Endovascular repair and open repair resulted in similar long-term survival. The perioperative survival advantage with endovascular repair was sustained for several years, but rupture after repair remained a concern. Endovascular repair led to increased long-term survival among younger patients but not among older patients, for whom a greater benefit from the endovascular approach had been expected. (Funded by the Department of Veterans Affairs Office of Research and Development; OVER ClinicalTrials.gov number, NCT00094575.).

The preferential placement of autogenous fistulas may increase primary patency and decrease the incidence of revisions. Vein transpositions had similar secondary patency compared with simple fistulas, but required more revisions. The greatest benefit of a vein transposition fistula was seen in women and in patients with a history of access failure.

Intimal hyperplasia is a primary cause of failure after vascular reconstruction and may be affected by blood flow. We have studied the effects of increased blood flow on intimal hyperplasia in porous polytetrafluoroethylene grafts implanted in baboons. These grafts develop an endothelial lining by 2 weeks and neointimal thickening due to proliferation of underlying smooth muscle cells by 1 month. Creation of a distal arteriovenous fistula increased flow (from 230 +/- 35 to 785 +/- 101 ml/min, p less than 0.001) and mean shear (from 26 +/- 4 to 78 +/- 10 dynes/cm2, p less than 0.001) without causing a drop in pressure across the grafts. Fistula flow did not alter the pattern of endothelial coverage but did cause a marked reduction in the cross-sectional area of the neointima (from 2.60 +/- 0.52 to 0.42 +/- 0.07 mm2 at 3 months, p less than 0.01). Detailed morphometric analysis revealed an equivalent percentage decrease in smooth muscle cells and matrix content, suggesting that the primary effect of increased flow was to reduce smooth muscle cell number without affecting the amount of matrix produced by individual cells. The neointima remained sensitive to changes in flow at late times; ligation of the fistula after 2 months resulted in a rapid increase in neointimal thickness (from 0.60 +/- 0.03 mm2 after 2 months of fistula flow to 3.88 +/- 0.55 mm2 1 month after ligation of fistula, p less than 0.01). These results support the hypothesis that changes in blood flow affect the structure of diseased as well as normal vessels.

During the last decade (1980 to 1989) 186 patients with ruptured abdominal aortic aneurysm were admitted to a single urban hospital. Ninety-six percent of these patients had a prehospital systolic blood pressure less than 90 mm Hg. Management included paramedic field resuscitation and transport, an emergency department diagnostic protocol completed in an average of 12 minutes, rapid transport to a dedicated emergency operating room, aneurysmorrhaphy by general surgery chief residents under the supervision of specialist vascular surgeons, and skilled postoperative intensive care unit care. Nevertheless, 130 (70%) patients died in the first 30 postoperative days--3% in the emergency department, 13% in the operating room, 51% in the intensive care unit, and 3% on the ward or at home. Certain features--age greater than 80 years, female gender, persistent preoperative hypotension despite aggressive crystalloid and blood replacement, admission hematocrit less than 25, transfusion requirements exceeding 15 units--were associated with a greater than 90% likelihood of death. No patient with preoperative cardiac arrest survived more than 24 hours. From this experience we conclude that, although "optimal" prehospital, emergency department, operating room, and postoperative care can improve the outcome of patients with ruptured abdominal aortic aneurysms in shock, most such patients will die. Certain clinical features predict such excessive mortality rates after ruptured abdominal aortic aneurysms that withholding operation may be reasonable. Screening of patients at high risk for abdominal aortic aneurysm, followed by elective aneurysmorrhaphy, is clearly indicated.

Use of an algorithm favoring endovascular repair resulted in a highly significant reduction in rAAA mortality in our urban hospital. Thirty-day mortality for open repair was no different between pre- and post-protocol eras. With modern techniques of resuscitation and surgical management, a majority of patients presenting with rAAA can survive.

We have previously shown that high shear stress inhibits growth of developing neointima in a primate model of polytetrafluoroethylene (PTFE) graft healing. We used this model to test the hypothesis that increased shear stress can cause atrophy of an established neointima. High porosity PTFE grafts were inserted into the aorto-iliac circulation bilaterally in baboons. These grafts develop neointimal hyperplasia comprising smooth muscle cells and a luminal surface of confluent endothelium. Neointima was allowed to develop for 2 months. At that time 8 animals were sacrificed. In eight other animals blood flow in one of two grafts was increased by construction of a femoral arterio-venous fistula. These animals were sacrificed 2 months later (4 months after graft placement). At four months, intimal cross sectional area was smaller on the high shear stress side compared to the contralateral, normal shear stress side (2.53 +/- 0.75 versus 6.83 +/- 0.65 mm2, P < .05). Neointima from grafts exposed to 2 months normal shear stress followed by 2 months of high shear stress had regressed when compared to normal-shear stress grafts studied at 2 months (2.53 +/- 0.75 versus 4.56 +/- 0.68 mm2, P < .05). Morphometric analysis using transmission electron microscopy revealed that the decrease in intimal cross sectional area was attributable to a loss of both smooth muscle cells and matrix. Endothelial nitric oxide synthase was induced in high-flow graft intima. These observations support the conclusion that elevated shear stress can cause vessel wall atrophy. This process might be mediated by nitric oxide.

We compared ultrasonic duplex scanning and angiography for the localization and classification of arterial stenoses and occlusions in 32 patients. The criteria for the detection of a greater than 50% diameter reducing stenosis was an increase in peak systolic velocity of greater than 100%, loss of reverse flow, and spectral broadening. Duplex studies and angiograms were evaluated in a blinded fashion. locations along visualized arteries. The path of the Doppler beam is indicated by a white line on the B mode image, and the region from which velocity data are obtained (the sample volume) is indicated by a cross mark on that line (figure 1). Because this system permits measurement of the angle of incidence of the Doppler beam with the vessel axis, velocity can be calculated by the Doppler equation. All examinations were performed by one of two technologists (M. C. or N. V.). Our technique has been previously described. 1 2 Patients are asked to fast for 12 hr before the examination to decrease interference by abdominal gas. This has allowed us to obtain velocity signals from aortoiliac segments in approximately 90% of patients. Study of the recumbent patient starts at the proximal abdominal aorta, with a 3 MHz transducer for average-sized adults and a 5 MHz transducer for asthenic individuals. The transducer is placed just above the umbilicus to image the aorta and is then moved distally to the inguinal ligament, following the course of the iliac arteries. Examination of the more superficial distal arteries is performed with higher-resolution, 5 or 7.5 MHz, transducers. The popliteal artery is examined with the patient prone and the knee slightly flexed. When time permits we attempt to study all segments in each patient. Occasionally limited examinations directed at specific arterial sites are performed. A single extremity can be studied in less than an hour, whereas a complete study may take 2 hr or more.We prospectively applied classification criteria previously described by Jager et al. 1' 2Each arterial segment is graded into five categories of stenosis: normal, 1% to 19% diameter reduction, 20% to 49% diameter reduction, 50% to 99% diameter reduction, and total occlusion. Typical waveforms for each category are shown in figure 2. Normal arteries have a triphasic signal and minimal spectral broadening. The spectral band is narrow with a clear area below the systolic peak (systolic window

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