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Objective:This study was an attempt to determine risk factors for rupture and to improve management of patients with type B aortic dissection who survive the acute phase without operation. Methods: We studied 50 patients by means of serial computer-generated 3-dimensional computed tomographic scans. All patients who did not undergo operative treatment before the completion of at least 2 computed tomographic scans a minimum of 3 months apart after an acute type B dissection were included in the study. The median duration of follow-up was 40 months (range 0.9-112 months). Only 1 patient died of causes unrelated to the aneurysm during follow-up. Nine patients had fatal rupture (18%); 10 patients underwent elective aneurysm resection because of rapid expansion or development of symptoms, and 31 patients remained alive without operation or rupture. Possible risk factors for rupture in patients in the rupture, operative, and event-free groups were compared, as were dimensional data from first follow-up and last computed tomographic scans. Results: Older age, chronic obstructive pulmonary disease, and elevated mean blood pressures were unequivocally associated with rupture (rupture versus event-free survival, P < .05), and pain was marginally significantly associated. Analysis of dimensional factors contributing to rupture was complicated by the fact that patients who underwent elective operation had significantly larger aneurysms and faster expansion rates than did either of the other groups, leaving comparisons of aneurysmal diameter between groups with and without rupture showing only marginal statistical significance. The last median descending aortic diameter before rupture in the rupture group was 5.4 cm (range 3.2-6.7 cm). Conclusions: In an environment in which patients with large and rapidly expanding aneurysms are usually referred for surgical treatment, older patients with chronic type B dissections, especially if they have uncontrolled hypertension and a history of chronic obstructive pulmonary disease, are significantly more likely to have rupture than are younger, normotensive patients without lung disease. Neither the presence of a persistently patent false lumen nor a large abdominal aortic diameter appears to increase the risk of rupture. Overall, our nondimensional data strikingly resemble the natural history of patients with nondissecting aneurysms, suggesting that calculations derived from data on chronic descending thoracic and thoracoabdominal aneurysms would provide an overly conservative individual estimate of rupture risk for patients with chronic type B dissection, who tend toward earlier rupture of smaller aneurysms. A more aggressive surgical approach toward treatment of patients with chronic type B dissection seems warranted. (J Thorac Cardiovasc Surg 1999;117:776-86)

Objective: We assessed the impact on histologic and behavioral outcome of an interval of retrograde cerebral perfusion after arterial embolization, comparing retrograde cerebral perfusion with and without inferior vena caval occlusion with continued antegrade perfusion. Methods: Sixty Yorkshire pigs (27 to 30 kg) were randomly assigned to the following groups: antegrade cerebral perfusion control; antegrade cerebral perfusion after embolization; retrograde cerebral perfusion control; retrograde cerebral perfusion after embolization; retrograde cerebral perfusion with inferior vena cava occlusion, retrograde cerebral perfusion with inferior vena cava occlusion control, and retrograde cerebral perfusion with inferior vena cava occlusion after embolization. After cooling to 20^o C, a bolus of 200 mg of polystyrene microspheres 250 to 750 (@mm diameter (or saline solution) was injected into the isolated aortic arch. After 5 minutes of antegrade cerebral perfusion, 25 minutes of antegrade cerebral perfusion, retrograde cerebral perfusion, or retrograde cerebral perfusion with inferior vena cava occlusion was instituted. After the operation, all animals underwent daily assessment of neurologic status until the time of death on day 7. Results: Aortic arch return, cerebral vascular resistance, and oxygen extraction data during retrograde cerebral perfusion showed differences, suggesting that more effective flow occurs during retrograde cerebral perfusion with inferior vena cava occlusion, which also resulted in more pronounced fluid sequestration. Microsphere recovery from the brain revealed significantly fewer emboli after retrograde cerebral perfusion with inferior vena cava occlusion. Behavioral scores showed full recovery in all but one control animal (after retrograde cerebral perfusion with inferior vena cava occlusion) by day 7 but were considerably lower after embolization, with no significant differences between groups. The extent of histopathologic injury was not significantly different among embolized groups. Although no histopathologic lesions were present in either the antegrade cerebral perfusion control group or the retrograde cerebral perfusion control group, mild significant ischemic damage occurred after retrograde cerebral perfusion with inferior vena cava occlusion even in control animals. Conclusions: Although effective washout of particulate emboli from the brain can be achieved with retrograde cerebral perfusion with inferior vena cava occlusion, no advantage of retrograde cerebral perfusion with inferior vena cava occlusion after embolization is seen from behavioral scores, electro- encephalographic recovery, or histopathologic examination; retrograde cerebral perfusion with inferior vena cava occlusion results in greater fluid sequestration and mild histopathologic injury even in control animals. Retrograde cerebral perfusion with inferior vena cava occlusion shows clear promise in the management of embolization, but further refinements must be sought to address its still worrisome potential for harm.(J Thorac Cardiovasc Surg 1998;115:1142-59) J Thorac Cardiovasc Surg 1998;115:1142-59