Peter A. Schneider

Effect of internal carotid artery occlusion on intracranial hemodynamics. Transcranial Doppler evaluation and clinical correlation.

Neurologic deficits that occur simultaneously with or subsequent to internal carotid artery occlusion may be influenced by the adequacy of the intracerebral collateral circulation. Transcranial Doppler ultrasonography was used to evaluate mean middle cerebral artery blood velocity and blood flow in major collateral arteries in 78 patients, including 39 patients with 40 internal carotid artery occlusions and 39 control patients with less severe extracranial cerebrovascular disease, matched for age and sex distribution. Middle cerebral artery blood velocity was 38.9 +/- 17.9 cm/sec ipsilateral to an occlusion, 50.9 +/- 18.3 cm/sec contralateral to an occlusion (p less than 0.01), and 56.8 +/- 14.4 cm/sec in the controls (p less than 0.01). Pulsatility index ipsilateral to an occlusion (0.86 +/- 0.32) was reduced compared with contralateral and control pulsatility indexes (1.05 +/- 0.33 and 1.03 +/- 0.18) respectively; p less than 0.05). Major intracerebral collateral arteries were detectable in 94.9% of occlusion patients and in 53.8% of controls (p less than 0.01). A posterior communicating artery was demonstrated ipsilateral to an occlusion in 80.0% of the patients and contralateral to an occlusion in 39.5% (p less than 0.01). An ipsilateral posterior communicating artery was identified in all 10 asymptomatic occlusions and in 75.8% of the symptomatic ones. Pulsatility index was 1.02 +/- 0.34 for asymptomatic occlusions and 0.76 +/- 0.30 for symptomatic occlusions (p less than 0.01). Transcranial Doppler ultrasonography permits noninvasive quantification of the cerebral hemodynamic consequences of internal carotid artery occlusion and direct evaluation of the collateral blood supply, which can be correlated with symptomatology.

Preformed confluent endothelial cell monolayers prevent early platelet deposition on vascular prostheses in baboons

We assessed the capacity of preformed confluent endothelial cell (EC) monolayers on small-caliber prosthetic grafts to prevent early platelet deposition in a baboon model. Cultured human umbilical vein ECs were attached to expanded polytetrafluoroethylene (Gore-Tex, 4 mm inner diameter, 3 cm length) precoated with type I collagen and perfused in vitro for 2 hours at 15 ml/min with serum-containing culture medium to achieve cell spreading into confluent monolayers. Cell numbers were quantified by deoxyribonucleic acid assay or isotopic counting of indium 111-labeled ECs. Saturation density for cell attachment was 3.55 +/- 0.29 x 10(5) cells per square centimeter of graft. After 1 hour of in vitro perfusion at 100 ml/min, 92.8% +/- 1.8% of cells remained attached and the flow surface was morphologically confluent. When grafts were inserted as extension segments into arteriovenous silicone rubber (Silastic) shunts in baboons, thereby exposing the endothelialized grafts to native flowing blood (100 ml/min) for 1 hour, the EC monolayers remained confluent with 81.05% +/- 5.88% of the cells attached. Indium 111-labeled platelet deposition onto grafts was quantified by dynamic scintillation camera imaging. Platelet deposition on 10 endothelialized grafts was markedly reduced (0.16 +/- 0.04 x 10(9) platelets per graft) compared with 10 untreated control grafts (1.84 +/- 0.59 x 10(9) platelets, p less than 0.02), eight grafts with early attached unspread ECs (2.38 +/- 0.66 x 10(9) platelets, p less than 0.005), and 11 grafts treated with collagen alone (5.93 +/- 0.72 x 10(9) platelets, p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive assessment of cerebral collateral blood supply through the ophthalmic artery.

We assessed the potential of 2-MHz pulsed-wave transorbital Doppler ultrasonography to delineate the role of the ophthalmic artery as a source of collateral cerebral blood supply by comparing oculopneumoplethysmography, transorbital Doppler ultrasonography, periorbital continuous-wave Doppler ultrasonography, and transcranial Doppler ultrasonography in 25 patients with unilateral internal carotid artery occlusion and five controls with 10 normal internal carotid arteries. Systolic ophthalmic artery blood velocity was reduced ipsilateral to an internal carotid artery occlusion (38.2 +/- 10.2 cm/sec) compared with the contralateral and control velocities (46.0 +/- 10.3 and 47.5 +/- 6.8 cm/sec, respectively; p less than 0.05). Ophthalmic systolic pressure measured by oculopneumoplethysmography was 94.7 +/- 13.2 mm Hg ipsilateral to an internal carotid artery occlusion compared with 108.4 +/- 15.3 mm Hg on the contralateral side (p less than 0.01). Transorbital and periorbital Doppler ultrasonography detected reversed ophthalmic artery blood flow ipsilateral to an internal carotid artery occlusion in 44.0% and 40.0% of the patients, respectively. Systolic middle cerebral artery blood velocity was 55.2 +/- 22.3 cm/sec ipsilateral to an internal carotid artery occlusion compared with 79.4 +/- 23.5 cm/sec on the contralateral side (p less than 0.05) and 101.2 +/- 18.9 cm/sec in the controls (p less than 0.05). Reversed ophthalmic artery blood flow was associated with a low middle cerebral artery blood velocity and lack of major intracerebral collaterals. Transorbital Doppler ultrasonography permits noninvasive evaluation of the ophthalmic artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Importance of cerebral collateral pathways during carotid endarterectomy.

Before surgery, we evaluated major intracranial collateral pathways using transcranial Doppler ultrasonography (TCD) in 50 patients who then underwent carotid endarterectomy with concurrent multimodality cerebral monitoring. Patients were grouped with respect to collateral pathways demonstrated preoperatively by TCD: Group 1, good collateralization with an anterior and/or posterior communicating artery ipsilateral to the operative carotid lesion (29 patients, 58%); Group 2, collateral pathways present but impeded by other proximal stenoses (nine patients, 18%); and Group 3, no collateralization identified (nine patients, 18%). Three patients (6%) could not be classified. TCD identified major collateral pathways with a sensitivity of 89% and a specificity of 80% when compared with arteriography. During carotid endarterectomy mean middle cerebral artery velocity, pulsatility index, and stump pressure were higher and the decrease in middle cerebral artery velocity with extracranial carotid artery cross clamping was significantly less among Group 1 patients than among Group 2 and 3 patients (p less than 0.05 for both groups). Group 1 patients required fewer intraoperative carotid artery shunts and developed fewer ischemic electroencephalographic abnormalities than did patients in Groups 2 and 3 (p less than 0.05 for both groups). TCD assessment of cerebral collateralization helps predict hemodynamic consequences of cross clamping during carotid endarterectomy.

Transcranial Doppler in the management of extracranial cerebrovascular disease: implications in diagnosis and monitoring

Transcranial Doppler (TCD) insonation permits quantitative noninvasive evaluation of intracerebral arterial velocity. With the use of a 2 MHz Doppler through a transtemporal approach, middle cerebral artery blood velocity (MCA-V, centimeters per second) and major collaterals were measured in 96 patients, including 15 normal control subjects, 66 patients with extracranial cerebrovascular disease (ECCVD), and 15 patients with other medical problems without ECCVD. MCA-V was higher in control subjects (62.7 ± 15.1) than in patients with ECCVD (45.0 ± 16.3, p < 0.05). There was a significant inverse correlation between MCA-V and the degree of internal carotid artery stenosis present by duplex examination. Twenty-three patients monitored during carotid endarterectomy had a mean MCA-V under anesthesia of 37.0 ± 16.9, which decreased to 22.4 ± 14.8 during cross-clamping (p < 0.01). MCA-V during cross-clamping correlated directly with stump pressure (R = 0.87) and was higher when major collaterals were identified before operation by TCD than when none were seen (31.7 ± 9.5 vs. 8.8 ± 8.5, p < 0.01). Shunt function was verified in all 11 patients shunted. Electroencephalographic changes occurred in four patients with an MCA-V of 14.7 ± 8.5 compared with an average of 24.1 ± 15.5 for patients with normal electroencephalograms. MCA-V increased from 46.6 ± 21.2 before operation to 61.0 ± 22.4 after carotid endarterectomy (p < 0.05). TCD can quantitate intracerebral blood flow in specific vessels, collateralization, the degree of cerebral ischemia caused by ECCVD, intraoperative changes in MCA-V that correlate with stump pressure and the electroencephalogram, shunt function, and the increases in cerebral blood flow resulting from carotid surgery. It is a new and important tool. (J VASC SURG 1988;7:223-31.)

Confluent durable endothelialization of endarterectomized baboon aorta by early attachment of cultured endothelial cells

Since surgical endarterectomy produces a highly thrombogenic vascular flow surface, we evaluated in baboons the capacity of acutely attached, unspread, cultured, homologous aortic endothelial cells to form durable, confluent endothelial cell monolayers and to interrupt acute thrombus formation during exposure to arterial blood flow conditions. When cultured baboon aortic endothelial cells were incubated with segments of freshly endarterectomized baboon aorta for 20 minutes in vitro, 3.8 x 10(5) endothelial cells/cm2 became attached. The endarterectomized surface treated with endothelial cells showed the presence of rounded, unspread endothelial cells with intervening bare areas of vascular media. Platelet deposition onto the endothelial cell--treated surface during exposure to blood under high flow conditions for 1 hour in vivo was markedly reduced by the attached but unspread endothelial cells. Moreover, these attached endothelial cells underwent spreading on the endarterectomized surface in the presence of high shear blood flow to form a confluent endothelial monolayer at the end of 1 hour. Thus acutely attached cultured endothelial cells form a durable thromboresistant monolayer on surgically denuded vascular surfaces during exposure to arterial blood flow.

Monoclonal antibody-induced inhibition of platelet function: effects on hemostasis and vascular graft thrombosis in baboons.

The usefulness of antiplatelet agents in vascular graft recipients remains controversial because of uncertainties regarding drug mechanisms of action and dose-duration effects. In our study, a well-characterized murine monoclonal antibody (LJ-CP8, 10 mg/kg) was infused into baboons to assess the hemostatic consequences and antithrombotic effectiveness of blocking the platelet glycoprotein IIb-IIIa receptor for fibrinogen and other adhesive glycoproteins. Five treated animals and six control animals were evaluated with serial measurements of platelet count, bleeding time, and platelet aggregation ex vivo (in response to adenosine diphosphate and collagen). Indium 111-labeled platelet deposition onto femoral vascular grafts (4 mm inner diameter Gore-Tex) implanted immediately after antibody infusion was measured by quantitative gamma camera imaging. Although the antibody did not alter circulating platelet counts, bleeding times were immediately prolonged to more than 30 minutes (vs. 4.8 +/- 0.4 minutes pretreatment) with only partial normalization by 48 hours (8.3 +/- 1.0 minutes, p less than 0.05). Platelet aggregation in response to both collagen and adenosine diphosphate was abolished immediately and remained impaired for 48 hours. Despite the profound inhibition of platelet function, graft platelet deposition was equivalent postoperatively in both the treated and untreated groups (p greater than 0.5), averaging approximately 5 x 10(9) platelets per graft. Graft-associated indium 111-labeled platelet activity increased over 48 hours and was not reduced by the antibody treatment (p greater than 0.5 at all times). All grafts were removed at 8 days; only one graft from a treated animal was found patent.(ABSTRACT TRUNCATED AT 250 WORDS)

The natural history of amaurosis fugax with minor degrees of internal carotid artery stenosis.

The natural history of amaurosis fugax with hemodynamically insignificant degrees of internal carotid artery stenosis is uncertain. Seventy-three patients over age 40 who presented with amaurosis fugax without obvious cause and had ipsilateral stenoses of 50% or less with carotid duplex scanning were followed for a mean period of 35.5 months (range 3–110) without surgical intervention. At the initial vascular laboratory duplex evaluation, 35 patients had normal arteries (47.9%), 29 had minor (0–19%) stenoses of the ipsilateral internal carotid arteries (39.7%), and 11 had 20–50% stenosis (15.1%). Four patients with 0–19% stenosis and one patient with 20–50% stenosis experienced a subsequent stroke or permanent ipsilateral blindness. When analyzed by life-table format, stroke, blindness, and early death were more frequent in patients with minor degrees of stenosis than in those with normal arteries. Investigations in all patients with amaurosis fugax should be aimed at identifying whether the symptoms are explained by arteriosclerotic, systemic, collagen, cardiac, hematologic, or ophthalmologic disease. When no other etiology is found, and localized carotid bifurcation atherosclerosis of even modest degrees is identified, an atheroembolic etiology should be considered.