs should be included as a serious but potentially reversible component of the postoperative hyperperfusion syndrome. NEUROLOGY 1996;46: 175-181

Long-term follow-up of patients operated on for recurrent carotid stenosis*

We reviewed our experience with 29 operations for recurrent carotid stenosis in 27 patients who underwent both their primary carotid endarterectomy and their reoperations at our institution. These 27 patients represent 4% of the 667 patients who underwent primary carotid endarterectomies at our institution and who are included in our carotid follow-up registry. Reoperation was prompted by recurrent symptoms in 19/29 (65.5%) cases. Comparison of long-term stroke prevention in those patients who did (84% at 5 years, 78.6% at 10 years) and did not (90.3% at 5 years, 83.6% at 10 years) develop recurrent stenosis requiring reoperation revealed no statistically significant difference (p = 0.48) when measured from the time of primary operation. The perioperative stroke and death rates for reoperation (3.4% and 0%) were acceptable. We conclude that with our acceptably low perioperative stroke morbidity (3.4%), surgery for recurrent carotid stenosis in symptomatic patients or in asymptomatic patients with high-grade (greater than or equal to 75%) stenosis maintains the durable stroke prevention offered by primary carotid endarterectomy.

Late stroke after carotid endarterectomy: The role of recurrent stenosis

Perioperative stroke after carotid endarterectomy has been well studied, although little information is available regarding later strokes. We determined the etiology of late stroke after carotid endarterectomy by examining the records of those patients in our carotid registry who had a stroke more than 30 days after surgery. Thirty-five (5.1%) of the 688 patients in our registry had a stroke more than 30 days after surgery (mean follow-up, 59.3 months; standard error, 1.8 months; range, 1 to 292 months). The cause of late stroke was established by input from consulting neurologists, CT scanning of the head, magnetic resonance imaging results, angiograms, noninvasive studies, and postmortem examinations. Eight of the 11 strokes of unknown origin were massive fatal events for which no further evaluation was undertaken. Restenosis or occlusion accounted for fewer strokes (3 of 20, 15%) in the 1- to 36-month postoperative interval than in the greater than 36-month interval (8 of 15, 53.7%) (p less than 0.02 by Fishers Exact Test). These data support the hypothesis that the early pseudointimal hyperplastic lesion is less likely to result in stroke than is later recurrent stenosis, which is usually related to atherosclerosis.

Common carotid artery occlusion with patent internal and external carotid arteries: Diagnosis and surgical management

PURPOSE Occlusion of the common carotid artery (CCA) is generally associated with occlusion of the ipsilateral internal carotid artery (ICA) and external carotid artery (ECA). Occasionally, however, collateral circulation to the ECA may preserve patency of the ICA via retrograde perfusion through the bulb. These patients may suffer ongoing transient ischemic attacks and risk for stroke. Recognition of this pathologic variant may allow for effective surgical intervention. METHODS We have performed seven operations in six patients with occluded CCAs and patent ECA and ICAs. The occluded CCA was on the left side in each case (p < 0.01). Six of the operations were performed for ischemic symptoms, including amaurosis fugax in five patients, hemispheric TIA in one patient, and profound global ischemia in two patients who had concomitant occlusions of other extracranial vessels. In the five most recent cases the patent ECA and ICA above the occluded CCA were recognized by preoperative duplex scanning, which prompted cerebral angiography. A variety of reconstructive procedures were used, depending on the pathologic anatomy. These procedures included subclavian or axillary artery to carotid artery bypass with carotid endarterectomy (five), carotid endarterectomy with thrombectomy of the proximal CCA (one), and ascending aorta to carotid artery bypass (one). RESULTS There were no strokes associated with the surgery, although one patient had transient neurologic symptoms and a seizure associated with documented reperfusion edema. Three of the patients had preoperative and postoperative transcranial Doppler studies that documented significant improvement in intracranial hemodynamics. Five of the patients have had continuously patent grafts with relief of symptoms for an average of 40 months (range 3 to 155 months). The remaining patient had graft occlusion after 72 months and underwent repeat operation for amaurosis fugax and global ischemia. His second graft remains patent, and he is symptom free 21 months later. CONCLUSIONS Recognition of patent distal vessels above a CCA occlusion depends on a high index of suspicion, careful investigation of the carotid bulb with duplex scanning, and delayed arteriographic views of the bulb allowing for late collateral vessel filling. The favorable results in this small series of patients supports an aggressive surgical approach when patients with symptoms are encountered with patent distal vessels above an occluded CCA.

Routine postendarterectomy duplex surveillance: Does it prevent late stroke? ☆

Our recent finding that less than 50% of late postendarterectomy strokes are related to recurrent carotid stenosis led us to question the utility of routine postendarterectomy duplex surveillance (RpCEADS) in the prevention of late stroke. To evaluate our RpCEADS program, we reviewed our postoperative duplex studies and correlated their results with clinical data. A total of 1053 postendarterectomy scans was carried out on 348 carotid arteries (258 patients) (3.0 +/- 0.1 studies/artery) during an average follow-up of 52.6 (+/- 2.3) months. Less than 50% of recurrent carotid stenosis was documented throughout follow-up in 292 (83.9%) of 348 arteries. Recurrent carotid stenosis of greater than 50% or occlusion of either the common or internal carotid artery was noted in the remaining 56 arteries (16.1%). Of the 56 duplex-detected recurrent stenoses, only two (3.6%) resulted directly in an unheralded stroke, whereas eight (14.3%) underwent prophylactic reoperation, eight (14.3%) resulted in transient ischemia requiring reoperation, eight (14.3%) occluded without causing stroke, and 29 (51.8%) remained asymptomatic and did not progress to occlusion. Assuming that each of our eight patients who underwent prophylactic reoperation would have had a stroke if operation had not been carried out and our two unheralded strokes could have been prevented with more rigorous follow-up, RpCEADS might have prevented late stroke related to 10 (2.9%) of 348 arteries in 10 (3.9%) of 258 patients after surgery. All other cases of duplex-detected recurrent carotid stenosis or occlusion were asymptomatic or manifest by transient cerebral ischemia. Therefore RpCEADS cannot be justified as a means of preventing late strokes related to recurrent stenosis.

The variation in vein graft flow velocity with luminal diameter and outflow level

Duplex scanning has recently been used to monitor the patency of infrainguinal vein grafts. Empirically derived criteria that have been used for identifying the failing graft have never accounted for the effect of vein graft diameter or varying outflow resistance, despite the fact that they are major determinants of flow. We prospectively examined the variation in graft peak systolic flow velocity with graft diameter and outflow level in a consecutive series of 68 patients with 72 normally functioning vein grafts returning for routine follow-up. Images were obtained of vein grafts with a duplex scanner throughout their lengths, and the distal peak systolic flow velocity and intraluminal diameters were recorded. There were 15 popliteal, 26 tibial, and 21 inframalleolar grafts. The mean ankle-brachial index of inframalleolar grafts was 1.01 +/- 0.04 and did not differ significantly from tibial (0.96 +/- 0.03) or popliteal (0.93 +/- 0.06) grafts (p = 0.32). Grafts to the three outflow levels differed significantly in diameter, with inframalleolar grafts measuring 3.95 +/- 0.17 mm, tibial grafts 4.78 +/- 0.21 mm, and popliteal grafts 5.65 +/- 0.38 mm (p = 0.0001). In a similar manner inframalleolar grafts had significantly lower peak systolic flow velocities (59.1 +/- 3.4 cm/sec) than tibial (77.2 +/- 5.6 cm/sec) or popliteal (71.0 +/- 7.6 cm/sec) grafts (p = 0.04). Inframalleolar grafts did not demonstrate a significant correlation (r = -0.21, p = 0.29) between peak systolic flow velocity and graft diameter. Conversely, both tibial (r = -0.49, p = 0.005) and popliteal (r = -0.73, p = 0.002) grafts demonstrated significant inverse correlations.(ABSTRACT TRUNCATED AT 250 WORDS)

Modification of the Thrombogenicity of a Self-Expanding Vascular Stent

When placed in the iliac arteries of normal healthy animals, the Wall-stent self-expanding endovascular prosthesis exhibits minimal thrombogenicity, measured by 111In-labeled platelet uptake. Preliminary clinical reports suggest a greater thrombogenicity in diseased human arteries. When evaluated in an ex vivo shunt, these stents exhibit significant thrombogenicity. The ex vivo shunt may therefore provide a model to evaluate strategies to reduce thrombogenicity in the clinical setting. Stents were released into shunts and the uptake of In111-labeled platelets was measured by gamma imaging for 2 h at a flow rate of 100 mL/min. The effect of systemic heparin, 100 U/kg, oral aspirin, 325 mg, and local application of heparin-benzalkonium chloride complex were evaluated. At the end of each study the stents were fixed in situ and evaluated with scanning electron microscopy (SEM). Control stents exhibited a rapid, significant uptake of platelet associated 111In activity, which reached a maximum in approximately 1 h. Twenty-two percent of control stents occluded before 2 h. Aspirin reduced maximum platelet uptake by 46%. Systemic heparin, with a clotting time greater than five times control, reduced maximum platelet uptake by 86%. The benzalkonium-heparin complex coating, with no increase in clotting time, reduced maximum platelet uptake by 84%. No occlusions were observed with the anti-thrombotic regimes. SEM evaluation of the stents supports the results of the isotope uptake studies.

Critical carotid and vertebral arterial occlusive disease and cough syncope.

Background and Purpose Cough syncope typically occurs in patients with known chronic lung disease. The mechanism usually involves a combination of decreased venous return, increased cerebrospinal fluid pressure, and secondary hypocapnia, all resulting in cerebral arterial vasoconstriction. Cough syncope has not in the past been associated with occlusive cerebrovascular disease. Case Description We describe a 50-year-old man with a 6-month history of episodes of loss of consciousness during paroxysms of coughing. Physical examination showed asymmetrical upper extremity blood pressures and carotid and subclavian artery bruits. Pulmonary function studies were normal. Ultrasound and angiography showed total occlusion of the left common carotid artery, right internal carotid artery, and right vertebral artery; tight stenosis of the right subclavian artery; and a hypoplastic left vertebral artery. The patient had a left subclavian-to-left common carotid artery bypass and has had no syncope since that time. Conclusions To our knowledge, this is the first reported case of cough syncope and severe cerebrovascular disease in which surgery led to amelioration of symptoms. Cerebrovascular occlusive disease may contribute to cough syncope.

Superiority of Balloon Occlusion Arteriography to Reactive Hyperemic Arteriography in Visualization of Distal Lower Limb Vessels

Balloon occlusion arteriography was performed in 38 lower limbs; reactive hyperemic arteriography was also performed in 16 of these limbs. To assess the safety and utility of this technique the balloon occlusion arteriograms of all 38 patients were reviewed retrospectively by a vascular surgeon and vascular radiologist who were unaware of the patients identity and ultimate treatment. After the arteriograms were reviewed and the outflow vessels identified, a decision was made regarding operability and optimal recipient vessel for distal bypass. Twenty-two of the 38 patients underwent balloon occlusion arteriography only, and 21/22 (95.5%) of these patients only had studies deemed adequate for surgical planning. Twelve of the 16 (75%) patients underwent both reactive hyperemic arteriography and balloon occlusion arteriography; potential distal outflow vessels not seen on reactive hyperemic arteriograms were observed on balloon occlusion arteriograms. In only 4/16 (25%) patients the balloon occlusion arteriograms did not yield additional information. No complications were associated with this technique. Approximately 8.5 g of iodine per run is used for balloon occlusion arteriography compared with approximately 37 g of iodine per run for reactive hyperemic arteriography. Balloon occlusion arteriography is a safe and accurate adjunctive technique that can be used when identification of lower limb vessels is critical.