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Eur J Cardiothorac Surg 2002;22:746-752
© 2002 Elsevier Science NL


Hemodynamic effects of inhaled aerosolized iloprost and inhaled nitric oxide in heart transplant candidates with elevated pulmonary vascular resistance

Armin Sablotzkia*, Thomas Hentschela, Ekkehard Gruenigb, Susann Schuberta, Ivar Friedrichc, Jörg Mühlingd, Marius G. Dehned, Elke Czeslicka

a Clinic of Anesthesiology and Intensive Care Medicine, Martin-Luther-University Halle/Wittenberg, Ernst-Grube-Strasse 40, 06120 Halle/Saale, Germany
b Clinic of Internal Medicine III, University of Heidelberg, 69117 Heidelberg, Germany
c Clinic of Cardiothoracic Surgery, Martin-Luther-University Halle/Wittenberg, 06120 Halle/Saale, Germany
d Department of Anaesthesiology and Intensive Care Medicine, University of Giessen, 35392 Giessen, Germany

Received 8 March 2002; received in revised form 29 June 2002; accepted 10 August 2002.

* Corresponding author. Tel.: +49-345-557-3300; fax: +49-345-557-3306
e-mail: sablotzki{at}aol.com

Objective: An elevated pulmonary vascular resistance (PVR) is described as a predictor of postoperative right heart failure and increased mortality in patients undergoing orthotopic heart transplantation. The use of intravenous vasodilators is limited by their systemic effects. We evaluated the pulmonary and systemic hemodynamic effects of inhaled nitric oxide (NO) and inhaled aerosolized iloprost (IP) in heart transplant candidates with elevated PVR. Methods: Fourteen male heart transplant candidates due to dilative or ischemic cardiomyopathia with elevated PVR (>=180 dyn s cm-5) were included in the study. Increasing concentrations of NO (5, 10 and 30 ppm) and 50 µg aerosolized IP were administered by inhalation. Hemodynamic measurements preceded and followed administration of each agent. Results: Inhalation of IP, 10, and 30 ppm NO reduced PVR and mean pulmonary artery pressure (MPAP), but did not affect blood pressure or systemic vascular resistance. Comparing the effectiveness of 10 ppm NO and IP, we found a significant higher reduction of MPAP in patients treated with IP. An increase of cardiac index and stroke index could only be shown with IP-inhalation. Conclusions: Inhaled iloprost induces pulmonary vasodilation which is significantly greater than the effects of 10 and 30 ppm NO. The results of our study show, that inhaled iloprost induces a reliable hemodynamic response in the evaluation of heart transplant candidates. Further advantages of iloprost inhalation are the lack of adverse reactions and toxic side effects and an easier administration. Due to this facts we recommend iloprost as a routine screening drug for vascular reactivity in HTx-candidates. Based on our results it would be of great interest to investigate the role of iloprost in management of postoperative right heart insufficiency following cardiac transplantation.

Key Words: Nitric oxide • Iloprost • Heart transplantation • Pulmonary hypertension




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