Safe ex vivo coronary angiography with isosmotic contrast agent.

Plain-film coronary angiography of the cardiac explant on the operating table should be considered when conventional cardiac catheterization is desired but unavailable. We compared the effects of three contrast solutions on cold-preserved, isolated guinea pig hearts. Hearts were excised, perfused for 30 minutes, and arrested with Plegisol solution at 7 degree C. Twenty minutes after arrest, experimental hearts were perfused with one of three solutions: hyperosmolar Hexabrix solution (n = 6), hyperosmolar Renografin-76 solution (n = 6), or diluted, isosmotic Omnipaque solution (n = 8). The hearts were flushed with cold Plegisol solution 5 minutes later. Control hearts received no contrast during arrest (n = 9). The hearts were reperfused after 1 hour of arrest, and coronary blood flow (in millimeters per minute), left ventricular developed pressure (in millimeters of mercury), and rate of developed pressure (in millimeters of mercury per second) were measured. Endothelium-dependent smooth muscle relaxation to bradykinin administration and endothelium-independent relaxation to sodium nitroprusside administration were also assessed. No significant difference in myocardial or endothelial function was noted between control hearts and hearts perfused with Omnipaque solution. Hearts perfused with Renografin solution or Hexabrix solution, however, were found to have significantly impaired endothelial and myocardial function. We conclude that an isosmotic contrast solution should be used for ex vivo coronary angiography in cold-preserved hearts to avoid impairment of endothelial and myocardial function.

Euro-Collins solution exacerbates lung injury in the setting of high-flow reperfusion.

Single-lung transplantation has been abandoned for the treatment of pulmonary hypertension by many centers because of overperfusion of the graft following implantation. Euro-Collins solution is currently used for lung preservation despite the vasoconstrictive effect of this intracellular-type solution. We hypothesized that high-flow reperfusion, alone or in combination with Euro-Collins-induced vasoconstriction, may cause lung dysfunction. Twenty-eight New Zealand White rabbit lungs were harvested and studied in an isolated, blood-perfused model of lung function after 4 hours of cold ischemia. Control lungs were preserved with 50 ml/kg cold saline solution flush and reperfused at either normal flow (60 ml/min) or high flow (120 ml/min). Experimental lungs were preserved with 50 ml/kg cold Euro-Collins solution and reperfused at normal or high flow rates. The arteriovenous oxygen gradient at the end of the 30-minute reperfusion period was significantly lower in the high-flow versus the low-flow experimental group (31.1 +/- 4.2 vs 130.6 +/- 41.6 mm Hg, p < 0.05). The pulmonary vascular resistance was increased in the high-flow groups and the experimental groups, with a statistically significant difference between low-flow experimental and control groups (64374.4 +/- 5722.6 vs 37041.5 +/- 2110.9 dynes x sec x cm(-5), p < 0.001). The percentage decrease in dynamic airway compliance in the high-flow experimental group was markedly different from that in the high-flow control group (-51% +/- 13.3% vs -10.15% +/- 3.4%, p < 0.05). Similarly, the wet/dry ratio of the lungs in the high-flow experimental group (13.92 +/- 2.32) was significantly greater than that in the low-flow experimental group (6.27 +/- 0.19, p < 0.01) and than that in the high-flow control group (5.88 +/- 0.23, p < 0.001). These data demonstrate that high-flow reperfusion and preservation with Euro-Collins solution are deleterious to lung function, both individually and in combination, in an ex vivo rabbit lung model. Lung preservation with Euro-Collins solution may not be optimal when high-flow reperfusion is anticipated, as in the setting of unilateral lung transplantation for pulmonary hypertension.

Enhanced isolated lung function after ischemia with anti-intercellular adhesion molecule antibody.

The binding of leukocytes to intercellular adhesion molecules expressed on endothelial surfaces during ischemia and subsequent reperfusion initiates leukocyte-mediated reperfusion injury. Interruption of this leukocyte-endothelium interaction may therefore prevent reperfusion injury. In an isolated, ventilated, blood-perfused rabbit lung preparation, we studied the effect of a monoclonal anti-intercellular adhesion molecule antibody on lung function during reperfusion. Lungs were harvested with 50 ml/kg cold Euro-Collins flush and 30 micrograms prostaglandin E1 before storage for 18 hours at 4 degrees C. Experimental groups received low-dose (100 micrograms) or high-dose (200 micrograms) anti-intercellular adhesion molecule antibody added to the pulmonary flush at harvest and to the initial reperfusate. Eighteen-hour control preparations were preserved for 18 hours and received saline solution vehicle. Immediate control preparations were harvested and immediately reperfused. The oxygen tension in the recirculated pulmonary venous effluent was measured after 30 minutes of reperfusion. Histologic specimens were graded by blinded observers for degree of leukocyte infiltration (0, normal, to 4, severe infiltration). The mean oxygen tensions (+/-standard error of the mean) were 138.29 +/- 6.23, 58.86 +/- 9.14, 86.87 +/- 11.32, and 139.33 +/- 16.15 mm Hg in immediate control preparations, 18-hour control preparations, low-dose antibody group, and high-dose antibody group, respectively (p = 0.0001). The leukocyte grades (mean +/- standard error of the mean) were 1.5 +/- 0.723, 3.0 +/- 0.955, 1.9 +/- 0.899, and 1.2 +/- 0.834, respectively (p = 0.0002). We conclude that anti-intercellular adhesion molecule antibody added to the pulmonary flush and initial reperfusate results in a dose-dependent enhancement of the reperfused lung's ability to oxygenate blood, possibly as a result of decreased leukocyte sequestration.

Neutrophil endopeptidase inhibitor improves pulmonary function during reperfusion after eighteen-hour preservation.

BACKGROUND: Reperfusion injury remains a significant problem after lung transplantation and is thought to be in part mediated by neutrophils. Ulinastatin inhibits release of elastase and cathepsin G from neutrophil granules. We hypothesized that inhibition of these neutrophi endopeptidases (proteases) would attenuate pulmonary reperfusion injury. METHODS: With an isolated, whole blood-perfused, ventilated rabbit lung model, we studied the effects of ulinastatin. All lungs were flushed with cold Euro-Collins solution, harvested en bloc, stored inflated at 4 degrees C for 18 hours, and reperfused with whole blood. The 18-hour control lungs (n = 8) were stored and reperfused. Low-dose (n = 8) and high-dose (n = 7) groups were treated with total doses of ulinastatin of 25,000 and 50,000 units, respectively, during flush and reperfusion. An additional control group of lungs (n = 8) was harvested, flushed, and immediately reperfused. RESULTS: The pulmonary artery pressure was significantly lower in the high-dose group than in the 18-hour control group (36.7 +/- 1.8 vs 44.8 +/- 2.9 mm Hg, p = 0.034). The percentage decrease in dynamic airway compliance was significantly less in the high-dose group than in the 18-hour control group (-13.8% +/- 4.4% vs -25.1% +/- 3.7%, p = 0.032). Both low-dose and high-dose ulinastatin treatments did not result in a significant improvement in oxygenation with respect to the 18-hour control group (72.2 +/- 25.8 vs 32.5 +/- 4.9 mm Hg, p = 0.21). CONCLUSIONS: Ulinastatin diminishes reperfusion injury after 18 hours of hypothermic pulmonary ischemia, with resultant improvements in pulmonary artery pressure and airway compliance. Improvement in pulmonary function after preservation and reperfusion with a neutrophil endopeptidase inhibitor confirms the role of endopeptidases in reperfusion injury and suggests an intervention to reduce their detrimental effects on early graft function.

The physiologic basis of warm cardioplegia.

BACKGROUND: Advances in myocardial protection have been instrumental in making cardiac surgery safer. Debate exists over the optimal medium and the optimal temperature for cardioplegia. Currently blood cardioplegia is preferred over crystalloid; the optimal temperature, however, remains controversial. METHODS: Both warm and cold blood cardioplegia use potassium-induced electromechanical arrest, thereby reducing oxygen consumption by 90% in the working heart. Hypothermic blood cardioplegia given every 15 to 30 minutes provides a bloodless operative field and reduces oxygen consumption an additional 5% to 20%. Continuous warm cardioplegia avoids the deleterious effects of hypothermic ischemia and minimizes reperfusion injury. Perfusion is often interrupted for 5 to 10 minutes to allow adequate visualization of the operative site. Both warm and cold cardioplegia can be given either antegrade or retrograde. RESULTS: Retrospective studies from Toronto support the safety and efficacy of warm cardioplegia. Two large prospective, randomized trials of warm cardioplegia versus intermittent cold blood or cold crystalloid cardioplegia demonstrated equally low incidences of death, perioperative myocardial infarction, and need of intraaortic balloon pump support. CONCLUSIONS: Warm blood cardioplegia represents the latest development in myocardial protection. Preliminary studies support its efficacy. Additional studies are needed to determine the ideal route of delivery and to identify any risks associated with the inherent warm cardiopulmonary bypass required.

Intrathoracic fibrin sealant application using computed tomography fluoroscopy.

Persistent intrathoracic airspace and bronchopleural fistula remain a problem following lung resection or in patients with severe bullous disease experiencing a spontaneous pneumothorax. Although fibrin sealant has been used successfully to manage such air-leaks, precise nonoperative intrathoracic application is difficult. This report describes a novel technique using computed tomography fluoroscopy for catheter-directed FS application through a previously placed thoracostomy tube. Continuous computed tomography-fluoroscopy images allowed real-time catheter manipulation for precise placement of fibrin sealant.

Effects of internal mammary artery dissection on phrenic nerve perfusion and function.

The effects of left internal mammary artery (LIMA) dissection and distal division on phrenic nerve perfusion and function were examined in an adult swine model. Phrenic nerve perfusion was determined by left atrial injection of radioactively labeled microspheres. Phrenic nerve function was determined by measuring nerve and diaphragm potentials evoked by bilateral phrenic nerve stimulation. In the first group of animals (n = 9), the LIMA was dissected with ligation of all its branches. Left phrenic nerve perfusion and function decreased after LIMA dissection in every animal studied, whereas only minimal changes were observed on the right. Sixty minutes after LIMA dissection, left phrenic nerve mean perfusion decreased 71%. Left phrenic nerve and left diaphragm mean action potential amplitudes decreased 54% and 80%, respectively. In the second group of animals (n = 4), the LIMA dissection was performed without division of the pericardiacophrenic artery, a small proximal branch of the internal mammary artery that supplies the phrenic nerve. Sixty minutes after LIMA dissection, left phrenic nerve perfusion had decreased by 21% from control values, with a corresponding decrease in left phrenic nerve and diaphragm mean action potential amplitudes of 19% and 23%, respectively. These results indicate that LIMA dissection with division of all its branches in this model is associated with a significant impairment in left phrenic nerve perfusion and function and suggests a causal relationship. These results may also explain the apparent increased phrenic nerve cold sensitivity and increased incidence of phrenic nerve dysfunction associated with LIMA grafting.(ABSTRACT TRUNCATED AT 250 WORDS)

Intraoperative hetastarch infusion impairs hemostasis after cardiac operations.

BACKGROUND: An outbreak of excessive bleeding after cardiac operations occurred at our institution when 5% albumin was in short supply and hetastarch became the preferred intraoperative colloid. As hetastarch may impair coagulation, we investigated the effects of its intraoperative administration on post-cardiac surgical hemostasis. METHODS: Indices of postoperative hemostasis were analyzed in 189 consecutive patients undergoing coronary artery bypass grafting. Three groups were compared: one group (n = 68) received a mean of 796 mL of hetastarch only in the operating room (a few minutes after cessation of cardiopulmonary bypass), another group (n = 59) received a mean of 856 mL postoperatively only, and a third group (n = 62) received no hetastarch. RESULTS: Compared with the other two groups, those patients administered hetastarch intraoperatively exhibited significant reductions in hematocrit and platelet count, a significant prolongation in the prothrombin time, and significant increases in both blood loss and hemostatic drug requirement. Also identified were obvious trends toward a greater transfusion requirement and reexploration rate for bleeding in the latter group. CONCLUSIONS: Hetastarch infusion just after weaning from cardiopulmonary bypass produces a clinically important impairment in post-cardiac surgical hemostasis. Intraoperative use of this agent during heart operations should be avoided until the safe timing of its administration is clarified.

Prevention of spinal cord injury after repair of the thoracic or thoracoabdominal aorta.

Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. The incidence of postoperative neurologic deficits varies from 4% to 38%. Factors associated with a greater risk for injury include the presence of dissection or extensive thoracoabdominal disease, and a prolonged cross-clamp time. Spinal cord ischemia initiates a deleterious cascade of biochemical events that ultimately result in an increased intracellular calcium concentration. Calcium-activated proteases, lipases, and nucleases mediate the processes that cause cell injury. The accumulation of oxygen-derived free radicals and the occurrence of hyperemia during reperfusion are also contributing causes of spinal cord injury. Increasing the spinal cord blood flow with shunts, oxygenated bypass circuits, cerebrospinal fluid drainage, the intrathecal administration of vasodilators, and the reattachment of intercostal arteries has been tried in an effort to increase spinal cord perfusion. Pharmacologically based measures to prevent spinal cord injury have been pursued, and these have consisted of hypothermia, anesthetic agents, calcium channel blockers, free radical scavengers, and immune system modulation. However, no single technique has proved to be consistently effective in preventing ischemia-induced spinal cord injury.

Ambulatory intraaortic balloon counterpulsation.

A technique is described for the retroperitoneal placement of a balloon pump that preserves patient mobility. This technique may be superior to standard femoral placement when prolonged support is required for cardiac transplant candidates awaiting donor organs.

Low-potassium solution for lung preservation in the setting of high-flow reperfusion.

BACKGROUND: We previously demonstrated that standard preservation using Euro-Collins solution impairs lung function in the setting of high-flow reperfusion because of potassium-induced vasoconstriction. Preservation strategies for single-lung transplantation are an important factor in patients with pulmonary hypertension. This study investigates the hypothesis that low-potassium preservation solution will improve function of lungs subjected to high-flow reperfusion. METHODS: Twenty-one New Zealand white rabbit lungs were harvested and studied on an isolated, blood-perfused model of lung function after 4 hours of cold ischemia at 4 degrees C. Control lungs were preserved with 50 mL/kg of cold saline solution flush (group I). Experimental lungs were preserved with low-potassium solution (group II) or Euro-Collins solution (group III) at similar temperatures and volumes. RESULTS: The pulmonary arteriovenous oxygen gradient at the end of the 30-minute high-flow reperfusion period was significantly higher in group II compared with group III (121.3 +/- 19.2 mm Hg versus 31.1 +/- 4.2 mm Hg; p < 0.001). The pulmonary vascular resistance was significantly lower in group II than in group III (46.3 +/- 1.8 x 10(3) dynes x s x cm(-5) versus 79.8 +/- 8.4 x 10(3) dynes x s x cm(-5); p < 0.01. The percent decrease in dynamic airway compliance in group III was significantly greater than in group I and II (-51.0% +/- 13.3% versus -10.2% +/- 3.4% and -11.2% +/- 2.8%, respectively; p < 0.001). Similarly, the wet to dry ratio of the lungs in group III was significantly greater than in groups I and II (13.9 +/- 2.3 versus 5.9 +/- 0.2 and 6.0 +/- 0.4, respectively; p < 0.001). CONCLUSIONS: These data demonstrate that a low-potassium preservation solution yields improved lung function after high-flow reperfusion in an ex vivo rabbit lung model. Lung preservation should be aimed at the clinical setting.

Controlled reperfusion of cardiac grafts from non-heart-beating donors.

BACKGROUND: Hearts harvested from non-heart-beating donors sustain severe injury during procurement and implantation, mandating interventions to preserve their function. We tested the hypothesis that limiting oxygen delivery during initial reperfusion of such hearts would reduce free-radical injury. METHODS: Rabbits sustained hypoxic arrest after ventilatory withdrawal, followed by 20 minutes of in vivo ischemia. Hearts were excised and reperfused with blood under conditions of high arterial oxygen tension (PaO2) (approximately 400 mm Hg), low PaO2 (approximately 60 to 70 mm Hg), high pressure (80 mm Hg), and low pressure (40 mm Hg), with or without free-radical scavenger infusion. Non-heart-beating donor groups were defined by the initial reperfusion conditions: high PaO2/ high pressure (n = 8), low PaO2/high pressure (n = 7), high PaO2/low pressure (n = 8), low PaO2/low pressure (n = 7), and high PaO2/high pressure/free-radical scavenger infusion (n = 7). RESULTS: After 45 minutes of reperfusion, low PaO2/ high pressure and high PaO2/low pressure had a significantly higher left ventricular developed pressure (63.6 +/- 5.6 and 63.1 +/- 5.6 mm Hg, respectively) than high PaO2/high pressure (40.9 +/- 4.5 mm Hg; p < 0.0000001 versus both). However, high PaO2/high pressure/free-radical scavenger infusion displayed only a trend toward improved ventricular recovery compared with high PaO2/ high pressure. CONCLUSIONS: Initially reperfusing nonbeating cardiac grafts at low PaO2 or low pressure improves recovery, but may involve mechanisms other than decreased free-radical injury.

Intratracheal surfactant administration preserves airway compliance during lung reperfusion.

BACKGROUND: Decreased airway compliance after lung transplantation has been observed with severe ischemia-reperfusion injury. Further, it has been shown that the surfactant system is impaired after lung preservation and reperfusion. We hypothesized that surfactant replacement after allograft storage could preserve airway compliance during reperfusion. METHODS: Rabbit lungs were harvested after flush with 50 mL/kg of cold saline solution. Immediate control lungs were studied with an isolated ventilation/perfusion apparatus using venous rabbit blood recirculated at 40 mL/min, room-air ventilation at 20 breaths/min, and constant airway pressure (n = 8). Twenty-four-hour control lungs were preserved at 4 degrees C for 24 hours and then similarly studied (n = 7). Surfactant lungs underwent similar harvest and preservation for 24 hours, but received 1.5 mL/kg of intratracheal surfactant 5 minutes before reperfusion (n = 10). Airway pressure and flow were recorded continuously during 30 minutes of reperfusion. Tidal volume and airway compliance were calculated at 30 minutes. RESULTS: Tidal volume was 33.67 +/- 0.57, 15.75 +/- 5.72, and 29.83 +/- 1.07 mL in the immediate control, 24-hour control, and surfactant groups, respectively (p = 0.004, surfactant versus 24-hour control). Airway compliance was 1.94 +/- 0.27, 0.70 +/- 0.09, and 1.46 +/- 0.10 mL/mm Hg in the immediate control, 24-hour control, and surfactant groups, respectively (p = 0.002, surfactant versus 24-hour control). CONCLUSIONS: We conclude that surfactant administration before reperfusion after 24 hours of cold storage preserves tidal volume and airway compliance in the isolated ventilated/perfused rabbit model of lung reperfusion injury.

Compensatory growth of porcine right lungs after chronic rejection of transplanted left lungs.

Neonatal lung hypoplasia is frequently a fatal condition often associated with congenital diaphragmatic hernia. Unilateral lung transplantation rarely has been performed for this indication, although it is a potential solution. It is not known whether the transplant needs to function permanently or to act as a bridge until the native lung develops. It is also not known whether the native lung will grow in the face of an immunosuppressed state and chronic rejection of the transplanted lung. We therefore developed a porcine model of left lung rejection to study this. Infant swine underwent left lung transplantation. Chronic rejection occurred in all, resulting in nonfunction of the transplanted lung. The right lungs of these animals were compared with the right lungs of size-matched and age-matched control animals not given immunosuppressive treatment and not undergoing transplantation. There were no differences in terms of the functional residual capacity, airway compliance, and airway resistance among the groups. There was a significant increase in the pulmonary vascular resistance in the animals with transplanted lungs. There was also a significant increase in the lung weight in these animals. Unilateral pneumonectomies were done in 4 infant pigs to serve as controls. Three of the 4 did not survive the operation because of acute pulmonary failure. In conclusion, the study group exhibited evidence of compensatory growth that was not seen in the control animals, as shown by the increase in lung weight. This suggests that contralateral lung growth occurs in a growing animal, despite the effects of immunosuppression therapy and chronic rejection of the transplanted lung.

Pulmonary function after non-heart-beating lung donation in a survival model.

BACKGROUND: Lung procurement from recently deceased cadavers has been suggested to enlarge the limited donor pool. We hypothesized that lungs harvested from non-heart-beating donors (NHBD) would function as well as those harvested from heart-beating donors. METHODS: Sixteen adult swine underwent left lung allotransplantation. Controls received lungs procured from heart-beating donors, NHBD pigs received lungs immediately harvested from donors after death from asphyxiation, and NHBD-15 and NHBD-30 pigs received lungs harvested after 15 and 30 minutes after asphyxiation. RESULTS: After 1 week of survival, mean dynamic airway compliance (mL/cm H2O +/- standard error of the mean) was 16.3 +/- 0.7 in controls, and 17.3 +/- 1.0, 16.4 +/- 6.0, and 7.3 +/- 1.6 in the NHBD, NHBD-15, and NHBD-30 groups, respectively (p = 0.02, NHBD-30 versus others combined). No significant differences were noted in the pulmonary venous partial pressure of oxygen or pulmonary vascular hemodynamics compared with controls. CONCLUSIONS: The decrease in airway compliance noted in the NHBD-30 group may reflect an exacerbation of reperfusion injury caused by 30 minutes of warm ischemia during organ retrieval. We conclude that posttransplantation lung function using an NHBD with up to 15 minutes of warm ischemia is equivalent to lung function after heart-beating harvest.

Intravenous phenylephrine preconditioning of cardiac grafts from non-heart-beating donors.

BACKGROUND: Hypoxia and warm ischemia produce severe injury to cardiac grafts harvested from non-heartbeating donors. To potentially improve recovery of such grafts, we studied the effects of intravenous phenylephrine preconditioning. METHODS: Thirty-seven blood-perfused rabbit hearts were studied. Three groups of non-heart-beating donors underwent intravenous treatment with phenylephrine at 12.5 (n = 8), 25 (n = 7), or 50 microg/kg (n = 7) before initiation of apnea. Non-heart-beating controls (n = 8) received saline vehicle. Hypoxic cardiac arrest occurred after 6 to 12 minutes of apnea, followed by 20 minutes of warm in vivo ischemia. A 45-minute period of ex vivo reperfusion ensued. Nonischemic controls (n = 7) were perfused without antecedent hypoxia or ischemia. RESULTS: Phenylephrine 25 microg/kg significantly delayed the onset of hypoxic cardiac arrest compared with saline controls (9.6 +/- 0.5 versus 7.7 +/- 0.4 minutes; p = 0.00001), yet improved recovery of left ventricular developed pressure compared with saline controls (57.1 +/- 5.3 versus 41.0 +/- 3.4 mm Hg; p = 0.04). Phenylephrine 25 microg/kg also yielded a trend toward less myocardial edema than saline vehicle (p = 0.09). CONCLUSIONS: Functional recovery of nonbeating cardiac grafts is improved by preconditioning. We provide evidence that the myocardium can be preconditioned with phenylephrine against hypoxic cardiac arrest.

Non-heart-beating donors: a model of thoracic allograft injury.

4ACKGROUND. Non-heart-beating donors (NHBDs) have been proposed for the critical shortage of donors for cardiac and pulmonary transplantation. We determined the effects of prearrest hypoxia and postarrest warm ischemia on cardiac and pulmonary allografts procured from NHBDs undergoing hypoxic arrest. METHODS. Rabbit hearts and lungs were procured from separate donors and placed on isolated blood perfusion circuits. Controls were excised and perfused without ischemia. Heart from NHBDs underwent either prearrest hypoxic perfusion alone or consecutive periods of prearrest hypoxic perfusion and 20 minutes of postarrest warm ischemia. A third group of hearts underwent 30 minutes of warm, global ischemia alone. Two groups of pulmonary allografts were studied using similar hypoxic perfusion/20-minute ischemia and 30-minute ischemia donors. RESULTS. Prearrest hypoxic perfusion clearly causes significant dysfunction of cardiac allografts from NHBDs compared with nonischemic controls. Prearrest hypoxic perfusion combined with postarrest ischemia results in an additive degree of dysfunction more severe than a similar period of warm ischemia alone. Both groups of experimental lungs displayed function similar to that of nonischemic controls in terms of pulmonary hemodynamics, airway resistance, and oxygenation potential. CONCLUSIONS. We conclude that prearrest hypoxic perfusion significantly contributes to the dysfunction of NHBD cardiac allografts. Pulmonary allografts may be more amenable to procurement of NHBDs.

Optimal timing of abdominal aortic aneurysm repair after coronary artery revascularization.

OBJECTIVE: The authors ascertained the optimal timing of repair of an abdominal aortic aneurysm (AAA) after coronary artery revascularization. SUMMARY BACKGROUND DATA: Cardiac events are the most common cause of death after elective repair of AAA. Preoperative coronary revascularization has significantly reduced postoperative cardiac complications after elective AAA repair. Currently, most patients undergo repair of asymptomatic AAA within 6 months after the coronary revascularization. METHODS: The authors performed a retrospective review of patients who underwent repair or scheduled repair of an asymptomatic AAA within 6 months after coronary artery bypass graft (CABG) between March 1988 and October 1993. RESULTS: There was no mortality in the group of patients (n = 14) who underwent repair of AAA simultaneously or within 14 days of coronary revascularization. In contrast, there was a significantly increased mortality rate of 3 of 9 (33%) in patients scheduled to undergo repair of the AAA more than 2 weeks after coronary revascularization (p < 0.05). All nonsurvivors died between 16 and 29 days after CABG, and died as a result of ruptured AAA. CONCLUSION: Elective AAA repair should be undertaken simultaneously or within 2 weeks of coronary artery revascularization because of an increased risk of postoperative AAA rupture seen after this time period. In addition, simultaneous or early postoperative AAA repair does not increase the overall operative risk.

Management of renal tumors involving the inferior vena cava.

PURPOSE: We reviewed our experience of the resection of renal tumors involving the inferior vena cava (IVC) from 1987 to 1992 with the hypothesis that retrohepatic IVC involvement of renal tumors can be managed without cardiopulmonary bypass (CPB) and circulatory arrest with acceptable morbidity and mortality rates. METHODS: We retrospectively reviewed our experience of radical nephrectomies for renal tumors from 1987 to 1992 (n = 69). Of these, 13 had involvement of the IVC (19%). Three of the patients had right atrial extension requiring CPB with circulatory arrest. Three patients had retrohepatic involvement, and seven had infrahepatic involvement. All thirteen patients underwent operative removal of the tumor and tumor thrombus. RESULTS: The patients with atrial extension who were treated with CPB and circulatory arrest had hospital and 1-year survival rates of 100% (three of three). The patients with retrohepatic extension treated without CPB and circulatory arrest had hospital and 1-year survival rates of 100% (three of three). The patients with infrahepatic extension treated without CPB and circulatory arrest had hospital and 1-year survival rates of 85% (six of seven) and 50% (three of six), respectively. There was no statistically significant difference between groups. The hospital death occurred in a patient who had a massive pulmonary embolism and disseminated intravascular coagulation before operation. The deaths that occurred before 1 year were due to metastatic disease and unresectable disease at the time of operation. CONCLUSION: CPB with circulatory arrest is not required in patients with retrohepatic IVC extension of renal tumors, and aggressive resection can be performed in these patients with acceptable morbidity and mortality rates.

Stroke rate is markedly reduced after carotid endarterectomy by avoidance of protamine.

PURPOSE: Postoperative neurologic injury remains a significant risk of carotid endarterectomy. Mechanisms include embolization of debris and formation of thrombus on the newly endarterectomized surface. We hypothesized that the risk of postoperative neurologic injury would be lower in those patients who did not receive protamine for reversal of heparin anticoagulation. METHODS: We reviewed 348 consecutive primary carotid endarterectomies performed since January 1, 1986, to determine the relationship between surgical outcomes and reversal of heparin anticoagulation. Patients undergoing additional simultaneous cardiovascular procedures were excluded. One hundred ninety-three patients received protamine after completion of the endarterectomy. The remaining 155 patients did not receive any protamine. RESULTS: All patients in both groups survived to discharge. There were no strokes in those patients who did not receive any protamine; however, the stroke rate in the protamine group was 2.6% (5 of 193), p < 0.045. The incidence of hematoma requiring reexploration was 1.0% (2 of 193) and 1.9% (3 of 155) in the protamine and no-protamine groups, respectively (p = NS). Intraoperative shunting was used more frequently in the no-protamine group (84% vs 67%, p < 0.001), and patch angioplasty was performed more frequently in the protamine group (35% vs 15%, p < 0.001). However, neither shunting nor patching significantly influenced stroke rates. CONCLUSIONS: We conclude that carotid endarterectomy without reversal of heparin anticoagulation is associated with a reduced postoperative stroke rate without a significant increase in morbidity rates.