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Eur J Cardiothorac Surg 2005;28:514-515
© 2005 Elsevier Science NL
Letter to the Editor |
Division of Cardiac Surgery, University of Maryland School of Medicine, N4W94 22 S. Greene St., Baltimore, MD 21201, USA
Received 4 May 2005; accepted 9 May 2005.
* Corresponding author. Tel.:+1 410 328 5089; fax: +1 410 328 2750. (Email: rposton{at}smail.umaryland.edu).
Key Words: Aspirin Thrombosis Off-pump Platelets
I appreciate the interest that Dr Isbir et al. have expressed in our work on platelet function monitoring after OPCAB and the opportunity to clarify three important issues that they raise in their letter [1]: (1) the role of the TEG after OPCAB, (2) the method of diagnosing ASA resistance and (3) recommendations about use of clopidogrel after OPCAB.
Well-regulated platelet function is critical for balancing hemostasis without thrombosis after cardiac surgery. Perioperative monitoring of platelet function is likely to be the best means for establishing an appropriate balance. The correlation of the maximum amplitude (MA) of the Thrombelastography tracing with postoperative bleeding seen in our study and others reflects effective modeling of the in vivo hemostatic plug with this in vitro assay. On the other hand, the ability of this test to model thrombus formation in other conditions, such as within the bypass graft, appears to be limited [2]. A more specific analysis of platelet function, such as that provided by an analysis of aspirin resistance (ASA-R), is required to accurately discriminate patients who are at risk for thrombosis [3].
A growing appreciation of the clinical importance of ASA-R has increased the need to establish a cheap, simple, reproducible and generalizable diagnostic strategy. It seems unlikely that this can be accomplished with a single diagnostic test given the relatively low predictive values of currently available assays. We addressed this problem in a more recent follow-up study [3] by considering the diagnosis of ASA-R established only if findings were compatible in two of three separate assays performed in all patients: modified TEG, whole blood aggregometry and thromboxane metabolites in the serum. The strong correlation between these three complementary methods used to diagnose ASA-R with flow cytometry, a more established method of quantifying platelet function, justifies confidence regarding our choice of diagnostic criteria. We have found that ASA-R is infrequent prior to surgery but is acquired in 10% of patients on the first day after surgery, increasing further to about a third of patients by day 3 after OPCAB.
Finally, clopidogrel is used frequently after OPCAB based on widespread concerns of a hypercoagulable state. However, the absolute requirement of a loading dose for effective use of clopidogrel [4] creates a narrow therapeutic window that increases the risks of bleeding and possibly mortality in the cardiac surgical patient [5]. Perhaps a better strategy for improving graft patency after OPCAB would be to treat the cause of acquired aspirin resistance itself. Preliminary data from our lab suggests that perioperative thrombin formation plays an important role in the development of ASA-R after OPCAB. Aprotinin is known to inhibit the formation of thrombin and its effect on the platelet. In a recently reported randomized trial of aprotinin use during OPCAB, we found a reduction in perioperative thrombin formation and ASA-R in the aprotinin group compared to placebo. Pending confirmation in ongoing studies, aprotinin may prove to be a novel intraoperative adjunct to safely promote the patency of the saphenous vein graft.
References
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