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Ann Thorac Surg 1996;62:1335-1336
© 1996 The Society of Thoracic Surgeons
DR MEHMET C. OZ (New York, NY): There is an adult equivalent to this operation, and it is called a left ventricular assist device placement. We have done a similar analysis. We used aprotinin in 31 of 116 left ventricular assist device patients, and again many of them had true Fontan physiology with either arrhythmias or very poor right ventricular function. The anaphylaxis rate was low as you showed also, but the right ventricular assist device incidence was also lower in the aprotinin group than in the control group. Interestingly, the thromboembolic incidence was higher in the control group, I think because flows were often so low in these patients because they were bleeding. This translated to a significant 7-day mortality in the control group compared with the aprotinin group.
Aprotinin inhibits the detrimental inflammation effects of cardiopulmonary bypass and bleeding. I think it is not just the effects of cardiopulmonary bypass with neutrophil degranulation and thromboxane A2release that result in elevated pulmonary vascular resistance, but also the bleeding and resuscitation and resulting elevated circulating cytokines.
So my question for you is: Is there a patient in whom you would not use aprotinin? And do you have experience with redosing of aprotinin, and what do you do in that situation?
DR TWEDDELL: Thank you. None of the patients who underwent bidirectional cavopulmonary shunts or Fontan procedures in this study had previously received aprotinin. All patients receive a 1.4-mg test dose of aprotinin before receiving the full dose. In patients being redosed with aprotinin, I believe the test dose is particularly important to avoid a hypersensitivity reaction. I agree with you that the mechanism of action by which aprotinin improves postoperative pulmonary function may be to prevent increased capillary permeability, which leads to increased pulmonary vascular resistance. Alternatively, the mechanism of action may be to decrease the release of vasoactive substances normally elevated by cardiopulmonary bypass including thromboxane A2 and endothelin-1. At this point, we can only speculate as to the mechanism of action. Future efforts by our group are aimed at identifying the mechanism by which aprotinin improves postoperative pulmonary function.
DR EDWARD L. BOVE (Ann Arbor, MI): Doctor Tweddell, were any of your patients operated on using circulatory arrest?
DR TWEDDELL: Yes, we have used aprotinin in 2 patients undergoing procedures using profound hyperthermic circulatory arrest. Both of these patients had previously undergone the Norwood procedure and underwent repair of recurrent coarctation using profound hyperthermic circulatory arrest.
In 1 patient this procedure was combined with a bidirectional cavopulmonary shunt and he is included in this study. The second patient underwent revision of his Blalock-Taussig shunt and repair of branch pulmonary artery stenosis at the same procedure. Subsequently, he went on to a bidirectional cavopulmonary shunt but did not receive aprotinin during that procedure. We identified no complications or adverse sequelae in either of these patients.
DR BOVE: Would you have any hesitation using aprotinin in a patient who is going to have a planned circulatory arrest?
DR TWEDDELL: I have some hesitation in using aprotinin in the setting of profound hyperthermic circulatory arrest. I am not certain that the action of aprotinin in the local microvascular environment in the setting of stasis is completely understood. In these 2 patients in whom we have used aprotinin in the setting of profound hyperthermic circulatory arrest, the circulatory arrest time was between 15 and 20 minutes. I felt comfortable using it for this relatively short period of time, but I would be concerned about using it for longer periods. I must admit, however, that I have no data to support that conclusion.
DR BOVE: We have used it in our patients undergoing Fontan procedures, even those with circulatory arrest, and have had no adverse sequelae from it and feel fairly comfortable with that.
I have one other question. As you may know, in the coronary bypass literature there is some evidence to suggest that it may actually be effective even after cardiopulmonary bypass to reduce bleeding and not for reasons you have discussed. Have you had any experience using it in patients after bypass?
DR TWEDDELL: We have not used aprotinin to attempt to decrease bleeding after cardiopulmonary bypass. None of the patients in this study required reoperation for bleeding. We have used aprotinin in an attempt to control bleeding in 1 patient on postcardiotomy extracorporeal membrane oxygenation support. Although this patient did not have any complications attributable to the use of aprotinin (in particular, there was no thrombus formation or renal failure), I do not believe we had an impact on the bleeding situation either.
DR DONALD C. WATSON, JR (Memphis, TN): There is a difference in oxygen saturation between your two groups. One explanation may be a difference in baffle fenestration rate. Did you fenestrate the baffles, or were they all complete Fontans?
DR TWEDDELL: That is an excellent question. All the Fontans were constructed using a lateral tunnel technique. All of them were initially fenestrated. In 8 of the 10 aprotinin patients and 5 of 6 control patients the fenestration was closed before leaving the operating room. All the procedures were performed with the use of transesophageal echocardiography, and we were able to demonstrate that the fenestrations were, in fact, closed. Therefore, there were essentially equal rates of fenestrations in the aprotinin and control groups, and I do not think this had an impact on our findings or conclusions.
DR CARLO MARCELLETTI (Rome, Italy): Have you used nitrous oxide in any of your patients when you were concerned that pulmonary vascular resistance might be high postoperatively?
DR TWEDDELL: Yes, we have used nitric oxide to reduce pulmonary vascular resistance in a postoperative Fontan patient. This patient was a 6-year-old boy who underwent a combined Damus-Kaye-Stansel and Fontan procedure. He went on to be supported with extracorporeal membrane oxygenation and was successfully weaned from extracorporeal membrane oxygenation with the help of nitric oxide. At that point, he was hemodynamically stable on mechanical ventilation until eventually he succumbed to sepsis. This suggests to me that the patient was probably a good hemodynamic candidate for a Fontan procedure. It suggests further that the extensive nature of his operative procedure was responsible for his initial inability to function initially as a Fontan. We have used inhaled nitric oxide in a number of other patients undergoing operation for congenital heart disease who had an elevated pulmonary vascular resistance with generally very positive results.
Nitric oxide may also be useful as an agent to test the effectiveness of aprotinin in reducing postoperative pulmonary vascular resistance. Inhaled nitric oxide could be administered in the postoperative period to determine how much further the pulmonary vascular resistance can be reduced by aprotinin or other agents one might wish to study.
Related Article
Ann. Thorac. Surg. 1996 62: 1329-1335.
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