Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control: Insights From Simultaneous Cardioneural Mapping

BACKGROUND—Variability in premature ventricular contraction (PVC) coupling interval (CI) increases the risk of cardiomyopathy and sudden death. The autonomic nervous system regulates cardiac electrical and mechanical indices, and its dysregulation plays an important role in cardiac disease pathogene...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Circulation. Arrhythmia and electrophysiology 2017-04, Vol.10 (4), p.e004937-e004937
Hauptverfasser: Hamon, David, Rajendran, Pradeep S, Chui, Ray W, Ajijola, Olujimi A, Irie, Tadanobu, Talebi, Ramin, Salavatian, Siamak, Vaseghi, Marmar, Bradfield, Jason S, Armour, J Andrew, Ardell, Jeffrey L, Shivkumar, Kalyanam
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page e004937
container_issue 4
container_start_page e004937
container_title Circulation. Arrhythmia and electrophysiology
container_volume 10
creator Hamon, David
Rajendran, Pradeep S
Chui, Ray W
Ajijola, Olujimi A
Irie, Tadanobu
Talebi, Ramin
Salavatian, Siamak
Vaseghi, Marmar
Bradfield, Jason S
Armour, J Andrew
Ardell, Jeffrey L
Shivkumar, Kalyanam
description BACKGROUND—Variability in premature ventricular contraction (PVC) coupling interval (CI) increases the risk of cardiomyopathy and sudden death. The autonomic nervous system regulates cardiac electrical and mechanical indices, and its dysregulation plays an important role in cardiac disease pathogenesis. The impact of PVCs on the intrinsic cardiac nervous system, a neural network on the heart, remains unknown. The objective was to determine the effect of PVCs and CI on intrinsic cardiac nervous system function in generating cardiac neuronal and electric instability using a novel cardioneural mapping approach. METHODS AND RESULTS—In a porcine model (n=8), neuronal activity was recorded from a ventricular ganglion using a microelectrode array, and cardiac electrophysiological mapping was performed. Neurons were functionally classified based on their response to afferent and efferent cardiovascular stimuli, with neurons that responded to both defined as convergent (local reflex processors). Dynamic changes in neuronal activity were then evaluated in response to right ventricular outflow tract PVCs with fixed short, fixed long, and variable CI. PVC delivery elicited a greater neuronal response than all other stimuli (P
doi_str_mv 10.1161/CIRCEP.116.004937
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1888682264</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1888682264</sourcerecordid><originalsourceid>FETCH-LOGICAL-c2286-77a8ac57fa38c92ceda617b6e50c776c107a149b235a8b23939e3fb36c8690fa3</originalsourceid><addsrcrecordid>eNo9UctuFDEQHCEQCYEP4IJ85DLBj1nbww0NG7JSgIhHrlaP17tr8IwnfhAtP8UvxpvZcHC7pK4qt7uq6jXB54Rw8q5bfeuW1wd8jnHTMvGkOiVtQ2qGZfP0EZOmPalexPgLY04k4c-rEyobLPmCnlb_roMZIOVg0I0ZU7A6Owio8wWDTtaPBefJ2XGLVmMy4Q84dAPBQm-dTXv00cT0gP-aiDoIawsafTE5-LEwYVyjpTM6BT_t9tF657dWl8bDA969L6bRbncpoovgB_TdDtklGI3PRzc_Fq8i-AzTVIZ4WT3bgIvm1fE-q35eLH90l_XV10-r7sNVrSmVvBYCJOiF2ACTuqXarIET0XOzwFoIrgkWUPbSU7YAWWrLWsM2PeNa8hYX1Vn1dvadgr_N5Y9qsFEb5-bZFJFSckkpbwqVzFQdfIzBbNQU7ABhrwhWh5zUnNMBqzmnonlztM_9YNb_FY_BFEIzE-68K1uPv12-M0HtDLi0U5gwJopRTTERuMEY1-Vgzu4BfQ2jJA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1888682264</pqid></control><display><type>article</type><title>Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control: Insights From Simultaneous Cardioneural Mapping</title><source>MEDLINE</source><source>American Heart Association Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Hamon, David ; Rajendran, Pradeep S ; Chui, Ray W ; Ajijola, Olujimi A ; Irie, Tadanobu ; Talebi, Ramin ; Salavatian, Siamak ; Vaseghi, Marmar ; Bradfield, Jason S ; Armour, J Andrew ; Ardell, Jeffrey L ; Shivkumar, Kalyanam</creator><creatorcontrib>Hamon, David ; Rajendran, Pradeep S ; Chui, Ray W ; Ajijola, Olujimi A ; Irie, Tadanobu ; Talebi, Ramin ; Salavatian, Siamak ; Vaseghi, Marmar ; Bradfield, Jason S ; Armour, J Andrew ; Ardell, Jeffrey L ; Shivkumar, Kalyanam</creatorcontrib><description>BACKGROUND—Variability in premature ventricular contraction (PVC) coupling interval (CI) increases the risk of cardiomyopathy and sudden death. The autonomic nervous system regulates cardiac electrical and mechanical indices, and its dysregulation plays an important role in cardiac disease pathogenesis. The impact of PVCs on the intrinsic cardiac nervous system, a neural network on the heart, remains unknown. The objective was to determine the effect of PVCs and CI on intrinsic cardiac nervous system function in generating cardiac neuronal and electric instability using a novel cardioneural mapping approach. METHODS AND RESULTS—In a porcine model (n=8), neuronal activity was recorded from a ventricular ganglion using a microelectrode array, and cardiac electrophysiological mapping was performed. Neurons were functionally classified based on their response to afferent and efferent cardiovascular stimuli, with neurons that responded to both defined as convergent (local reflex processors). Dynamic changes in neuronal activity were then evaluated in response to right ventricular outflow tract PVCs with fixed short, fixed long, and variable CI. PVC delivery elicited a greater neuronal response than all other stimuli (P&lt;0.001). Compared with fixed short and long CI, PVCs with variable CI had a greater impact on neuronal response (P&lt;0.05 versus short CI), particularly on convergent neurons (P&lt;0.05), as well as neurons receiving sympathetic (P&lt;0.05) and parasympathetic input (P&lt;0.05). The greatest cardiac electric instability was also observed after variable (short) CI PVCs. CONCLUSIONS—Variable CI PVCs affect critical populations of intrinsic cardiac nervous system neurons and alter cardiac repolarization. These changes may be critical for arrhythmogenesis and remodeling, leading to cardiomyopathy.</description><identifier>ISSN: 1941-3149</identifier><identifier>EISSN: 1941-3084</identifier><identifier>DOI: 10.1161/CIRCEP.116.004937</identifier><identifier>PMID: 28408652</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Action Potentials ; Animals ; Autonomic Nervous System - physiopathology ; Cardiac Pacing, Artificial ; Cardiomyopathies - etiology ; Cardiomyopathies - physiopathology ; Disease Models, Animal ; Electrophysiologic Techniques, Cardiac ; Female ; Heart - innervation ; Heart Rate ; Male ; Myocardial Contraction ; Sus scrofa ; Time Factors ; Ventricular Function ; Ventricular Premature Complexes - complications ; Ventricular Premature Complexes - diagnosis ; Ventricular Premature Complexes - physiopathology</subject><ispartof>Circulation. Arrhythmia and electrophysiology, 2017-04, Vol.10 (4), p.e004937-e004937</ispartof><rights>2017 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2286-77a8ac57fa38c92ceda617b6e50c776c107a149b235a8b23939e3fb36c8690fa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28408652$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hamon, David</creatorcontrib><creatorcontrib>Rajendran, Pradeep S</creatorcontrib><creatorcontrib>Chui, Ray W</creatorcontrib><creatorcontrib>Ajijola, Olujimi A</creatorcontrib><creatorcontrib>Irie, Tadanobu</creatorcontrib><creatorcontrib>Talebi, Ramin</creatorcontrib><creatorcontrib>Salavatian, Siamak</creatorcontrib><creatorcontrib>Vaseghi, Marmar</creatorcontrib><creatorcontrib>Bradfield, Jason S</creatorcontrib><creatorcontrib>Armour, J Andrew</creatorcontrib><creatorcontrib>Ardell, Jeffrey L</creatorcontrib><creatorcontrib>Shivkumar, Kalyanam</creatorcontrib><title>Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control: Insights From Simultaneous Cardioneural Mapping</title><title>Circulation. Arrhythmia and electrophysiology</title><addtitle>Circ Arrhythm Electrophysiol</addtitle><description>BACKGROUND—Variability in premature ventricular contraction (PVC) coupling interval (CI) increases the risk of cardiomyopathy and sudden death. The autonomic nervous system regulates cardiac electrical and mechanical indices, and its dysregulation plays an important role in cardiac disease pathogenesis. The impact of PVCs on the intrinsic cardiac nervous system, a neural network on the heart, remains unknown. The objective was to determine the effect of PVCs and CI on intrinsic cardiac nervous system function in generating cardiac neuronal and electric instability using a novel cardioneural mapping approach. METHODS AND RESULTS—In a porcine model (n=8), neuronal activity was recorded from a ventricular ganglion using a microelectrode array, and cardiac electrophysiological mapping was performed. Neurons were functionally classified based on their response to afferent and efferent cardiovascular stimuli, with neurons that responded to both defined as convergent (local reflex processors). Dynamic changes in neuronal activity were then evaluated in response to right ventricular outflow tract PVCs with fixed short, fixed long, and variable CI. PVC delivery elicited a greater neuronal response than all other stimuli (P&lt;0.001). Compared with fixed short and long CI, PVCs with variable CI had a greater impact on neuronal response (P&lt;0.05 versus short CI), particularly on convergent neurons (P&lt;0.05), as well as neurons receiving sympathetic (P&lt;0.05) and parasympathetic input (P&lt;0.05). The greatest cardiac electric instability was also observed after variable (short) CI PVCs. CONCLUSIONS—Variable CI PVCs affect critical populations of intrinsic cardiac nervous system neurons and alter cardiac repolarization. These changes may be critical for arrhythmogenesis and remodeling, leading to cardiomyopathy.</description><subject>Action Potentials</subject><subject>Animals</subject><subject>Autonomic Nervous System - physiopathology</subject><subject>Cardiac Pacing, Artificial</subject><subject>Cardiomyopathies - etiology</subject><subject>Cardiomyopathies - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Electrophysiologic Techniques, Cardiac</subject><subject>Female</subject><subject>Heart - innervation</subject><subject>Heart Rate</subject><subject>Male</subject><subject>Myocardial Contraction</subject><subject>Sus scrofa</subject><subject>Time Factors</subject><subject>Ventricular Function</subject><subject>Ventricular Premature Complexes - complications</subject><subject>Ventricular Premature Complexes - diagnosis</subject><subject>Ventricular Premature Complexes - physiopathology</subject><issn>1941-3149</issn><issn>1941-3084</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9UctuFDEQHCEQCYEP4IJ85DLBj1nbww0NG7JSgIhHrlaP17tr8IwnfhAtP8UvxpvZcHC7pK4qt7uq6jXB54Rw8q5bfeuW1wd8jnHTMvGkOiVtQ2qGZfP0EZOmPalexPgLY04k4c-rEyobLPmCnlb_roMZIOVg0I0ZU7A6Owio8wWDTtaPBefJ2XGLVmMy4Q84dAPBQm-dTXv00cT0gP-aiDoIawsafTE5-LEwYVyjpTM6BT_t9tF657dWl8bDA969L6bRbncpoovgB_TdDtklGI3PRzc_Fq8i-AzTVIZ4WT3bgIvm1fE-q35eLH90l_XV10-r7sNVrSmVvBYCJOiF2ACTuqXarIET0XOzwFoIrgkWUPbSU7YAWWrLWsM2PeNa8hYX1Vn1dvadgr_N5Y9qsFEb5-bZFJFSckkpbwqVzFQdfIzBbNQU7ABhrwhWh5zUnNMBqzmnonlztM_9YNb_FY_BFEIzE-68K1uPv12-M0HtDLi0U5gwJopRTTERuMEY1-Vgzu4BfQ2jJA</recordid><startdate>201704</startdate><enddate>201704</enddate><creator>Hamon, David</creator><creator>Rajendran, Pradeep S</creator><creator>Chui, Ray W</creator><creator>Ajijola, Olujimi A</creator><creator>Irie, Tadanobu</creator><creator>Talebi, Ramin</creator><creator>Salavatian, Siamak</creator><creator>Vaseghi, Marmar</creator><creator>Bradfield, Jason S</creator><creator>Armour, J Andrew</creator><creator>Ardell, Jeffrey L</creator><creator>Shivkumar, Kalyanam</creator><general>American Heart Association, 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>201704</creationdate><title>Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control: Insights From Simultaneous Cardioneural Mapping</title><author>Hamon, David ; Rajendran, Pradeep S ; Chui, Ray W ; Ajijola, Olujimi A ; Irie, Tadanobu ; Talebi, Ramin ; Salavatian, Siamak ; Vaseghi, Marmar ; Bradfield, Jason S ; Armour, J Andrew ; Ardell, Jeffrey L ; Shivkumar, Kalyanam</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2286-77a8ac57fa38c92ceda617b6e50c776c107a149b235a8b23939e3fb36c8690fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Action Potentials</topic><topic>Animals</topic><topic>Autonomic Nervous System - physiopathology</topic><topic>Cardiac Pacing, Artificial</topic><topic>Cardiomyopathies - etiology</topic><topic>Cardiomyopathies - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Electrophysiologic Techniques, Cardiac</topic><topic>Female</topic><topic>Heart - innervation</topic><topic>Heart Rate</topic><topic>Male</topic><topic>Myocardial Contraction</topic><topic>Sus scrofa</topic><topic>Time Factors</topic><topic>Ventricular Function</topic><topic>Ventricular Premature Complexes - complications</topic><topic>Ventricular Premature Complexes - diagnosis</topic><topic>Ventricular Premature Complexes - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hamon, David</creatorcontrib><creatorcontrib>Rajendran, Pradeep S</creatorcontrib><creatorcontrib>Chui, Ray W</creatorcontrib><creatorcontrib>Ajijola, Olujimi A</creatorcontrib><creatorcontrib>Irie, Tadanobu</creatorcontrib><creatorcontrib>Talebi, Ramin</creatorcontrib><creatorcontrib>Salavatian, Siamak</creatorcontrib><creatorcontrib>Vaseghi, Marmar</creatorcontrib><creatorcontrib>Bradfield, Jason S</creatorcontrib><creatorcontrib>Armour, J Andrew</creatorcontrib><creatorcontrib>Ardell, Jeffrey L</creatorcontrib><creatorcontrib>Shivkumar, Kalyanam</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>Circulation. Arrhythmia and electrophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hamon, David</au><au>Rajendran, Pradeep S</au><au>Chui, Ray W</au><au>Ajijola, Olujimi A</au><au>Irie, Tadanobu</au><au>Talebi, Ramin</au><au>Salavatian, Siamak</au><au>Vaseghi, Marmar</au><au>Bradfield, Jason S</au><au>Armour, J Andrew</au><au>Ardell, Jeffrey L</au><au>Shivkumar, Kalyanam</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control: Insights From Simultaneous Cardioneural Mapping</atitle><jtitle>Circulation. Arrhythmia and electrophysiology</jtitle><addtitle>Circ Arrhythm Electrophysiol</addtitle><date>2017-04</date><risdate>2017</risdate><volume>10</volume><issue>4</issue><spage>e004937</spage><epage>e004937</epage><pages>e004937-e004937</pages><issn>1941-3149</issn><eissn>1941-3084</eissn><abstract>BACKGROUND—Variability in premature ventricular contraction (PVC) coupling interval (CI) increases the risk of cardiomyopathy and sudden death. The autonomic nervous system regulates cardiac electrical and mechanical indices, and its dysregulation plays an important role in cardiac disease pathogenesis. The impact of PVCs on the intrinsic cardiac nervous system, a neural network on the heart, remains unknown. The objective was to determine the effect of PVCs and CI on intrinsic cardiac nervous system function in generating cardiac neuronal and electric instability using a novel cardioneural mapping approach. METHODS AND RESULTS—In a porcine model (n=8), neuronal activity was recorded from a ventricular ganglion using a microelectrode array, and cardiac electrophysiological mapping was performed. Neurons were functionally classified based on their response to afferent and efferent cardiovascular stimuli, with neurons that responded to both defined as convergent (local reflex processors). Dynamic changes in neuronal activity were then evaluated in response to right ventricular outflow tract PVCs with fixed short, fixed long, and variable CI. PVC delivery elicited a greater neuronal response than all other stimuli (P&lt;0.001). Compared with fixed short and long CI, PVCs with variable CI had a greater impact on neuronal response (P&lt;0.05 versus short CI), particularly on convergent neurons (P&lt;0.05), as well as neurons receiving sympathetic (P&lt;0.05) and parasympathetic input (P&lt;0.05). The greatest cardiac electric instability was also observed after variable (short) CI PVCs. CONCLUSIONS—Variable CI PVCs affect critical populations of intrinsic cardiac nervous system neurons and alter cardiac repolarization. These changes may be critical for arrhythmogenesis and remodeling, leading to cardiomyopathy.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>28408652</pmid><doi>10.1161/CIRCEP.116.004937</doi></addata></record>
fulltext fulltext
identifier ISSN: 1941-3149
ispartof Circulation. Arrhythmia and electrophysiology, 2017-04, Vol.10 (4), p.e004937-e004937
issn 1941-3149
1941-3084
language eng
recordid cdi_proquest_miscellaneous_1888682264
source MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects Action Potentials
Animals
Autonomic Nervous System - physiopathology
Cardiac Pacing, Artificial
Cardiomyopathies - etiology
Cardiomyopathies - physiopathology
Disease Models, Animal
Electrophysiologic Techniques, Cardiac
Female
Heart - innervation
Heart Rate
Male
Myocardial Contraction
Sus scrofa
Time Factors
Ventricular Function
Ventricular Premature Complexes - complications
Ventricular Premature Complexes - diagnosis
Ventricular Premature Complexes - physiopathology
title Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control: Insights From Simultaneous Cardioneural Mapping
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T09%3A14%3A05IST&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=Premature%20Ventricular%20Contraction%20Coupling%20Interval%20Variability%20Destabilizes%20Cardiac%20Neuronal%20and%20Electrophysiological%20Control:%20Insights%20From%20Simultaneous%20Cardioneural%20Mapping&rft.jtitle=Circulation.%20Arrhythmia%20and%20electrophysiology&rft.au=Hamon,%20David&rft.date=2017-04&rft.volume=10&rft.issue=4&rft.spage=e004937&rft.epage=e004937&rft.pages=e004937-e004937&rft.issn=1941-3149&rft.eissn=1941-3084&rft_id=info:doi/10.1161/CIRCEP.116.004937&rft_dat=%3Cproquest_cross%3E1888682264%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=1888682264&rft_id=info:pmid/28408652&rfr_iscdi=true