Faculty Bibliography

PURPOSE: It is believed that cerebral hyperperfusion syndrome (CHS) is caused by loss of cerebral autoregulation resulting from chronic cerebral ischemia and that factors including increased intraoperative cerebral blood flow, ipsilateral or contralateral carotid disease, and postoperative hypertension may cause CHS. We describe our experience with CHS, which diverges from published reports. MATERIALS AND METHODS: From March 2000 to February 2002 we performed 455 carotid endarterectomy (CEA) procedures in 404 patients at our institution. CHS developed 1 to 8 days (mean, 3.2 +/- 2.5 days) postoperatively in 9 patients (2%), 6 women and 3 men, whose age ranged from 52 to 84 years (mean, 69 +/- 8 years). Indications for surgery in 8 patients without neurologic symptoms were ipsilateral internal carotid artery (ICA) stenoses ranging from 70% to 99% (mean, 80% +/- 7%); the remaining patient had an ipsilateral stroke, with good clinical recovery, 7 weeks before CEA. Only 1 patient had significant contralateral ICA stenosis (70%). However, 5 patients had undergone contralateral CEA within the previous 3 months. CHS symptoms were severe headache in 5 patients, seizures in 3 patients (1 stroke), and visual disturbance and ataxia in 1 patient. All 404 patients (455 cases) underwent intraoperative and early (2 weeks) postoperative carotid artery duplex scanning. The 9 patients with CHS also underwent carotid artery duplex scanning at the time of the neurologic event. RESULTS: Mean intraoperative ICA volume flow (MICAVF) in the 9 CHS cases was not significantly different from that in the other 446 cases (170 +/- 47 mL/min and 182 +/- 81 mL/min, respectively). However, mean ICA volume flow (481 +/- 106 mL/min) and peak systolic velocity (PSV) (108 +/- 33 cm/s) for the 9 CHS cases measured at onset of symptoms were higher than those for the remaining 446 cases (267 +/- 87 mL/min and 80 +/- 26 cm/s, respectively) (P <.01). Of the 9 patients with CHS, only 3 had systolic blood pressures more than 160 mm Hg at onset of symptoms. Severity of ipsilateral and contralateral ICA stenoses was not significantly different between the 9 CHS cases and the remaining 446 cases. CONCLUSIONS: These data do not corroborate the common belief that CHS occurs preferentially in patients with severe ipsilateral or contralateral carotid disease, increased intraoperative cerebral perfusion, or severe hypertension. Recently performed contralateral CEA (<3 months) appears to be predictive of CHS.

The TrapEase filter is a permanent, symmetric nitinol filter that can be deployed through a low-profile sheath. Although the TrapEase is enjoying an increasing market share of inferior vena cava (IVC) filters, there are still limited clinical follow-up data on its use. This study is a retrospective review of 189 consecutive infrarenal TrapEase filters placed at our institution. The study included 80 men and 109 women, with an average age of 73 years (24-102). The most common indication for filter placement was a contraindication to warfarin. In total, 13% of the patients were treated with warfarin. The filter was successfully deployed in all cases, via the right femoral vein in 57% of the patients, via the left femoral vein in 32%, and via the right internal jugular vein in 11%. Follow-up studies were performed as clinically indicated. During the investigation, there were three cases of IVC thrombosis (1.5%) and one case of retroperitoneal hemorrhage potentially caused by filter placement. Two of the thrombosis cases resulted in serious sequelae. This study also represents the first report of a symptomatic pulmonary embolism (PE) after TrapEase filter placement. While this investigation does demonstrate a low overall complication rate of this new device, it raises the concern of an increase in IVC thrombosis rate.

BACKGROUND: We have previously demonstrated that programmed cell death, proteolytic activity, and inflammatory infiltrate in the aneurysmal wall may have a role in the pathogenesis of popliteal artery aneurysms (PAA). This investigation examines the expression of a cell death-promoting molecule, a cysteine protease, YAMA/CPP-32 in a series of PAA specimens. METHODS: Twenty PAA specimens were obtained from patients undergoing elective surgical repair. Normal controls were popliteal arteries obtained from patients without PAA who were undergoing infrainguinal bypass surgery (n = 8). Standard histochemistry techniques were used to assess inflammatory infiltrates in PAA. Expression of apoptosis-promoting molecule, CPP-32, vascular smooth muscle cells (VSMC), macrophages, and T lymphocytes was detected by immunohistochemistry. RESULTS: There is a conspicuous disruption and fragmentation of elastic lamellae and increased inflammatory infiltrate in the PAA as compared with normal arteries. As compared with normal popliteal artery tissues, the PAA demonstrated large number of cells immunopositive for CPP-32 (60.45 +/- 4.25% P < 0.05). This study revealed significantly increased expression of CPP-32 in the T-cell population of the PAA as compared with the other cells (P < 0.01). Dual immunolabeling and investigation of serial sections demonstrated that co-expression of CPP-32 was maximum in the CD8+ subset (37 +/- 3.3% of the total CPP-32 immunoreactive cells identified). CONCLUSIONS: The data emphasize that the inflammatory infiltrate in the PAA walls has a significant role in the pathogenesis of this vascular disorder. Cells expressing death-promoting molecules are present in large numbers and are predominantly T lymphocytes in PAA. In addition to compromising the mechanical integrity of the vessel wall, apoptosis in the inflammatory infiltrate may contribute to the production of cytokines, activation of other signaling molecules such as stress proteins that could eventually favor PAA development.

OBJECTIVE: Upper extremity embolic complications of occluded axillofemoral bypass grafts are infrequent. However, traditional management of dissection of axillary anastomosis for removal of the stump can be challenging. We report two patients with critical upper extremity ischemia secondary to stump syndrome and its successful management with endovascular techniques. METHODS: One hundred fifty-two patients underwent axillofemoral bypass grafting over 10 years from 1991-2001. Two patients from this series had acute ischemia involving the ipsilateral upper extremity of occluded axillofemoral bypass graft. Duplex ultrasound scans revealed occlusion of the axillofemoral bypass graft and acute occlusion of ipsilateral upper extremity arteries. Both patients underwent brachial artery exploration and embolectomy. Completion angiograms revealed persistent axillofemoral bypass graft stump as the source of embolus. The stump was obliterated with a 10-mm/40-mm Wallgraft introduced through the same arteriotomy made for brachial embolectomy. Transesophageal echocardiography and magnetic resonance angiography of the arch and great vessels were performed to exclude other sources of origin for the embolus. RESULTS: Both patients remained symptom-free and with patent stent grafts, as seen on duplex scans at 3, 6, and 9 months of follow-up. CONCLUSIONS: Upper extremity embolism is a rare complication after occlusion of axillofemoral bypass grafts. The endovascular approach to obliterate the stump of occluded axillofemoral bypass grafts is minimally invasive and an effective alternative treatment of this rare condition.