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The heart regulates the endocrine response to heart failure: cardiac contribution to circulating neprilysin
Abstract Aims Heart failure (HF) is accompanied by major neuroendocrine changes including the activation of the natriuretic peptide (NP) pathway. Using the unique model of patients undergoing implantation of the CARMAT total artificial heart and investigating regional differences in soluble neprilys...
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Published in: | European heart journal 2018-05, Vol.39 (20), p.1794-1798 |
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creator | Arrigo, Mattia Vodovar, Nicolas Nougué, Hélène Sadoune, Malha Pemberton, Chris J Ballan, Pamela Ludes, Pierre-Olivier Gendron, Nicolas Carpentier, Alain Cholley, Bernard Bizouarn, Philippe Cohen-Solal, Alain Singh, Jagmeet P Szymonifka, Jackie Latremouille, Christian Samuel, Jane-Lise Launay, Jean-Marie Pottecher, Julien Richards, A Mark Truong, Quynh A Smadja, David M Mebazaa, Alexandre |
description | Abstract
Aims
Heart failure (HF) is accompanied by major neuroendocrine changes including the activation of the natriuretic peptide (NP) pathway. Using the unique model of patients undergoing implantation of the CARMAT total artificial heart and investigating regional differences in soluble neprilysin (sNEP) in patients with reduced or preserved systolic function, we studied the regulation of the NP pathway in HF.
Methods and results
Venous blood samples from two patients undergoing replacement of the failing ventricles with a total artificial heart were collected before implantation and weekly thereafter until post-operative week 6. The ventricular removal was associated with an immediate drop in circulating NPs, a nearly total disappearance of circulating glycosylated proBNP and furin activity and a marked decrease in sNEP. From post-operative week 1 onwards, NP concentrations remained overall unchanged. In contrast, partial recoveries in glycosylated proBNP, furin activity, and sNEP were observed. Furthermore, while in patients with preserved systolic function (n = 6), sNEP concentrations in the coronary sinus and systemic vessels were similar (all P > 0.05), in patients with reduced left-ventricular systolic function, sNEP concentration, and activity were ∼three-fold higher in coronary sinus compared to systemic vessels (n = 21, all P |
doi_str_mv | 10.1093/eurheartj/ehx679 |
format | article |
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Aims
Heart failure (HF) is accompanied by major neuroendocrine changes including the activation of the natriuretic peptide (NP) pathway. Using the unique model of patients undergoing implantation of the CARMAT total artificial heart and investigating regional differences in soluble neprilysin (sNEP) in patients with reduced or preserved systolic function, we studied the regulation of the NP pathway in HF.
Methods and results
Venous blood samples from two patients undergoing replacement of the failing ventricles with a total artificial heart were collected before implantation and weekly thereafter until post-operative week 6. The ventricular removal was associated with an immediate drop in circulating NPs, a nearly total disappearance of circulating glycosylated proBNP and furin activity and a marked decrease in sNEP. From post-operative week 1 onwards, NP concentrations remained overall unchanged. In contrast, partial recoveries in glycosylated proBNP, furin activity, and sNEP were observed. Furthermore, while in patients with preserved systolic function (n = 6), sNEP concentrations in the coronary sinus and systemic vessels were similar (all P > 0.05), in patients with reduced left-ventricular systolic function, sNEP concentration, and activity were ∼three-fold higher in coronary sinus compared to systemic vessels (n = 21, all P < 0.0001), while the trans-pulmonary gradient was neutral (n = 5, P = 1.0).
Conclusion
The heart plays a pivotal role as a regulator of the endocrine response in systolic dysfunction, not only by directly releasing NPs but also by contributing to circulating sNEP, which in turn determines the bioavailability of other numerous vasoactive peptides.</description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehx679</identifier><identifier>PMID: 29244074</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Aged ; Biomarkers - blood ; EHJ Brief Communication ; Female ; Heart - physiopathology ; Heart Failure - blood ; Heart Failure - physiopathology ; Heart Failure - surgery ; Heart, Artificial ; Humans ; Male ; Middle Aged ; Natriuretic Peptide, Brain - blood ; Natriuretic Peptides - physiology ; Neprilysin - blood ; Neprilysin - genetics ; Neprilysin - physiology ; Peptide Fragments - blood ; Postoperative Period ; RNA, Messenger - genetics ; Signal Transduction - physiology ; Systole - physiology</subject><ispartof>European heart journal, 2018-05, Vol.39 (20), p.1794-1798</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c432t-530cac36d01ad6bcf72fb57c427996b68a361009b08d3393d0e448dad1fadd023</citedby><cites>FETCH-LOGICAL-c432t-530cac36d01ad6bcf72fb57c427996b68a361009b08d3393d0e448dad1fadd023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29244074$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arrigo, Mattia</creatorcontrib><creatorcontrib>Vodovar, Nicolas</creatorcontrib><creatorcontrib>Nougué, Hélène</creatorcontrib><creatorcontrib>Sadoune, Malha</creatorcontrib><creatorcontrib>Pemberton, Chris J</creatorcontrib><creatorcontrib>Ballan, Pamela</creatorcontrib><creatorcontrib>Ludes, Pierre-Olivier</creatorcontrib><creatorcontrib>Gendron, Nicolas</creatorcontrib><creatorcontrib>Carpentier, Alain</creatorcontrib><creatorcontrib>Cholley, Bernard</creatorcontrib><creatorcontrib>Bizouarn, Philippe</creatorcontrib><creatorcontrib>Cohen-Solal, Alain</creatorcontrib><creatorcontrib>Singh, Jagmeet P</creatorcontrib><creatorcontrib>Szymonifka, Jackie</creatorcontrib><creatorcontrib>Latremouille, Christian</creatorcontrib><creatorcontrib>Samuel, Jane-Lise</creatorcontrib><creatorcontrib>Launay, Jean-Marie</creatorcontrib><creatorcontrib>Pottecher, Julien</creatorcontrib><creatorcontrib>Richards, A Mark</creatorcontrib><creatorcontrib>Truong, Quynh A</creatorcontrib><creatorcontrib>Smadja, David M</creatorcontrib><creatorcontrib>Mebazaa, Alexandre</creatorcontrib><title>The heart regulates the endocrine response to heart failure: cardiac contribution to circulating neprilysin</title><title>European heart journal</title><addtitle>Eur Heart J</addtitle><description>Abstract
Aims
Heart failure (HF) is accompanied by major neuroendocrine changes including the activation of the natriuretic peptide (NP) pathway. Using the unique model of patients undergoing implantation of the CARMAT total artificial heart and investigating regional differences in soluble neprilysin (sNEP) in patients with reduced or preserved systolic function, we studied the regulation of the NP pathway in HF.
Methods and results
Venous blood samples from two patients undergoing replacement of the failing ventricles with a total artificial heart were collected before implantation and weekly thereafter until post-operative week 6. The ventricular removal was associated with an immediate drop in circulating NPs, a nearly total disappearance of circulating glycosylated proBNP and furin activity and a marked decrease in sNEP. From post-operative week 1 onwards, NP concentrations remained overall unchanged. In contrast, partial recoveries in glycosylated proBNP, furin activity, and sNEP were observed. Furthermore, while in patients with preserved systolic function (n = 6), sNEP concentrations in the coronary sinus and systemic vessels were similar (all P > 0.05), in patients with reduced left-ventricular systolic function, sNEP concentration, and activity were ∼three-fold higher in coronary sinus compared to systemic vessels (n = 21, all P < 0.0001), while the trans-pulmonary gradient was neutral (n = 5, P = 1.0).
Conclusion
The heart plays a pivotal role as a regulator of the endocrine response in systolic dysfunction, not only by directly releasing NPs but also by contributing to circulating sNEP, which in turn determines the bioavailability of other numerous vasoactive peptides.</description><subject>Aged</subject><subject>Biomarkers - blood</subject><subject>EHJ Brief Communication</subject><subject>Female</subject><subject>Heart - physiopathology</subject><subject>Heart Failure - blood</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Failure - surgery</subject><subject>Heart, Artificial</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Natriuretic Peptide, Brain - blood</subject><subject>Natriuretic Peptides - physiology</subject><subject>Neprilysin - blood</subject><subject>Neprilysin - genetics</subject><subject>Neprilysin - physiology</subject><subject>Peptide Fragments - blood</subject><subject>Postoperative Period</subject><subject>RNA, Messenger - genetics</subject><subject>Signal Transduction - physiology</subject><subject>Systole - physiology</subject><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNqFkc9LHDEYhoNUdP1x76nMsSBTvyQzmUkPBRFtC4IXhd5CJvlmN3Y2WZMZ0f_ebHe76MlcAl-e78kLLyGfKXyjIPk5TnGBOo4P57h4Fo3cIzNaM1ZKUdWfyAyorEsh2j-H5CilBwBoBRUH5JBJVlXQVDPy926BxT9HEXE-DXrEVIx5ht4GE53HPE-r4BMWY9iSvXbDFPF7YXS0TpvCBD9G102jC36NGRfN2uX8vPC4im54Sc6fkP1eDwlPt_cxub--urv8Vd7c_vx9eXFTmoqzsaw5GG24sEC1FZ3pG9Z3dWMq1kgpOtFqLiiA7KC1nEtuAauqtdrSXlsLjB-THxvvauqWaA3mcHpQOcZSxxcVtFPvX7xbqHl4UkKyppWQBV-3ghgeJ0yjWrpkcBi0xzAlRWWTj5QtzShsUBNDShH73TcU1LojtetIbTrKK1_extst_C8lA2cbIEyrj3WvbdukKQ</recordid><startdate>20180521</startdate><enddate>20180521</enddate><creator>Arrigo, Mattia</creator><creator>Vodovar, Nicolas</creator><creator>Nougué, Hélène</creator><creator>Sadoune, Malha</creator><creator>Pemberton, Chris J</creator><creator>Ballan, Pamela</creator><creator>Ludes, Pierre-Olivier</creator><creator>Gendron, Nicolas</creator><creator>Carpentier, Alain</creator><creator>Cholley, Bernard</creator><creator>Bizouarn, Philippe</creator><creator>Cohen-Solal, Alain</creator><creator>Singh, Jagmeet P</creator><creator>Szymonifka, Jackie</creator><creator>Latremouille, Christian</creator><creator>Samuel, Jane-Lise</creator><creator>Launay, Jean-Marie</creator><creator>Pottecher, Julien</creator><creator>Richards, A Mark</creator><creator>Truong, Quynh A</creator><creator>Smadja, David M</creator><creator>Mebazaa, Alexandre</creator><general>Oxford University Press</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180521</creationdate><title>The heart regulates the endocrine response to heart failure: cardiac contribution to circulating neprilysin</title><author>Arrigo, Mattia ; Vodovar, Nicolas ; Nougué, Hélène ; Sadoune, Malha ; Pemberton, Chris J ; Ballan, Pamela ; Ludes, Pierre-Olivier ; Gendron, Nicolas ; Carpentier, Alain ; Cholley, Bernard ; Bizouarn, Philippe ; Cohen-Solal, Alain ; Singh, Jagmeet P ; Szymonifka, Jackie ; Latremouille, Christian ; Samuel, Jane-Lise ; Launay, Jean-Marie ; Pottecher, Julien ; Richards, A Mark ; Truong, Quynh A ; Smadja, David M ; Mebazaa, Alexandre</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c432t-530cac36d01ad6bcf72fb57c427996b68a361009b08d3393d0e448dad1fadd023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Aged</topic><topic>Biomarkers - blood</topic><topic>EHJ Brief Communication</topic><topic>Female</topic><topic>Heart - physiopathology</topic><topic>Heart Failure - blood</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Failure - surgery</topic><topic>Heart, Artificial</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Natriuretic Peptide, Brain - blood</topic><topic>Natriuretic Peptides - physiology</topic><topic>Neprilysin - blood</topic><topic>Neprilysin - genetics</topic><topic>Neprilysin - physiology</topic><topic>Peptide Fragments - blood</topic><topic>Postoperative Period</topic><topic>RNA, Messenger - genetics</topic><topic>Signal Transduction - physiology</topic><topic>Systole - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arrigo, Mattia</creatorcontrib><creatorcontrib>Vodovar, Nicolas</creatorcontrib><creatorcontrib>Nougué, Hélène</creatorcontrib><creatorcontrib>Sadoune, Malha</creatorcontrib><creatorcontrib>Pemberton, Chris J</creatorcontrib><creatorcontrib>Ballan, Pamela</creatorcontrib><creatorcontrib>Ludes, Pierre-Olivier</creatorcontrib><creatorcontrib>Gendron, Nicolas</creatorcontrib><creatorcontrib>Carpentier, Alain</creatorcontrib><creatorcontrib>Cholley, Bernard</creatorcontrib><creatorcontrib>Bizouarn, Philippe</creatorcontrib><creatorcontrib>Cohen-Solal, Alain</creatorcontrib><creatorcontrib>Singh, Jagmeet P</creatorcontrib><creatorcontrib>Szymonifka, Jackie</creatorcontrib><creatorcontrib>Latremouille, Christian</creatorcontrib><creatorcontrib>Samuel, Jane-Lise</creatorcontrib><creatorcontrib>Launay, Jean-Marie</creatorcontrib><creatorcontrib>Pottecher, Julien</creatorcontrib><creatorcontrib>Richards, A Mark</creatorcontrib><creatorcontrib>Truong, Quynh A</creatorcontrib><creatorcontrib>Smadja, David M</creatorcontrib><creatorcontrib>Mebazaa, Alexandre</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arrigo, Mattia</au><au>Vodovar, Nicolas</au><au>Nougué, Hélène</au><au>Sadoune, Malha</au><au>Pemberton, Chris J</au><au>Ballan, Pamela</au><au>Ludes, Pierre-Olivier</au><au>Gendron, Nicolas</au><au>Carpentier, Alain</au><au>Cholley, Bernard</au><au>Bizouarn, Philippe</au><au>Cohen-Solal, Alain</au><au>Singh, Jagmeet P</au><au>Szymonifka, Jackie</au><au>Latremouille, Christian</au><au>Samuel, Jane-Lise</au><au>Launay, Jean-Marie</au><au>Pottecher, Julien</au><au>Richards, A Mark</au><au>Truong, Quynh A</au><au>Smadja, David M</au><au>Mebazaa, Alexandre</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The heart regulates the endocrine response to heart failure: cardiac contribution to circulating neprilysin</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>2018-05-21</date><risdate>2018</risdate><volume>39</volume><issue>20</issue><spage>1794</spage><epage>1798</epage><pages>1794-1798</pages><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract>Abstract
Aims
Heart failure (HF) is accompanied by major neuroendocrine changes including the activation of the natriuretic peptide (NP) pathway. Using the unique model of patients undergoing implantation of the CARMAT total artificial heart and investigating regional differences in soluble neprilysin (sNEP) in patients with reduced or preserved systolic function, we studied the regulation of the NP pathway in HF.
Methods and results
Venous blood samples from two patients undergoing replacement of the failing ventricles with a total artificial heart were collected before implantation and weekly thereafter until post-operative week 6. The ventricular removal was associated with an immediate drop in circulating NPs, a nearly total disappearance of circulating glycosylated proBNP and furin activity and a marked decrease in sNEP. From post-operative week 1 onwards, NP concentrations remained overall unchanged. In contrast, partial recoveries in glycosylated proBNP, furin activity, and sNEP were observed. Furthermore, while in patients with preserved systolic function (n = 6), sNEP concentrations in the coronary sinus and systemic vessels were similar (all P > 0.05), in patients with reduced left-ventricular systolic function, sNEP concentration, and activity were ∼three-fold higher in coronary sinus compared to systemic vessels (n = 21, all P < 0.0001), while the trans-pulmonary gradient was neutral (n = 5, P = 1.0).
Conclusion
The heart plays a pivotal role as a regulator of the endocrine response in systolic dysfunction, not only by directly releasing NPs but also by contributing to circulating sNEP, which in turn determines the bioavailability of other numerous vasoactive peptides.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>29244074</pmid><doi>10.1093/eurheartj/ehx679</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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source | Oxford Journals Online |
subjects | Aged Biomarkers - blood EHJ Brief Communication Female Heart - physiopathology Heart Failure - blood Heart Failure - physiopathology Heart Failure - surgery Heart, Artificial Humans Male Middle Aged Natriuretic Peptide, Brain - blood Natriuretic Peptides - physiology Neprilysin - blood Neprilysin - genetics Neprilysin - physiology Peptide Fragments - blood Postoperative Period RNA, Messenger - genetics Signal Transduction - physiology Systole - physiology |
title | The heart regulates the endocrine response to heart failure: cardiac contribution to circulating neprilysin |
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