Carotid revascularization in the presence of contralateral carotid artery occlusion is safe and durable.

OBJECTIVE: Complete occlusion of the contralateral carotid artery has been thought to increase the risk of carotid endarterectomy (CEA). This study was conducted to determine whether contralateral occlusion (CO) leads to a higher rate of complications among patients undergoing CEA or alters long-term outcomes. METHODS: All CEAs (N = 221) performed at our institution between September 1997 and June 2002 were reviewed. Patients were divided into two groups, i.e., CO and contralateral patency. Statistical analyses were performed using Fisher's exact test for nominal values and the t test for continuous variables. Life-table analyses were performed for patency and survival. RESULTS: Complete data and follow-up results were available for 170 of the 221 operations performed during the study period. CO was present in 16 cases (9.4%). Preoperative demographic features, indications for surgery, and operative techniques did not vary between study groups; there was increased use of general anesthesia (p = 0.05) in the CO group. No surgical deaths occurred. The perioperative stroke rates were not statistically different between groups (CO group, 6.3%; contralateral patency group, 2.6%; p = 0.39). Long-term patency and stroke-free survival rates at 5 years exceeded 90% and did not vary significantly between groups. CONCLUSION: Patients undergoing CEA with occlusion of the contralateral carotid artery do not have unique preoperative demographic features or indications. Contralateral carotid artery occlusion does not increase risk or alter long-term outcomes after CEA. Carotid revascularization can be safely performed in tertiary military centers.

Extracranial cerebrovascular revascularization for chronic ocular ischemia.

We investigated the demographics, presentation, and outcome of patients undergoing cerebrovascular reconstruction for chronic ocular ischemia (COI) at a single institution through a review of 17 patients over a 9-year period. A total of 558 extracranial cerebrovascular reconstructions were performed during the period of study. Seventeen patients (3%) suffered symptoms of COI. There were 19 symptomatic eyes and 15 asymptomatic eyes. Two patients suffered bilateral symptoms. Eighteen (95%) symptomatic eyes experienced rapidly degenerating global visual acuity, and one suffered bright-light amaurosis. Concomitant ocular pathology was present in 10 (59%) patients, consisting of glaucoma (n = 4), cataracts (n = 4), diabetic retinopathy (n = 3), and macular degeneration (n = 1). Symptomatic eyes were found to have significantly worse ipsilateral internal carotid artery (p = 0.004), external carotid artery (p = 0.002), aortic arch branch disease (p = 0.04), and vertebral artery disease (p = 0.04). All 17 reconstructions treated ipsilateral disease. Twelve patients (70.6%) had significant bilateral disease at the time of operation. Three patients underwent staged contralateral reconstruction. Following revascularization, subjective visual improvement or stabilization occurred in 16 patients (94%). A single patient worsened after developing acute narrow angle glaucoma in the perioperative period. Worse cerebrovascular disease is present ipsilateral to symptomatic eyes. When revascularization is performed, arrest of progression or improvement of symptoms occurs in most patients.

Graft patency is not the only clinical predictor of success after exclusion and bypass of popliteal artery aneurysms.

PURPOSE: The traditional measure of success after exclusion and bypass of popliteal artery aneurysm (PAA) is graft patency. In addition to fate of the bypass, we hypothesize that late outcome after surgical treatment of PAA is influenced by completeness of exclusion. METHODS: Thirty patients who underwent 41 reconstructions for PAA over a 10-year period were reviewed. RESULTS: Excluded PAAs were examined with duplex ultrasound scan for size, patency, and patent feeding branches; bypass grafts and native inflow and outflow arteries were examined for patency and size. Thirty-six limbs were available for follow-up (mean follow-up period, 46 +/- 42 months). Only two aneurysms (5.6%) appeared patent on duplex ultrasound scan, but five limbs had patent arterial branches communicating with thrombosed excluded PAAs. PAA diameter decreased from 2.5 +/- 0.8 cm to 1.7 +/- 0.5 cm (P <.0001) in most. However, 12 excluded PAAs (33%) showed significant enlargement from 2.2 +/- 0.9 cm to 2.8 +/- 1.0 cm (P =.002). A quarter of enlarging excluded PAA were associated with new compressive symptoms. Three methods of PAA exclusion were used: proximal and distal ligation with short segment isolation (type 1), proximal and distal ligation with long segment isolation (type 2), and single ligature (type 3). In univariate analysis, type of exclusion significantly influenced late size of excluded PAA (P =.004). Type 1 exclusion was superior to both type 2 and 3 exclusions in producing aneurysm diameter reduction. Type 3 exclusion resulted in aneurysm growth. In addition, excluded aneurysms with visualized feeding branches were associated with significant growth compared with PAAs without feeding branches (P =.006). Graft primary and assisted primary patency rates at 5 years were 86% +/- 9.4% and 92% +/- 7.4%, respectively. Although graft diameter and native donor artery diameter significantly increased, this did not adversely affect graft patency. CONCLUSION: Enlargement of excluded PAA after surgical treatment can cause compressive symptoms. Exclusion requires adequate vascular isolation to prevent late PAA enlargement, with proximal and distal arterial ligation best performed adjacent to the aneurysm. Vein graft enlargement occurs, but this enlargement does not adversely influence patency.

Luminal thrombus disrupts nitric oxide-dependent endothelial physiology.

BACKGROUND: The goals of this study were: (1) to develop a large animal model to study endothelial function, and (2) to determine if arterial thrombosis induces endothelial dysfunction in vivo. METHODS: Surgical exposure of the porcine iliac and femoral arteries was performed. Normal porcine arteries were compared with arteries subjected to 90 min of arterial thrombosis. External iliac artery (EIA) luminal diameters were measured using M- and B-mode duplex ultrasound. Endothelium-dependent relaxation (EDR) and endothelium-independent relaxation (EIR) were measured using acetylcholine (ACh) and sodium nitroprusside (NTP), respectively. Endothelial integrity was determined by factor VIII immunohistochemistry (F8) and scanning electron microscopy (SEM). Nitric oxide levels were determined using a chemiluminescence assay of nitrite/nitrate metabolites (NO(x)). Continuous variables were analyzed using the two-tailed Student t test. RESULTS: Control artery EDR was 80 +/- 7.1% (+/- SE), while arteries exposed to luminal thrombus for 90 min had an EDR of 55.2 +/- 5.7% (ACh = 15 microg/min, n = 11, P = 0.0231). EIR was preserved in normal and thrombosis groups with uniform response to NTP (4.92 +/- 0.1 cm vs 5.07 +/- 0.42 cm, P = 0.76). F8 staining identified endothelium in all groups. SEM analysis revealed an intact monolayer of endothelium after thrombosis. Local NO(x) levels were 17.3% lower after 90 min of thrombosis (49.3 microM vs 40.8 microM, n = 16, P < 0.001). CONCLUSIONS: Luminal thrombus induces arterial dysfunction acutely without causing endothelial cell loss. EIR remains unaffected, indicating normal smooth muscle cell function. NO(x) levels suggest that nitric oxide levels are decreased acutely after thrombosis. The development of this porcine large animal model allows the in vivo study of vasospasm and alternative thrombolytic regimens.