Long-Term Effects of Pulmonary Endarterectomy on Right Ventricular Stiffness and Fibrosis in Chronic Thromboembolic Pulmonary Hypertension
BACKGROUNDSurgical removal of thromboembolic material by pulmonary endarterectomy (PEA) leads within months to the improvement of right ventricular (RV) function in the majority of patients with chronic thromboembolic pulmonary hypertension. However, RV mass does not always normalize. It is unknown...
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| creator | Braams, Natalia J. Kianzad, Azar van Wezenbeek, Jessie Wessels, Jeroen N. Jansen, Samara M.A. Andersen, Stine Boonstra, Anco Nossent, Esther J. Marcus, J. Tim Bayoumy, Ahmed A. Becher, Clarissa Goumans, Marie-José Andersen, Asger Vonk Noordegraaf, Anton de Man, Frances S. Bogaard, Harm Jan Meijboom, Lilian J. |
| description | BACKGROUNDSurgical removal of thromboembolic material by pulmonary endarterectomy (PEA) leads within months to the improvement of right ventricular (RV) function in the majority of patients with chronic thromboembolic pulmonary hypertension. However, RV mass does not always normalize. It is unknown whether incomplete reversal of RV remodeling results from extracellular matrix expansion (diffuse interstitial fibrosis) or cellular hypertrophy, and whether residual RV remodeling relates to altered diastolic function.METHODSWe prospectively included 25 patients with chronic thromboembolic pulmonary hypertension treated with PEA. Structured follow-up measurements were performed before, and 6 and 18 months after PEA. With single beat pressure-volume loop analyses, we determined RV end-systolic elastance (Ees), arterial elastance (Ea), RV-arterial coupling (Ees/Ea), and RV end-diastolic elastance (stiffness, Eed). The extracellular volume fraction of the RV free wall was measured by cardiac magnetic resonance imaging and used to separate the myocardium into cellular and matrix volume. Circulating collagen biomarkers were analyzed to determine the contribution of collagen metabolism.RESULTSRV mass significantly decreased from 43±15 to 27±11g/m2 (-15.9 g/m2 [95% CI, -21.4 to -10.5]; P |
| doi_str_mv | 10.1161/CIRCHEARTFAILURE.122.010336 |
| format | Article |
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Tim ; Bayoumy, Ahmed A. ; Becher, Clarissa ; Goumans, Marie-José ; Andersen, Asger ; Vonk Noordegraaf, Anton ; de Man, Frances S. ; Bogaard, Harm Jan ; Meijboom, Lilian J.</creator><creatorcontrib>Braams, Natalia J. ; Kianzad, Azar ; van Wezenbeek, Jessie ; Wessels, Jeroen N. ; Jansen, Samara M.A. ; Andersen, Stine ; Boonstra, Anco ; Nossent, Esther J. ; Marcus, J. Tim ; Bayoumy, Ahmed A. ; Becher, Clarissa ; Goumans, Marie-José ; Andersen, Asger ; Vonk Noordegraaf, Anton ; de Man, Frances S. ; Bogaard, Harm Jan ; Meijboom, Lilian J.</creatorcontrib><description>BACKGROUNDSurgical removal of thromboembolic material by pulmonary endarterectomy (PEA) leads within months to the improvement of right ventricular (RV) function in the majority of patients with chronic thromboembolic pulmonary hypertension. However, RV mass does not always normalize. It is unknown whether incomplete reversal of RV remodeling results from extracellular matrix expansion (diffuse interstitial fibrosis) or cellular hypertrophy, and whether residual RV remodeling relates to altered diastolic function.METHODSWe prospectively included 25 patients with chronic thromboembolic pulmonary hypertension treated with PEA. Structured follow-up measurements were performed before, and 6 and 18 months after PEA. With single beat pressure-volume loop analyses, we determined RV end-systolic elastance (Ees), arterial elastance (Ea), RV-arterial coupling (Ees/Ea), and RV end-diastolic elastance (stiffness, Eed). The extracellular volume fraction of the RV free wall was measured by cardiac magnetic resonance imaging and used to separate the myocardium into cellular and matrix volume. Circulating collagen biomarkers were analyzed to determine the contribution of collagen metabolism.RESULTSRV mass significantly decreased from 43±15 to 27±11g/m2 (-15.9 g/m2 [95% CI, -21.4 to -10.5]; P<0.0001) 6 months after PEA but did not normalize (28±9 versus 22±6 g/m2 in healthy controls [95% CI, 2.1 to 9.8]; P<0.01). On the contrary, Eed normalized after PEA. Extracellular volume fraction in the right ventricular free wall increased after PEA from 31.0±3.8 to 33.6±3.5% (3.6% [95% CI, 1.2-6.1]; P=0.013) as a result of a larger reduction in cellular volume than in matrix volume (Pinteraction=0.0013). Levels of MMP-1 (matrix metalloproteinase-1), TIMP-1 (tissue inhibitor of metalloproteinase-1), and TGF-β (transforming growth factor-β) were elevated at baseline and remained elevated post-PEA.CONCLUSIONSAlthough cellular hypertrophy regresses and diastolic stiffness normalizes after PEA, a relative increase in extracellular volume remains. Incomplete regression of diffuse RV interstitial fibrosis after PEA is accompanied by elevated levels of circulating collagen biomarkers, suggestive of active collagen turnover.</description><identifier>ISSN: 1941-3289</identifier><identifier>EISSN: 1941-3297</identifier><identifier>DOI: 10.1161/CIRCHEARTFAILURE.122.010336</identifier><identifier>PMID: 37675561</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Original</subject><ispartof>Circulation. Heart failure, 2023-10, Vol.16 (10), p.e010336-e010336</ispartof><rights>2023 The Authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c407t-50a7c908799557ee9c3916e022ff2f2009631a5e8d92bdd5bd5872d0a67162ea3</citedby><cites>FETCH-LOGICAL-c407t-50a7c908799557ee9c3916e022ff2f2009631a5e8d92bdd5bd5872d0a67162ea3</cites><orcidid>0000-0002-7153-1170 ; 0000-0001-9948-6407 ; 0000-0001-8541-6088 ; 0000-0003-3854-4137 ; 0000-0002-7528-8307 ; 0000-0002-1091-5445 ; 0000-0001-9344-6746 ; 0000-0002-1811-8037 ; 0000-0003-1238-4139 ; 0000-0003-3493-3573 ; 0000-0002-4459-1055 ; 0000-0001-5371-0346 ; 0000-0002-4057-758X ; 0000-0003-2401-7707 ; 0000-0002-5776-7793 ; 0000-0002-9102-3130</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3687,27924,27925</link.rule.ids></links><search><creatorcontrib>Braams, Natalia J.</creatorcontrib><creatorcontrib>Kianzad, Azar</creatorcontrib><creatorcontrib>van Wezenbeek, Jessie</creatorcontrib><creatorcontrib>Wessels, Jeroen N.</creatorcontrib><creatorcontrib>Jansen, Samara M.A.</creatorcontrib><creatorcontrib>Andersen, Stine</creatorcontrib><creatorcontrib>Boonstra, Anco</creatorcontrib><creatorcontrib>Nossent, Esther J.</creatorcontrib><creatorcontrib>Marcus, J. Tim</creatorcontrib><creatorcontrib>Bayoumy, Ahmed A.</creatorcontrib><creatorcontrib>Becher, Clarissa</creatorcontrib><creatorcontrib>Goumans, Marie-José</creatorcontrib><creatorcontrib>Andersen, Asger</creatorcontrib><creatorcontrib>Vonk Noordegraaf, Anton</creatorcontrib><creatorcontrib>de Man, Frances S.</creatorcontrib><creatorcontrib>Bogaard, Harm Jan</creatorcontrib><creatorcontrib>Meijboom, Lilian J.</creatorcontrib><title>Long-Term Effects of Pulmonary Endarterectomy on Right Ventricular Stiffness and Fibrosis in Chronic Thromboembolic Pulmonary Hypertension</title><title>Circulation. Heart failure</title><description>BACKGROUNDSurgical removal of thromboembolic material by pulmonary endarterectomy (PEA) leads within months to the improvement of right ventricular (RV) function in the majority of patients with chronic thromboembolic pulmonary hypertension. However, RV mass does not always normalize. It is unknown whether incomplete reversal of RV remodeling results from extracellular matrix expansion (diffuse interstitial fibrosis) or cellular hypertrophy, and whether residual RV remodeling relates to altered diastolic function.METHODSWe prospectively included 25 patients with chronic thromboembolic pulmonary hypertension treated with PEA. Structured follow-up measurements were performed before, and 6 and 18 months after PEA. With single beat pressure-volume loop analyses, we determined RV end-systolic elastance (Ees), arterial elastance (Ea), RV-arterial coupling (Ees/Ea), and RV end-diastolic elastance (stiffness, Eed). The extracellular volume fraction of the RV free wall was measured by cardiac magnetic resonance imaging and used to separate the myocardium into cellular and matrix volume. Circulating collagen biomarkers were analyzed to determine the contribution of collagen metabolism.RESULTSRV mass significantly decreased from 43±15 to 27±11g/m2 (-15.9 g/m2 [95% CI, -21.4 to -10.5]; P<0.0001) 6 months after PEA but did not normalize (28±9 versus 22±6 g/m2 in healthy controls [95% CI, 2.1 to 9.8]; P<0.01). On the contrary, Eed normalized after PEA. Extracellular volume fraction in the right ventricular free wall increased after PEA from 31.0±3.8 to 33.6±3.5% (3.6% [95% CI, 1.2-6.1]; P=0.013) as a result of a larger reduction in cellular volume than in matrix volume (Pinteraction=0.0013). Levels of MMP-1 (matrix metalloproteinase-1), TIMP-1 (tissue inhibitor of metalloproteinase-1), and TGF-β (transforming growth factor-β) were elevated at baseline and remained elevated post-PEA.CONCLUSIONSAlthough cellular hypertrophy regresses and diastolic stiffness normalizes after PEA, a relative increase in extracellular volume remains. Incomplete regression of diffuse RV interstitial fibrosis after PEA is accompanied by elevated levels of circulating collagen biomarkers, suggestive of active collagen turnover.</description><subject>Original</subject><issn>1941-3289</issn><issn>1941-3297</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpdkc1qGzEQx0VpadK07yDopZd19RFJK3ooZlnXBkOK6_QqtFrJVtmVXGk34FfoU0fBIaU9DDPDDL_5-APwEaMFxhx_bja7Zt0ud_vVcrO937ULTMgCYUQpfwWusbzFFSVSvH6Ja3kF3uX8CyFOGJNvwRUVXDDG8TX4s43hUO1tGmHrnDVThtHB7_MwxqDTGbah12myqVTieIYxwJ0_HCf404YpeTMPOsEfk3cu2JyhDj1c-S7F7DP0ATbHFIM3cF_82EVbbCjpX_z6fLIFH7KP4T144_SQ7YdnfwPuV-2-WVfbu2-bZrmtzC0SU8WQFkaiWkjJmLBWGioxt4gQ54gjCElOsWa27iXp-p51PasF6ZHmAnNiNb0BXy_c09yNtjdPl-hBnZIfy0oqaq_-rQR_VIf4oDBigiJZF8KnZ0KKv2ebJzX6bOww6GDjnBWpOcGy5jUurV8uraY8JSfrXuZgpJ7kVP_LqYqc6iInfQT5VZf4</recordid><startdate>20231001</startdate><enddate>20231001</enddate><creator>Braams, Natalia J.</creator><creator>Kianzad, Azar</creator><creator>van Wezenbeek, Jessie</creator><creator>Wessels, Jeroen N.</creator><creator>Jansen, Samara M.A.</creator><creator>Andersen, Stine</creator><creator>Boonstra, Anco</creator><creator>Nossent, Esther J.</creator><creator>Marcus, J. Tim</creator><creator>Bayoumy, Ahmed A.</creator><creator>Becher, Clarissa</creator><creator>Goumans, Marie-José</creator><creator>Andersen, Asger</creator><creator>Vonk Noordegraaf, Anton</creator><creator>de Man, Frances S.</creator><creator>Bogaard, Harm Jan</creator><creator>Meijboom, Lilian J.</creator><general>Lippincott Williams & Wilkins</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7153-1170</orcidid><orcidid>https://orcid.org/0000-0001-9948-6407</orcidid><orcidid>https://orcid.org/0000-0001-8541-6088</orcidid><orcidid>https://orcid.org/0000-0003-3854-4137</orcidid><orcidid>https://orcid.org/0000-0002-7528-8307</orcidid><orcidid>https://orcid.org/0000-0002-1091-5445</orcidid><orcidid>https://orcid.org/0000-0001-9344-6746</orcidid><orcidid>https://orcid.org/0000-0002-1811-8037</orcidid><orcidid>https://orcid.org/0000-0003-1238-4139</orcidid><orcidid>https://orcid.org/0000-0003-3493-3573</orcidid><orcidid>https://orcid.org/0000-0002-4459-1055</orcidid><orcidid>https://orcid.org/0000-0001-5371-0346</orcidid><orcidid>https://orcid.org/0000-0002-4057-758X</orcidid><orcidid>https://orcid.org/0000-0003-2401-7707</orcidid><orcidid>https://orcid.org/0000-0002-5776-7793</orcidid><orcidid>https://orcid.org/0000-0002-9102-3130</orcidid></search><sort><creationdate>20231001</creationdate><title>Long-Term Effects of Pulmonary Endarterectomy on Right Ventricular Stiffness and Fibrosis in Chronic Thromboembolic Pulmonary Hypertension</title><author>Braams, Natalia J. ; Kianzad, Azar ; van Wezenbeek, Jessie ; Wessels, Jeroen N. ; Jansen, Samara M.A. ; Andersen, Stine ; Boonstra, Anco ; Nossent, Esther J. ; Marcus, J. Tim ; Bayoumy, Ahmed A. ; Becher, Clarissa ; Goumans, Marie-José ; Andersen, Asger ; Vonk Noordegraaf, Anton ; de Man, Frances S. ; Bogaard, Harm Jan ; Meijboom, Lilian J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c407t-50a7c908799557ee9c3916e022ff2f2009631a5e8d92bdd5bd5872d0a67162ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Original</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Braams, Natalia J.</creatorcontrib><creatorcontrib>Kianzad, Azar</creatorcontrib><creatorcontrib>van Wezenbeek, Jessie</creatorcontrib><creatorcontrib>Wessels, Jeroen N.</creatorcontrib><creatorcontrib>Jansen, Samara M.A.</creatorcontrib><creatorcontrib>Andersen, Stine</creatorcontrib><creatorcontrib>Boonstra, Anco</creatorcontrib><creatorcontrib>Nossent, Esther J.</creatorcontrib><creatorcontrib>Marcus, J. Tim</creatorcontrib><creatorcontrib>Bayoumy, Ahmed A.</creatorcontrib><creatorcontrib>Becher, Clarissa</creatorcontrib><creatorcontrib>Goumans, Marie-José</creatorcontrib><creatorcontrib>Andersen, Asger</creatorcontrib><creatorcontrib>Vonk Noordegraaf, Anton</creatorcontrib><creatorcontrib>de Man, Frances S.</creatorcontrib><creatorcontrib>Bogaard, Harm Jan</creatorcontrib><creatorcontrib>Meijboom, Lilian J.</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Circulation. Heart failure</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Braams, Natalia J.</au><au>Kianzad, Azar</au><au>van Wezenbeek, Jessie</au><au>Wessels, Jeroen N.</au><au>Jansen, Samara M.A.</au><au>Andersen, Stine</au><au>Boonstra, Anco</au><au>Nossent, Esther J.</au><au>Marcus, J. Tim</au><au>Bayoumy, Ahmed A.</au><au>Becher, Clarissa</au><au>Goumans, Marie-José</au><au>Andersen, Asger</au><au>Vonk Noordegraaf, Anton</au><au>de Man, Frances S.</au><au>Bogaard, Harm Jan</au><au>Meijboom, Lilian J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long-Term Effects of Pulmonary Endarterectomy on Right Ventricular Stiffness and Fibrosis in Chronic Thromboembolic Pulmonary Hypertension</atitle><jtitle>Circulation. Heart failure</jtitle><date>2023-10-01</date><risdate>2023</risdate><volume>16</volume><issue>10</issue><spage>e010336</spage><epage>e010336</epage><pages>e010336-e010336</pages><issn>1941-3289</issn><eissn>1941-3297</eissn><abstract>BACKGROUNDSurgical removal of thromboembolic material by pulmonary endarterectomy (PEA) leads within months to the improvement of right ventricular (RV) function in the majority of patients with chronic thromboembolic pulmonary hypertension. However, RV mass does not always normalize. It is unknown whether incomplete reversal of RV remodeling results from extracellular matrix expansion (diffuse interstitial fibrosis) or cellular hypertrophy, and whether residual RV remodeling relates to altered diastolic function.METHODSWe prospectively included 25 patients with chronic thromboembolic pulmonary hypertension treated with PEA. Structured follow-up measurements were performed before, and 6 and 18 months after PEA. With single beat pressure-volume loop analyses, we determined RV end-systolic elastance (Ees), arterial elastance (Ea), RV-arterial coupling (Ees/Ea), and RV end-diastolic elastance (stiffness, Eed). The extracellular volume fraction of the RV free wall was measured by cardiac magnetic resonance imaging and used to separate the myocardium into cellular and matrix volume. Circulating collagen biomarkers were analyzed to determine the contribution of collagen metabolism.RESULTSRV mass significantly decreased from 43±15 to 27±11g/m2 (-15.9 g/m2 [95% CI, -21.4 to -10.5]; P<0.0001) 6 months after PEA but did not normalize (28±9 versus 22±6 g/m2 in healthy controls [95% CI, 2.1 to 9.8]; P<0.01). On the contrary, Eed normalized after PEA. Extracellular volume fraction in the right ventricular free wall increased after PEA from 31.0±3.8 to 33.6±3.5% (3.6% [95% CI, 1.2-6.1]; P=0.013) as a result of a larger reduction in cellular volume than in matrix volume (Pinteraction=0.0013). Levels of MMP-1 (matrix metalloproteinase-1), TIMP-1 (tissue inhibitor of metalloproteinase-1), and TGF-β (transforming growth factor-β) were elevated at baseline and remained elevated post-PEA.CONCLUSIONSAlthough cellular hypertrophy regresses and diastolic stiffness normalizes after PEA, a relative increase in extracellular volume remains. Incomplete regression of diffuse RV interstitial fibrosis after PEA is accompanied by elevated levels of circulating collagen biomarkers, suggestive of active collagen turnover.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>37675561</pmid><doi>10.1161/CIRCHEARTFAILURE.122.010336</doi><orcidid>https://orcid.org/0000-0002-7153-1170</orcidid><orcidid>https://orcid.org/0000-0001-9948-6407</orcidid><orcidid>https://orcid.org/0000-0001-8541-6088</orcidid><orcidid>https://orcid.org/0000-0003-3854-4137</orcidid><orcidid>https://orcid.org/0000-0002-7528-8307</orcidid><orcidid>https://orcid.org/0000-0002-1091-5445</orcidid><orcidid>https://orcid.org/0000-0001-9344-6746</orcidid><orcidid>https://orcid.org/0000-0002-1811-8037</orcidid><orcidid>https://orcid.org/0000-0003-1238-4139</orcidid><orcidid>https://orcid.org/0000-0003-3493-3573</orcidid><orcidid>https://orcid.org/0000-0002-4459-1055</orcidid><orcidid>https://orcid.org/0000-0001-5371-0346</orcidid><orcidid>https://orcid.org/0000-0002-4057-758X</orcidid><orcidid>https://orcid.org/0000-0003-2401-7707</orcidid><orcidid>https://orcid.org/0000-0002-5776-7793</orcidid><orcidid>https://orcid.org/0000-0002-9102-3130</orcidid><oa>free_for_read</oa></addata></record> |
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| source | American Heart Association Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Original |
| title | Long-Term Effects of Pulmonary Endarterectomy on Right Ventricular Stiffness and Fibrosis in Chronic Thromboembolic Pulmonary Hypertension |
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