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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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 < 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.</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. Karger AG</publisher><subject>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</subject><ispartof>Respiration, 2008-01, Vol.76 (2), p.154-159</ispartof><rights>2007 S. Karger AG, Basel</rights><rights>Copyright 2007 S. Karger AG, Basel.</rights><rights>Copyright (c) 2008 S. 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 < 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.</description><subject>Administration, Inhalation</subject><subject>Adult</subject><subject>Aged</subject><subject>Circulatory system</subject><subject>Clinical Investigations</subject><subject>Clinical outcomes</subject><subject>Drug therapy</subject><subject>Female</subject><subject>Hemodynamics</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension, Pulmonary - drug therapy</subject><subject>Hypertension, Pulmonary - etiology</subject><subject>Hypertension, Pulmonary - physiopathology</subject><subject>Iloprost - therapeutic use</subject><subject>Lung - blood supply</subject><subject>Lungs</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Prospective Studies</subject><subject>Pulmonary Embolism - complications</subject><subject>Vasoconstriction</subject><subject>Vasodilator Agents - therapeutic use</subject><subject>Vein & artery diseases</subject><issn>0025-7931</issn><issn>1423-0356</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpd0M9LwzAUB_AgipvTg3eR4kHwUE2a_kiOY6gbDPQwzyVNX7bONJlJq-y_N7qh4iE8Qj55vPdF6JzgW0IyfocxJrjgRXGAhiRNaIxplh-iIcZJFheckgE68X4dVMZYcowGpGA4ZZwP0XIs-w6iWbtx9h3qaAqtrbdGtI30kbJa24_GLKOZWQkdnmfaBui7qDHRZOWsaWS0CLWtLISjw_W51601wm2j6XYDrgPjG2tO0ZES2sPZvo7Qy8P9YjKN50-Ps8l4HkvKiy4WeZ0zJjJFSYplzaUCQXFRQU2VUkBpBYqwishaqoqRWqY4w5wUqhK5xEzSEbre9Q1jvvXgu7JtvASthQHb-zLnKeVZzgK8-gfXtncmzFYmCaM55YwGdLNDMiztHahy45o27FYSXH5FX_5EH-zlvmFftVD_yn3WAVzswKtwS3B_Wn3__wTxZYnc</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Krug, Sabine</creator><creator>Hammerschmidt, Stefan</creator><creator>Pankau, Hans</creator><creator>Wirtz, Hubert</creator><creator>Seyfarth, Hans-Jürgen</creator><general>S. Karger AG</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RQ</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20080101</creationdate><title>Acute Improved Hemodynamics following Inhaled Iloprost in Chronic Thromboembolic Pulmonary Hypertension</title><author>Krug, Sabine ; Hammerschmidt, Stefan ; Pankau, Hans ; Wirtz, Hubert ; Seyfarth, Hans-Jürgen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-a6d688a5f3140cd9cfea307bed3fffe33bef18b1cdcfb81dc4050917fba6c08c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Administration, Inhalation</topic><topic>Adult</topic><topic>Aged</topic><topic>Circulatory system</topic><topic>Clinical Investigations</topic><topic>Clinical outcomes</topic><topic>Drug therapy</topic><topic>Female</topic><topic>Hemodynamics</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension, Pulmonary - drug therapy</topic><topic>Hypertension, Pulmonary - etiology</topic><topic>Hypertension, Pulmonary - physiopathology</topic><topic>Iloprost - therapeutic use</topic><topic>Lung - blood supply</topic><topic>Lungs</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Prospective Studies</topic><topic>Pulmonary Embolism - complications</topic><topic>Vasoconstriction</topic><topic>Vasodilator Agents - therapeutic use</topic><topic>Vein & artery diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Krug, Sabine</creatorcontrib><creatorcontrib>Hammerschmidt, Stefan</creatorcontrib><creatorcontrib>Pankau, Hans</creatorcontrib><creatorcontrib>Wirtz, Hubert</creatorcontrib><creatorcontrib>Seyfarth, Hans-Jürgen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Career & Technical Education Database</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & 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 < 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.</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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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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