BACKGROUND: Chronic thromboembolic pulmonary hypertension (CTEPH) is a potential consequence to pulmonary embolism. The histologic picture is similar to idiopathic pulmonary hypertension (IPAH) suggesting that vascular remodeling also contributes to CTEPH. The treatment of choice is pulmonary endarterectomy. However, this treatment option is not adequate for all patients with CTEPH. Currently, no data exist on standard vasodilative therapy for CTEPH. Intravenous and oral prostanoids, both well-known vasodilators in IPAH, have been used with promising results, whereas the same has not been consistently observed for inhaled iloprost. OBJECTIVE: In this study, we examined acute hemodynamic effects of inhaled iloprost in patients with CTEPH. METHODS: In a prospective study, right heart catheterization was performed in 20 patients (mean age 56 years, New York Heart Association class II-IV) at the time of diagnosis of CTEPH. Pulmonary vascular resistance (PVR), mean pulmonary arterial pressure (mPAP), cardiac output (CO), mean systemic arterial pressure (MAP) and oxygen partial pressure (PaO(2)) were obtained before and 20 min after inhaling 5 mug iloprost. Subsequently, all patients were evaluated for pulmonary endarterectomy. Six patients were eligible for surgery. RESULTS: Significant changes in pulmonary and systemic hemodynamics were observed following the inhalation of iloprost (before to after inhalation): PVR: 1,057 +/- 404.3 to 821.3 +/- 294.3 dyn.s.cm(-5), p < 0.0001; mPAP: 50.55 +/- 8.43 to 45.75 +/- 8.09 mm Hg, p = 0.0002; CO: 3.66 +/- 1.05 to 4.05 +/- 0.91 l/min, p < 0.0106. MAP and PaO(2) decreased significantly (MAP: 94.15 +/- 11.58 to 89.45 +/- 14.29 mm Hg, p = 0.0111; PaO(2): 7.33 +/- 1.17 to 6.64 +/- 1.25 kPa, p = 0.0260). CONCLUSIONS: Hemodynamic changes directly following inhalation of iloprost suggest a significant contribution of a reversible component of vasoconstriction to pulmonary arterial hypertension in patients with CTEPH. Copyright 2007 S. Karger AG, Basel.
BACKGROUND:Chronic thromboembolic pulmonary hypertension (CTEPH) is a potential consequence to pulmonary embolism. The histologic picture is similar to idiopathic pulmonary hypertension (IPAH) suggesting that vascular remodeling also contributes to CTEPH. The treatment of choice is pulmonary endarterectomy. However, this treatment option is not adequate for all patients with CTEPH. Currently, no data exist on standard vasodilative therapy for CTEPH. Intravenous and oral prostanoids, both well-known vasodilators in IPAH, have been used with promising results, whereas the same has not been consistently observed for inhaled iloprost. OBJECTIVE: In this study, we examined acute hemodynamic effects of inhaled iloprost in patients with CTEPH. METHODS: In a prospective study, right heart catheterization was performed in 20 patients (mean age 56 years, New York Heart Association class II-IV) at the time of diagnosis of CTEPH. Pulmonary vascular resistance (PVR), mean pulmonary arterial pressure (mPAP), cardiac output (CO), mean systemic arterial pressure (MAP) and oxygen partial pressure (PaO(2)) were obtained before and 20 min after inhaling 5 mug iloprost. Subsequently, all patients were evaluated for pulmonary endarterectomy. Six patients were eligible for surgery. RESULTS: Significant changes in pulmonary and systemic hemodynamics were observed following the inhalation of iloprost (before to after inhalation): PVR: 1,057 +/- 404.3 to 821.3 +/- 294.3 dyn.s.cm(-5), p < 0.0001; mPAP: 50.55 +/- 8.43 to 45.75 +/- 8.09 mm Hg, p = 0.0002; CO: 3.66 +/- 1.05 to 4.05 +/- 0.91 l/min, p < 0.0106. MAP and PaO(2) decreased significantly (MAP: 94.15 +/- 11.58 to 89.45 +/- 14.29 mm Hg, p = 0.0111; PaO(2): 7.33 +/- 1.17 to 6.64 +/- 1.25 kPa, p = 0.0260). CONCLUSIONS: Hemodynamic changes directly following inhalation of iloprost suggest a significant contribution of a reversible component of vasoconstriction to pulmonary arterial hypertension in patients with CTEPH. Copyright 2007 S. Karger AG, Basel.
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