Cardiac afferent signaling partially underlies premature ventricular contraction–induced cardiomyopathy
The mechanisms underlying premature ventricular contraction (PVC)–induced cardiomyopathy (PIC) remain unknown. Transient receptor potential vanilloid-1 (TRPV1) afferent fibers are implicated in the reflex processing of cardiac stress. The purpose of this study was to determine whether cardiac TRPV1...
Gespeichert in:
| Veröffentlicht in: | Heart rhythm 2021-09, Vol.18 (9), p.1586-1595 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1595 |
|---|---|
| container_issue | 9 |
| container_start_page | 1586 |
| container_title | Heart rhythm |
| container_volume | 18 |
| creator | Hori, Yuichi Temma, Taro Wooten, Christian Sobowale, Christopher Chan, Christopher Swid, Mohammed Ajijola, Olujimi A. |
| description | The mechanisms underlying premature ventricular contraction (PVC)–induced cardiomyopathy (PIC) remain unknown. Transient receptor potential vanilloid-1 (TRPV1) afferent fibers are implicated in the reflex processing of cardiac stress.
The purpose of this study was to determine whether cardiac TRPV1 afferent signaling promote PIC.
A PIC swine model (50% PVC burden) was created via an implanted pacemaker. We selectively depleted cardiac TRPV1 afferent fibers using percutaneous epicardial application of resiniferatoxin (RTX). Animals were randomized to PVC only (n = 11), PVC+RTX (n = 11), or control (n = 6). We examined early-stage (4 weeks after implantation; n = 5) and late-stage PIC (8 weeks after implantation; n = 6). At terminal experimentation, animals underwent echocardiography, serum sampling, and physiological and autonomic reflex testing.
Depletion of cardiac TRPV1 afferents by RTX treatment was confirmed by absent sensory fibers and absent functional responses to TRPV1 activators. Left ventricular ejection fraction was worse in late-stage than early-stage PIC (P |
| doi_str_mv | 10.1016/j.hrthm.2021.04.004 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2512309252</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1547527121003271</els_id><sourcerecordid>2512309252</sourcerecordid><originalsourceid>FETCH-LOGICAL-c425t-25103288c8ced92c13a3c821ef749b2a926e46d96363468d73343c3a74f828233</originalsourceid><addsrcrecordid>eNp9kLtu3DAQRYkgRtaPfEEAQ2UayeQMJVFFCmORhwEDbuyaoKnRLhd6maQMbOd_8B_mS8LNOi5TzRRn7sUcxr4IXgguqqtdsfVxOxTAQRRcFpzLD-xUlGWVo6rFx8Mu67yEWqzYWQg7zqGpOH5iK0QlSxDylLm18a0zNjNdR57GmAW3GU3vxk02Gx-d6ft9towt-d5RyGZPg4mLp-w5wd7ZpTc-s1PajY1uGn-_vLqxXSy1mT1ET8N-mk3c7i_YSWf6QJ_f5jl7-PH9fv0rv737ebO-vs2thDLmUAqOoJRVKaIBK9CgVSCoq2XzCKaBimTVNhVWKCvV1ogSLZpadgoUIJ6zr8fc2U9PC4WoBxcs9b0ZaVqCTgWAvIESEopH1PopBE-dnr0bjN9rwfXBsd7pv471wbHmUifH6eryrWB5HKh9v_knNQHfjgClN58deR2sozH94zzZqNvJ_bfgD_VrkQk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2512309252</pqid></control><display><type>article</type><title>Cardiac afferent signaling partially underlies premature ventricular contraction–induced cardiomyopathy</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Hori, Yuichi ; Temma, Taro ; Wooten, Christian ; Sobowale, Christopher ; Chan, Christopher ; Swid, Mohammed ; Ajijola, Olujimi A.</creator><creatorcontrib>Hori, Yuichi ; Temma, Taro ; Wooten, Christian ; Sobowale, Christopher ; Chan, Christopher ; Swid, Mohammed ; Ajijola, Olujimi A.</creatorcontrib><description>The mechanisms underlying premature ventricular contraction (PVC)–induced cardiomyopathy (PIC) remain unknown. Transient receptor potential vanilloid-1 (TRPV1) afferent fibers are implicated in the reflex processing of cardiac stress.
The purpose of this study was to determine whether cardiac TRPV1 afferent signaling promote PIC.
A PIC swine model (50% PVC burden) was created via an implanted pacemaker. We selectively depleted cardiac TRPV1 afferent fibers using percutaneous epicardial application of resiniferatoxin (RTX). Animals were randomized to PVC only (n = 11), PVC+RTX (n = 11), or control (n = 6). We examined early-stage (4 weeks after implantation; n = 5) and late-stage PIC (8 weeks after implantation; n = 6). At terminal experimentation, animals underwent echocardiography, serum sampling, and physiological and autonomic reflex testing.
Depletion of cardiac TRPV1 afferents by RTX treatment was confirmed by absent sensory fibers and absent functional responses to TRPV1 activators. Left ventricular ejection fraction was worse in late-stage than early-stage PIC (P <.01). At 4 weeks (early stage), left ventricular ejection fraction was higher in PVC+RTX vs PVC animals (51.7% ± 1.6% vs 45.0% ± 2.1%; P = .030), whereas no significant difference between PVC and PVC+RTX was observed at 8 weeks (late stage). Histologic studies demonstrated reduced fibrosis in PVC+RTX vs PVC alone at 4 weeks (2.27% ± 0.14% vs 3.01% ± 0.21%; P = .020), suggesting that RTX mitigated profibrotic pathways induced by persistent PVCs.
TRPV1 afferent depletion alleviates left ventricular dysfunction in early- but not late-stage PIC. This temporal effect suggests that multiple pathways promote PIC, of which TRPV1 afferents are a part.</description><identifier>ISSN: 1547-5271</identifier><identifier>EISSN: 1556-3871</identifier><identifier>DOI: 10.1016/j.hrthm.2021.04.004</identifier><identifier>PMID: 33845214</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Afferent Pathways - physiopathology ; Animal model ; Animals ; Cardiac afferent ; Cardiomyopathies - etiology ; Cardiomyopathies - pathology ; Cardiomyopathies - physiopathology ; Diterpenes - pharmacology ; Echocardiography - methods ; Fibrosis ; Heart - innervation ; Models, Animal ; Neurotoxins - pharmacology ; Premature ventricular contraction ; Premature ventricular contraction cardiomyopathy ; Signal Transduction ; Stroke Volume ; Swine ; Transient receptor potential vanilloid-1 afferents ; TRPV Cation Channels - agonists ; Ventricular Function, Left ; Ventricular Premature Complexes - complications ; Ventricular Premature Complexes - physiopathology</subject><ispartof>Heart rhythm, 2021-09, Vol.18 (9), p.1586-1595</ispartof><rights>2021</rights><rights>Copyright © 2021. Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-25103288c8ced92c13a3c821ef749b2a926e46d96363468d73343c3a74f828233</citedby><cites>FETCH-LOGICAL-c425t-25103288c8ced92c13a3c821ef749b2a926e46d96363468d73343c3a74f828233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.hrthm.2021.04.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33845214$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hori, Yuichi</creatorcontrib><creatorcontrib>Temma, Taro</creatorcontrib><creatorcontrib>Wooten, Christian</creatorcontrib><creatorcontrib>Sobowale, Christopher</creatorcontrib><creatorcontrib>Chan, Christopher</creatorcontrib><creatorcontrib>Swid, Mohammed</creatorcontrib><creatorcontrib>Ajijola, Olujimi A.</creatorcontrib><title>Cardiac afferent signaling partially underlies premature ventricular contraction–induced cardiomyopathy</title><title>Heart rhythm</title><addtitle>Heart Rhythm</addtitle><description>The mechanisms underlying premature ventricular contraction (PVC)–induced cardiomyopathy (PIC) remain unknown. Transient receptor potential vanilloid-1 (TRPV1) afferent fibers are implicated in the reflex processing of cardiac stress.
The purpose of this study was to determine whether cardiac TRPV1 afferent signaling promote PIC.
A PIC swine model (50% PVC burden) was created via an implanted pacemaker. We selectively depleted cardiac TRPV1 afferent fibers using percutaneous epicardial application of resiniferatoxin (RTX). Animals were randomized to PVC only (n = 11), PVC+RTX (n = 11), or control (n = 6). We examined early-stage (4 weeks after implantation; n = 5) and late-stage PIC (8 weeks after implantation; n = 6). At terminal experimentation, animals underwent echocardiography, serum sampling, and physiological and autonomic reflex testing.
Depletion of cardiac TRPV1 afferents by RTX treatment was confirmed by absent sensory fibers and absent functional responses to TRPV1 activators. Left ventricular ejection fraction was worse in late-stage than early-stage PIC (P <.01). At 4 weeks (early stage), left ventricular ejection fraction was higher in PVC+RTX vs PVC animals (51.7% ± 1.6% vs 45.0% ± 2.1%; P = .030), whereas no significant difference between PVC and PVC+RTX was observed at 8 weeks (late stage). Histologic studies demonstrated reduced fibrosis in PVC+RTX vs PVC alone at 4 weeks (2.27% ± 0.14% vs 3.01% ± 0.21%; P = .020), suggesting that RTX mitigated profibrotic pathways induced by persistent PVCs.
TRPV1 afferent depletion alleviates left ventricular dysfunction in early- but not late-stage PIC. This temporal effect suggests that multiple pathways promote PIC, of which TRPV1 afferents are a part.</description><subject>Afferent Pathways - physiopathology</subject><subject>Animal model</subject><subject>Animals</subject><subject>Cardiac afferent</subject><subject>Cardiomyopathies - etiology</subject><subject>Cardiomyopathies - pathology</subject><subject>Cardiomyopathies - physiopathology</subject><subject>Diterpenes - pharmacology</subject><subject>Echocardiography - methods</subject><subject>Fibrosis</subject><subject>Heart - innervation</subject><subject>Models, Animal</subject><subject>Neurotoxins - pharmacology</subject><subject>Premature ventricular contraction</subject><subject>Premature ventricular contraction cardiomyopathy</subject><subject>Signal Transduction</subject><subject>Stroke Volume</subject><subject>Swine</subject><subject>Transient receptor potential vanilloid-1 afferents</subject><subject>TRPV Cation Channels - agonists</subject><subject>Ventricular Function, Left</subject><subject>Ventricular Premature Complexes - complications</subject><subject>Ventricular Premature Complexes - physiopathology</subject><issn>1547-5271</issn><issn>1556-3871</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kLtu3DAQRYkgRtaPfEEAQ2UayeQMJVFFCmORhwEDbuyaoKnRLhd6maQMbOd_8B_mS8LNOi5TzRRn7sUcxr4IXgguqqtdsfVxOxTAQRRcFpzLD-xUlGWVo6rFx8Mu67yEWqzYWQg7zqGpOH5iK0QlSxDylLm18a0zNjNdR57GmAW3GU3vxk02Gx-d6ft9towt-d5RyGZPg4mLp-w5wd7ZpTc-s1PajY1uGn-_vLqxXSy1mT1ET8N-mk3c7i_YSWf6QJ_f5jl7-PH9fv0rv737ebO-vs2thDLmUAqOoJRVKaIBK9CgVSCoq2XzCKaBimTVNhVWKCvV1ogSLZpadgoUIJ6zr8fc2U9PC4WoBxcs9b0ZaVqCTgWAvIESEopH1PopBE-dnr0bjN9rwfXBsd7pv471wbHmUifH6eryrWB5HKh9v_knNQHfjgClN58deR2sozH94zzZqNvJ_bfgD_VrkQk</recordid><startdate>202109</startdate><enddate>202109</enddate><creator>Hori, Yuichi</creator><creator>Temma, Taro</creator><creator>Wooten, Christian</creator><creator>Sobowale, Christopher</creator><creator>Chan, Christopher</creator><creator>Swid, Mohammed</creator><creator>Ajijola, Olujimi A.</creator><general>Elsevier Inc</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></search><sort><creationdate>202109</creationdate><title>Cardiac afferent signaling partially underlies premature ventricular contraction–induced cardiomyopathy</title><author>Hori, Yuichi ; Temma, Taro ; Wooten, Christian ; Sobowale, Christopher ; Chan, Christopher ; Swid, Mohammed ; Ajijola, Olujimi A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c425t-25103288c8ced92c13a3c821ef749b2a926e46d96363468d73343c3a74f828233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Afferent Pathways - physiopathology</topic><topic>Animal model</topic><topic>Animals</topic><topic>Cardiac afferent</topic><topic>Cardiomyopathies - etiology</topic><topic>Cardiomyopathies - pathology</topic><topic>Cardiomyopathies - physiopathology</topic><topic>Diterpenes - pharmacology</topic><topic>Echocardiography - methods</topic><topic>Fibrosis</topic><topic>Heart - innervation</topic><topic>Models, Animal</topic><topic>Neurotoxins - pharmacology</topic><topic>Premature ventricular contraction</topic><topic>Premature ventricular contraction cardiomyopathy</topic><topic>Signal Transduction</topic><topic>Stroke Volume</topic><topic>Swine</topic><topic>Transient receptor potential vanilloid-1 afferents</topic><topic>TRPV Cation Channels - agonists</topic><topic>Ventricular Function, Left</topic><topic>Ventricular Premature Complexes - complications</topic><topic>Ventricular Premature Complexes - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hori, Yuichi</creatorcontrib><creatorcontrib>Temma, Taro</creatorcontrib><creatorcontrib>Wooten, Christian</creatorcontrib><creatorcontrib>Sobowale, Christopher</creatorcontrib><creatorcontrib>Chan, Christopher</creatorcontrib><creatorcontrib>Swid, Mohammed</creatorcontrib><creatorcontrib>Ajijola, Olujimi A.</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><jtitle>Heart rhythm</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hori, Yuichi</au><au>Temma, Taro</au><au>Wooten, Christian</au><au>Sobowale, Christopher</au><au>Chan, Christopher</au><au>Swid, Mohammed</au><au>Ajijola, Olujimi A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiac afferent signaling partially underlies premature ventricular contraction–induced cardiomyopathy</atitle><jtitle>Heart rhythm</jtitle><addtitle>Heart Rhythm</addtitle><date>2021-09</date><risdate>2021</risdate><volume>18</volume><issue>9</issue><spage>1586</spage><epage>1595</epage><pages>1586-1595</pages><issn>1547-5271</issn><eissn>1556-3871</eissn><abstract>The mechanisms underlying premature ventricular contraction (PVC)–induced cardiomyopathy (PIC) remain unknown. Transient receptor potential vanilloid-1 (TRPV1) afferent fibers are implicated in the reflex processing of cardiac stress.
The purpose of this study was to determine whether cardiac TRPV1 afferent signaling promote PIC.
A PIC swine model (50% PVC burden) was created via an implanted pacemaker. We selectively depleted cardiac TRPV1 afferent fibers using percutaneous epicardial application of resiniferatoxin (RTX). Animals were randomized to PVC only (n = 11), PVC+RTX (n = 11), or control (n = 6). We examined early-stage (4 weeks after implantation; n = 5) and late-stage PIC (8 weeks after implantation; n = 6). At terminal experimentation, animals underwent echocardiography, serum sampling, and physiological and autonomic reflex testing.
Depletion of cardiac TRPV1 afferents by RTX treatment was confirmed by absent sensory fibers and absent functional responses to TRPV1 activators. Left ventricular ejection fraction was worse in late-stage than early-stage PIC (P <.01). At 4 weeks (early stage), left ventricular ejection fraction was higher in PVC+RTX vs PVC animals (51.7% ± 1.6% vs 45.0% ± 2.1%; P = .030), whereas no significant difference between PVC and PVC+RTX was observed at 8 weeks (late stage). Histologic studies demonstrated reduced fibrosis in PVC+RTX vs PVC alone at 4 weeks (2.27% ± 0.14% vs 3.01% ± 0.21%; P = .020), suggesting that RTX mitigated profibrotic pathways induced by persistent PVCs.
TRPV1 afferent depletion alleviates left ventricular dysfunction in early- but not late-stage PIC. This temporal effect suggests that multiple pathways promote PIC, of which TRPV1 afferents are a part.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>33845214</pmid><doi>10.1016/j.hrthm.2021.04.004</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1547-5271 |
| ispartof | Heart rhythm, 2021-09, Vol.18 (9), p.1586-1595 |
| issn | 1547-5271 1556-3871 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2512309252 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Afferent Pathways - physiopathology Animal model Animals Cardiac afferent Cardiomyopathies - etiology Cardiomyopathies - pathology Cardiomyopathies - physiopathology Diterpenes - pharmacology Echocardiography - methods Fibrosis Heart - innervation Models, Animal Neurotoxins - pharmacology Premature ventricular contraction Premature ventricular contraction cardiomyopathy Signal Transduction Stroke Volume Swine Transient receptor potential vanilloid-1 afferents TRPV Cation Channels - agonists Ventricular Function, Left Ventricular Premature Complexes - complications Ventricular Premature Complexes - physiopathology |
| title | Cardiac afferent signaling partially underlies premature ventricular contraction–induced cardiomyopathy |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T12%3A11%3A33IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cardiac%20afferent%20signaling%20partially%20underlies%20premature%20ventricular%20contraction%E2%80%93induced%20cardiomyopathy&rft.jtitle=Heart%20rhythm&rft.au=Hori,%20Yuichi&rft.date=2021-09&rft.volume=18&rft.issue=9&rft.spage=1586&rft.epage=1595&rft.pages=1586-1595&rft.issn=1547-5271&rft.eissn=1556-3871&rft_id=info:doi/10.1016/j.hrthm.2021.04.004&rft_dat=%3Cproquest_cross%3E2512309252%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2512309252&rft_id=info:pmid/33845214&rft_els_id=S1547527121003271&rfr_iscdi=true |