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J Thorac Cardiovasc Surg 2003;126:874-875
© 2003 The American Association for Thoracic Surgery
Brief communications |
a Department of Thoracic and Cardiovascular Surgery, University Hospitals, Homburg, Germany
b Department of Anesthesiology and Intensive Care Medicine, University Hospitals, Homburg, Germany
Received for publication March 18, 2003; accepted for publication April 1, 2003.
* Address for reprints: Hans-Joachim Schäfers, MD, Department of Thoracic and Cardiovascular Surgery, University Hospitals Homburg, Kirrberger Strasse, 66421 Homburg, Germany
chhjsc{at}uniklinik-saarland.de
Pulmonary hypertension (PHT) contributes significantly to morbidity and mortality in cardiac surgeryespecially in patients with long-standing mitral valve disease.1 Vasodilators administered intravenously can reduce pulmonary vascular resistance but also have an effect on the systemic circulation. Arterial hypotension must be expected, which results in reduction of right coronary blood flow and may lead to further deterioration of right ventricular performance.1
Inhaled nitric oxide (NO) is a more selective pulmonary vasodilator with virtually no systemic side effects.1 Recently, the inhalational use of the long-acting prostacyclin analog iloprost has been reported to offer superior selective pulmonary vasodilating properties relative to NO inhalation in primary PHT.2 We report our initial experience with the intraoperative use of iloprost inhalation in a case series of cardiac surgical patients.
Methods
Ten patients (age 69.4 ± 7.5 years, 3 male) had a diagnosis of mitral valve disease and associated PHT (mean pulmonary arterial pressure 28.0 ± 5.9 mm Hg) and underwent either mitral valve repair (n = 6) or mitral valve replacement (n = 4). Inhalational treatment with 16 µg nebulized iloprost (Ilomedin) was instituted after termination of cardiopulmonary bypass, when persistence of PHT (mean pulmonary arterial pressure >25 mm Hg) was observed. Iloprost was supplied through a common disposable nebulizer system (Ilo-Neb; Nebu-Tec, Elsenfeld, Germany) filled with 1.6 mL of a 10 µg · mL-1 solution in isotonic saline solution and introduced into the inspiratory limb of the ventilator circuit. Catecholamine and systemic vasodilator treatments remained unchanged during the inhalation cycle of 10 to 15 minutes. Hemodynamic profiles were obtained before and 15 minutes after starting the inhalation of iloprost.
The study was approved by a university hospital ethics review committee. Informed consent was obtained from all patients.
Results
With iloprost inhalation (Table 1) mean pulmonary arterial pressure decreased significantly from 31.6 ± 6.6 to 26.1 ± 3.1 mm Hg (P = .01). Pulmonary vascular resistance was significantly reduced from 394.3 ± 128.1 to 289.6 ± 94.6 dyne · s · cm-5 (P = .002). Cardiac index increased from 3.0 ± 0.5 to 3.2 ± 0.7 L · min-1 · m-2 (difference not significant). Nonsignificant changes were observed for mean arterial pressure (-1.1%) and systemic vascular resistance (-1.2%). Relevant side effects (bleeding complications, bronchospasm) did not occur. All patients were discharged home.
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PHT is recognized as a major risk factor for perioperative morbidity and mortality in cardiac surgical patients.1 Vasodilators administered intravenously may improve pulmonary hemodynamics but also decrease mean arterial pressure, thereby reducing right coronary perfusion with a further impairment of right ventricular contractility.1 Vasodilators administered by inhalation have more selective effects on the pulmonary circulation and thus appear ideal in a setting of hemodynamic instability.
Because of substantial problemsincluding increased methemoglobin, the toxic metabolite nitrogen dioxide, extremely short-lived hemodynamic effects, rebound phenomenon, specialized equipment, and financial implicationsthe inhalation of NO has some restrictions.1 Aerosolized prostacyclin has been introduced for the treatment of primary as well as secondary PHT.2 The hemodynamic effects of the inhaled prostacyclin analog iloprost appear to be similar, with an obvious difference in pharmacokinetics. The clinical effects of iloprost have been described to disappear after 1 to 2 hours (intravenous plasma half-life of prostacyclin <3 minutes vs 2030 minutes for iloprost). Aerosolized iloprost has shown vasodilating potency similar to that of inhaled NO in secondary PHT, and it actually appears to be superior in primary PHT.2
The intraoperative use of aerosolized prostanoids has been reported in only a few surgical cases,3 probably because of concerns regarding impaired platelet function. Both inhaled prostacyclin and NO are associated with impaired platelet aggregation in vitro4,5 but are without signs of platelet dysfunction in vivo.4 Increases in mediastinal drainage or transfusion requirements were not observed in any of our cases.
In conclusion, the intraoperative use of aerosolized iloprost is a clinical alternative to NO that warrants further comparative studies.
References
This article has been cited by other articles:
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K. Subramaniam and J.-P. Yared Management of Pulmonary Hypertension in the Operating Room Seminars in Cardiothoracic and Vascular Anesthesia, June 1, 2007; 11(2): 119 - 136. [Abstract] [PDF] |
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S. Takaoka, J. L. Faul, and R. Doyle Current Therapies for Pulmonary Arterial Hypertension Seminars in Cardiothoracic and Vascular Anesthesia, June 1, 2007; 11(2): 137 - 148. [Abstract] [PDF] |
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S. E Baker and R. H. Hockman Inhaled Iloprost in Pulmonary Arterial Hypertension Ann. Pharmacother., July 1, 2005; 39(7): 1265 - 1274. [Abstract] [Full Text] [PDF] |
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S. M. Lowson Alternatives to nitric oxide Br. Med. Bull., November 5, 2004; 70(1): 119 - 131. [Abstract] [Full Text] [PDF] |
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