Levosimendan and Platelet Function

LETTERS TO THE EDITOR

Levosimendan and Platelet Function To the Editor: We are very interested in a recent report by Zangrillo et al’s meta-analysis of 5 randomized controlled trials investigating the influence of levosimendan in patients’ outcome after cardiac surgery.1 Their primary endpoint of the meta-analysis was postoperative cardiac troponin release. They reported that levosimendan was associated with significant reductions in cardiac troponin peak release and in time to hospital discharge. In this meta-analysis, the authors concluded that levosimendan was associated with a significant reduction in cardiac troponin release in patients undergoing cardiac surgery and had cardioprotective effects. The authors did not investigate adverse events related to treatments in this meta-analysis. However, we should take into consideration the side effects of drugs when using them. For this reason, we would like to provide the possible effect of levosimendan on platelets. Recently, the effect of levosimendan on platelet function has been investigated.2 The study results displayed that levosimendan significantly inhibited aggregation of platelets induced by adenosine phosphatase and collagen, and there was a relationship between the levosimendan concentration and the inhibition of platelet aggregation, although the mechanism of action of it is not known. On the other hand, the clinical significance of the antiaggregatory effect of levosimendan is also not known. In studies in the meta-analysis, levosimendan was used in cardiac surgery with cardiopulmonary bypass or during off-pump coronary artery bypass graft surgery. It is well known that heart failure is the other indication for the use of levosimendan. It is possible that other medications used in these patient populations may have antiplatelet effects, and levosimendan also may aggravate this effect. Levosimendan also may have a potential problem in patients with platelet function defects or thrombocytopenia. A potential antiaggregatory effect of levosimendan may be overt in these patient populations and cause bleeding symptoms. It is also known that the active metabolite of levosimendan has a long half-life (⬃80 hours) and circulates for about 2 weeks.3 Because levosimendan is a drug with a long half-life, patients may be exposed to the drug after it is stopped. On the other hand, the antiaggregatory effect of levosimendan may have no clinical significance because of no reported bleeding problems in levosimendan-treated patients. However, we suggest that the potential effect of levosimendan should be kept in mind, especially in patients receiving concomitant medications that have possible effects on platelet function. Kürs¸ad Kaptan, MD Cengiz Beyan, MD Department of Hematology School of Medicine Gülhane Military Medical Academy Ankara, Turkey 532

REFERENCES 1. Zangrillo A, Biondi-Zoccai G, Mizzi A, et al: Levosimendan reduces cardiac troponin release after cardiac surgery: A meta-analysis of randomised controlled studies. J Cardiothorac Vasc Anesth 23:474-478, 2009 2. Kaptan K, Erinç K, Ifran A, et al: Levosimendan has an inhibitory effect on platelet function. Am J Hematol 83:46-49, 2008 3. Antila S, Pesonen U, Lehtonen L, et al: Pharmacokinetics of levosimendan and its active metabolite OR-1896 in rapid and slow acetylators. Eur J Pharm Sci 2:213-222, 2004 doi:10.1053/j.jvca.2009.05.011

Anesthetic Management of a Patient With Giant Right Atrial Myxoma To the Editor: A 68-year-old asymptomatic man presented to our hospital for excision of a right atrial mass. It was unexpectedly discovered by an abdominal computed tomography (CT) scan during evaluation for gastrointestinal bleeding. The CT scan showed an 8.9 ⫻ 6.7 ⫻ 6.7 cm large mass occupying most of the right atrial cavity (Fig 1). The patient was scheduled for excision of the mass by a median sternotomy. Monitors for cardiac surgery included invasive blood pressure, central venous pressure measurements, and transesophageal echocardiography (TEE). To ensure maintenance of circulation and to induce anesthesia safely, 1,000 mL of crystalloid were administered to maintain preload, and inotropic support was avoided to prevent obstruction of the tricuspid valve. Anesthesia was induced with 5 mg of midazolam, 10 mg of vecuronium, and 100 ␮g of fentanyl. After induction, a central venous catheter was inserted from the right internal jugular vein and TEE was performed. After a median sternotomy, aortic and femoral venous cannulation were performed for cardiopulmonary bypass because cannulation at the superior vena cava or the inferior vena cava was considered to be impossible due to the tumor. Although 2-dimensional TEE has its limitations, femoral venous cannulation for cardiopulmonary bypass and a central venous catheter were inserted under visualization with TEE to prevent embolization of tumor fragments that originate from contact between a catheter and the tumor into the pulmonary vessels. Similarly, a pulmonary artery catheter was avoided. Intraoperative TEE showed a mass occupying almost the entire space of the right atrial cavity (Fig 1). The mass was immobile, and therefore, fortunately, it did not obstruct the tricuspid valve. There was no significant tricuspid regurgitation and obstruction of ventricular inflow. However, TEE could not confirm whether the mass was pedunculated and where it attached because of its excessive large size. The right atrium was opened, revealing a huge mass without a stalk occupying almost all of the right atrial cavity and invading the interatrial septum. The root of the pedicle and the full thickness of the adjacent interatrial

Journal of Cardiothoracic and Vascular Anesthesia, Vol 24, No 3 (June), 2010: pp 532-539