Acetylsalicylic acid treatment until surgery reduces oxidative stress and inflammation in patients undergoing coronary artery bypass grafting
Selected in European Journal of Cardio-Thoracic Surgery by Rylski
Berg K, Langaas M, Ericsson M, Pleym H, Basu S, Nordrum IS, Vitale N, Haaverstad R
Eur J Cardiothorac Surg 2013;43:1154-63
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Acetylsalicylic acid (ASA) does not only prevent platelet aggregation but also reduces oxidative stress and thereby inflammation and vasoconstriction. To avoid bleeding in patients undergoing coronary artery bypass grafting (CABG), discontinuation of ASA is recommended (grade B recommendation) 2-10 days before elective cardiac surgery. The authors aimed to analyse the effect of ASA on reactive oxygen species (ROS) production, inflammation and myocardial damage in a well-designed prospective, randomised study on 20 patients referred for first-time CABG only. Patients were randomised by either ASA-treatment until the day before surgery or to ASA withdrawal 7 days earlier.
- Biomarkers predicting adverse outcome after CABG, C-reactive protein and 8-iso-prostaglandin F2alpha, were reduced in patients treated with ASA until surgery
- There was no significant difference in the myocardial injury assessed by troponin T levels, however a tendency towards reduced damage was noted in patients under ASA treatment until surgery
- Postoperative bleeding complications were not influenced by ASA
The authors made a significant contribution to the debate on the still controversial concept of ASA administration in patients scheduled for CABG. They proved a protective role of continued ASA treatment until the time of surgery. Their efforts were appreciated by representatives of the surgical society and published in one of the most read journals on cardiac surgery.
In the current era of interventional cardiology, patients under antiplatelet therapy are no longer unique in the operating room. Cardiac surgeons such as us, more and more frequently have to face the intra- and postoperative bleeding complications due to single or dual antiplatelet therapy, sometimes even combined with oral anticoagulants. We already learned how to reduce the risk of postoperative bleeding when antiplatelet drugs are not stopped before surgery. We operate more carefully which results in the extension of cardiopulmonary bypass time. This in turn leads to increased exposure of blood to unphysiological materials of the bypass circuit and consequently to increased ROS production. We manage the intraoperative enhanced bleeding by applying haemostatic techniques with one of the most effective techniques electrocauterization, which creates necrotic tissue and may increase the likelihood of infection. Together with anesthesiologists we try to reactivate the physiological blood hemostasis after weaning off cardiopulmonary bypass by administrating human blood plasma or platelets and hemostatic factors, which may lead to microembolism and in the worst-case scenario to coronary bypass occlusion. Dealing with increased bleeding tendency in the operating room takes time. The chest can be closed only if the operative field is ‘dry’, consequently the increased operating time introduces its own associated consequences. If the patients develop cardiac tamponade in the intensive care unit it enhances their risk enormously and they must emergently undergo reoperation. Furthermore, our experiences show that patients with prior to surgery antiplatelet medication require more blood products in the postoperative course.
Ultimately we have to pose the question: is the advantage of antiplatelet drugs in terms of antioxidative features greater than the disadvantage of enhanced intraoperative bleeding? According to the current literature making a definitive recommendation is not possible. Berg et al. have stimulated this discussion and should be congratulated for their results. There is a need for further research in this field, particularly on the true population of patients with complex cardiac disorders referred for cardiac surgery.