Acute Improved Hemodynamics following Inhaled Iloprost in Chronic Thromboembolic Pulmonary Hypertension

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 endart...

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Veröffentlicht in:Respiration 2008-01, Vol.76 (2), p.154-159
Hauptverfasser: Krug, Sabine, Hammerschmidt, Stefan, Pankau, Hans, Wirtz, Hubert, Seyfarth, Hans-Jürgen
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container_end_page 159
container_issue 2
container_start_page 154
container_title Respiration
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creator Krug, Sabine
Hammerschmidt, Stefan
Pankau, Hans
Wirtz, Hubert
Seyfarth, Hans-Jürgen
description 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 µg 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.
doi_str_mv 10.1159/000107977
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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 µg 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 &lt; 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 &lt; 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.</description><identifier>ISSN: 0025-7931</identifier><identifier>EISSN: 1423-0356</identifier><identifier>DOI: 10.1159/000107977</identifier><identifier>PMID: 17804899</identifier><language>eng</language><publisher>Basel, Switzerland: S. 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Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-a6d688a5f3140cd9cfea307bed3fffe33bef18b1cdcfb81dc4050917fba6c08c3</citedby><cites>FETCH-LOGICAL-c397t-a6d688a5f3140cd9cfea307bed3fffe33bef18b1cdcfb81dc4050917fba6c08c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17804899$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Krug, Sabine</creatorcontrib><creatorcontrib>Hammerschmidt, Stefan</creatorcontrib><creatorcontrib>Pankau, Hans</creatorcontrib><creatorcontrib>Wirtz, Hubert</creatorcontrib><creatorcontrib>Seyfarth, Hans-Jürgen</creatorcontrib><title>Acute Improved Hemodynamics following Inhaled Iloprost in Chronic Thromboembolic Pulmonary Hypertension</title><title>Respiration</title><addtitle>Respiration</addtitle><description>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 µg 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 &lt; 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 &lt; 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). 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Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Database (Alumni Edition)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Respiration</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Krug, Sabine</au><au>Hammerschmidt, Stefan</au><au>Pankau, Hans</au><au>Wirtz, Hubert</au><au>Seyfarth, Hans-Jürgen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acute Improved Hemodynamics following Inhaled Iloprost in Chronic Thromboembolic Pulmonary Hypertension</atitle><jtitle>Respiration</jtitle><addtitle>Respiration</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>76</volume><issue>2</issue><spage>154</spage><epage>159</epage><pages>154-159</pages><issn>0025-7931</issn><eissn>1423-0356</eissn><abstract>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 µg 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 &lt; 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 &lt; 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.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>17804899</pmid><doi>10.1159/000107977</doi><tpages>6</tpages></addata></record>
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source Karger Journals; MEDLINE
subjects Administration, Inhalation
Adult
Aged
Circulatory system
Clinical Investigations
Clinical outcomes
Drug therapy
Female
Hemodynamics
Humans
Hypertension
Hypertension, Pulmonary - drug therapy
Hypertension, Pulmonary - etiology
Hypertension, Pulmonary - physiopathology
Iloprost - therapeutic use
Lung - blood supply
Lungs
Male
Middle Aged
Prospective Studies
Pulmonary Embolism - complications
Vasoconstriction
Vasodilator Agents - therapeutic use
Vein & artery diseases
title Acute Improved Hemodynamics following Inhaled Iloprost in Chronic Thromboembolic Pulmonary Hypertension
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