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J Thorac Cardiovasc Surg 2003;125:960-962
© 2003 The American Association for Thoracic Surgery

Brief Communications

First experiences with the stable prostacyclin analog iloprost in the evaluation of heart transplant candidates with increased pulmonary vascular resistance

Armin Sablotzki, MDa, Elke Czeslick, MDb, Ekkehard Gruenig, MDc, Ivar Friedrich, MDa, Susann Schubert, MDb, Jochen Börgermann, MDa, Thomas Hentschel, MDb Halle/Salle and Heidelberg, Germany

From the Clinic of Cardiothoracic Surgerya and the Clinic of Anesthesiology and Intensive Care Medicine,b Martin-Luther-University Halle/Wittenberg, Halle/Salle, and the Clinic of Internal Medicine III,c University of Heidelberg, Germany.

Received for publication Feb 13, 2002. Accepted for publication Sept 9, 2002. Address for reprints: Armin Sablotzki, MD, Clinic of Cardiothoracic Surgery, Martin-Luther-University Halle/Wittenberg, Ernst-Grube-Str 40, 06120 Halle/Saale, Germany (E-mail: sablotzki@aol.com).

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  		Fig. 1. Influence of inhaled NO and iloprost on MPAP, mean arterial pressure (MAP), PVR, and SVR (n = 20). Data are expressed as means ± SEM. *P < .05, **P <. 01 compared with baseline values.

 
An increased pulmonary vascular resistance (PVR) is described as a predictor of increased mortality after orthotopic heart transplantation. The measurement of pulmonary hemodynamics is a routine procedure in the assessment of potential transplant recipients because the information about the response to vasodilator therapy is of great interest for the postoperative management of right-heart failure.Go 1

The therapeutic limitation of intravenous vasodilators is the systemic vasodilation and hypotension. Inhaled nitric oxide (NO) and prostacyclin (PGI2) have been shown to act as selective pulmonary vasodilators without systemic effects in patients with primary and secondary pulmonary hypertension as well.Go 2 Unfortunately, NO is a toxic molecule and requires specialized delivery systems and monitoring. Because of its short half-life, NO has to be administered continuously, and even brief interruptions can cause a dangerous rebound of pulmonary hypertension. Inhaled PGI2 shows advantages because of the lack of toxic reactions but no improved effects on hemodynamics.Go 2 Hoeper and colleaguesGo 3 described the use of aerosolized iloprost for severe pulmonary hypertension. Iloprost has a plasma half-life of 20 to 30 minutes and induces pulmonary vasodilation that persists for about 2 to 4 . . . [Full Text of this Article]






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