Ann Thorac Surg 2006;82:1575-1576
© 2006 The Society of Thoracic Surgeons
Correspondence
Reply
Edward H. Kincaid, MD,
Neal D. Kon, MD,
John W. Hammon, MD
Department of Cardiothoracic Surgery, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157
(Email: tkincaid{at}wfubmc.edu).
To the Editor:
We appreciate the interest of Dr Royston [1] in our study [2] and recognize his expertise in the area of hemostasis in cardiac surgery. Unfortunately, his critique of our article is incorrect on many levels. Aprotinin, like most other anti-inflammatory agents, affects intrarenal hemodynamics to an unknown degree. Perhaps Royston [1] overlooked the two references [3, 4] cited in our article that describe the effects as well as the potential interaction between aprotinin and ACE inhibitors.
Regarding his own data analysis of 1,800+ patients, this study seems to be slated for presentation at the 2006 Annual Meeting of the American Society of Anesthesiologists. His abstract describes a retrospective analysis of 1,881 patients enrolled in trials sponsored by Bayer Pharmaceuticals. Of the 20% of patients on preoperative ACE inhibitors, those that also received high-dose aprotinin had similar renal outcomes to those that did not. In his letter previously mentioned, Royston [1] did not reveal that more than 90% of these patients underwent isolated CABG and less than 10% isolated valve procedures. Apparently none of these patients underwent combined or other complex procedures, which represented 40% of our study group. It is this group of patients that seems to be most susceptible to renal injury with combined aprotinin and ACE inhibitor use as demonstrated in Figure 4 in our study. Two other recent studies also confirm that negative renal effects with aprotinin are more likely to occur with complex operations [5, 6]. Hopefully Royston [1] can share information from his center on similar patients.
In one area, we are in agreement with Royston [1]. Blood transfusions, as well as intraoperative anemia, are extremely important predictors of renal dysfunction in our data and many others. However, this finding then begs the question that if blood transfusions cause renal failure and aprotinin is so effective at decreasing transfusions, why does aprotinin not decrease the incidence of renal failure? Perhaps nephrotoxicity is the answer. We also agree with him that retrospective data such as ours can not prove or refute this speculation but only strengthen the argument for performance of appropriately registered, randomized, prospective studies.
Finally, aprotinin is a very powerful drug with many complex mechanisms that affect physiology during cardiopulmonary bypass. We urge Royston [1], with all his expertise in this area, to help further study the potential negative effects, for surely there must be some of this extremely important medication.
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References
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- Royston D. Does the combination of aprotinin and angiotensin-converting enzyme inhibitor cause renal failure after cardiac surgery?(letter) Ann Thorac Surg 2006;82:1575.[Free Full Text]
- Kincaid EH, Ashburn DA, Hoyle JR, Reichert MG, Hammon JW, Kon ND. Does the combination of aprotinin and angiotensin-converting-enzyme inhibitor cause renal failure after cardiac surgery? Ann Thorac Surg 2005;80:1388-1393.[Abstract/Free Full Text]
- Waxler B, Rabito SF. Aprotinin: a serine protease inhibitor with therapeutic actions: its interaction with ACE inhibitors Curr Pharm Des 2003;9:777-787.[Medline]
- Horl WH. Aprotinin and renal function in patients undergoing cardiac surgery Br J Anaesth 2000;84:3-5.[Free Full Text]
- Mangano DT, Tudor IC, Dietzel C. Multicenter study of Perioperative Ischemia Research Group, Ischemia Research and Education FoundationThe risk associated with aprotinin in cardiac surgery. N Engl J Med 2006;354:353-365.[Abstract/Free Full Text]
- Karkouti K, Beattie WS, Dattilo KM, et al. A propensity score case-control comparison of aprotinin and tranexamic acid in high-transfusion-risk cardiac surgery Transfusion 2006;46:327-338.[Medline]
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