Effects of Angiotensin Receptor-Neprilysin Inhibitor in Arrhythmogenicity Following Left Atrial Appendage Closure in an Animal Model
Purpose Left atrial appendage (LAA) closure decreases atrial natriuretic peptide (ANP) levels, which indirectly increases the risk of arrhythmogenicity. We aimed to determine the effect of a combined angiotensin receptor-neprilysin inhibitor (ARNi) on arrhythmogenicity following LAA closure in an an...
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| Veröffentlicht in: | Cardiovascular drugs and therapy 2021-08, Vol.35 (4), p.759-768 |
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| creator | Cheng, Wen-Han Lugtu, Isaiah C. Chang, Shih-Lin Liu, Shin-Huei Chen, Shih-Ann Lo, Li-Wei |
| description | Purpose
Left atrial appendage (LAA) closure decreases atrial natriuretic peptide (ANP) levels, which indirectly increases the risk of arrhythmogenicity. We aimed to determine the effect of a combined angiotensin receptor-neprilysin inhibitor (ARNi) on arrhythmogenicity following LAA closure in an animal model.
Methods
Twenty-four rabbits were randomized into four groups: (1) control, (2) LAA closure (LAAC), (3) heart failure (HF)-LAAC, and (4) HF-LAAC with sacubitril/valsartan (+ARNi). HF models were developed in the HF-LAAC and HF-LAAC+ARNi groups. Epicardial LAA exclusion was performed in the LAAC, HF-LAAC, and HF-LAAC+ARNi groups. ANP levels were measured. An electrophysiological study was performed. The myocardium was harvested for histopathological analysis.
Results
The ANP level decreased in the LAAC group (785 ± 103 pg/mL,
p
= 0.03), failed to increase in the HF-LAAC group (917 ± 172 pg/mL,
p
= 0.3), and increased in the HF-LAAC+ARNi group (1524 ± 126 pg/mL,
p
|
| doi_str_mv | 10.1007/s10557-021-07174-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2508890782</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2508890782</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-25ab014d1e2540655a24eb534efd0ae70713f2afd386974086b97beb62372dae3</originalsourceid><addsrcrecordid>eNp9kU1v1DAQhi1ERbeFP8ABReLCxdSfsXOMVv2SFpAQnC0nmWRdJXawE1V754fj7RaQOHAazczzvrbmRegtJR8pIeoqUSKlwoRRTBRVArMXaEOl4lgxQV-iDakYwZyR8hxdpPRAsqiq9Ct0zrmmutTVBv287ntol1SEvqj94MICPjlffIUW5iVE_Bnm6MbDcXbv965xeVjkpo5xf1j2UxjAu9Yth-ImjGN4dH4odtAvRb1EZ8einmfwnR2g2I4hrRGOYpv13k15_Sl0ML5GZ70dE7x5rpfo-831t-0d3n25vd_WO9xyJRfMpG0IFR0FJgUppbRMQCO5gL4jFlQ-Au-Z7Tuuy0oJosumUg00JeOKdRb4Jfpw8p1j-LFCWszkUgvjaD2ENRkmidYVUZpl9P0_6ENYo8-_y5SohKaEq0yxE9XGkFKE3uRjTTYeDCXmmJE5ZWRyRuYpI3O0fvdsvTYTdH8kv0PJAD8BKa_8APHv2_-x_QVoA51O</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2549481037</pqid></control><display><type>article</type><title>Effects of Angiotensin Receptor-Neprilysin Inhibitor in Arrhythmogenicity Following Left Atrial Appendage Closure in an Animal Model</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Cheng, Wen-Han ; Lugtu, Isaiah C. ; Chang, Shih-Lin ; Liu, Shin-Huei ; Chen, Shih-Ann ; Lo, Li-Wei</creator><creatorcontrib>Cheng, Wen-Han ; Lugtu, Isaiah C. ; Chang, Shih-Lin ; Liu, Shin-Huei ; Chen, Shih-Ann ; Lo, Li-Wei</creatorcontrib><description>Purpose
Left atrial appendage (LAA) closure decreases atrial natriuretic peptide (ANP) levels, which indirectly increases the risk of arrhythmogenicity. We aimed to determine the effect of a combined angiotensin receptor-neprilysin inhibitor (ARNi) on arrhythmogenicity following LAA closure in an animal model.
Methods
Twenty-four rabbits were randomized into four groups: (1) control, (2) LAA closure (LAAC), (3) heart failure (HF)-LAAC, and (4) HF-LAAC with sacubitril/valsartan (+ARNi). HF models were developed in the HF-LAAC and HF-LAAC+ARNi groups. Epicardial LAA exclusion was performed in the LAAC, HF-LAAC, and HF-LAAC+ARNi groups. ANP levels were measured. An electrophysiological study was performed. The myocardium was harvested for histopathological analysis.
Results
The ANP level decreased in the LAAC group (785 ± 103 pg/mL,
p
= 0.03), failed to increase in the HF-LAAC group (917 ± 172 pg/mL,
p
= 0.3), and increased in the HF-LAAC+ARNi group (1524 ± 126 pg/mL,
p
< 0.01) compared to that in the control group (1014 ± 56 pg/mL). The atrial effective refractory period (ERP) was prolonged in the HF-LAAC group and restored to baseline in the HF-LAAC+ARNi group. Ventricular ERP was the longest in the HF-LAAC group. The atrial fibrillation window of vulnerability (AF WOV) was elevated in the LAAC, HF-LAAC, and HF-LAAC+ARNi groups, with the latter group having lower AF WOV than the two former groups. Ventricular fibrillation (VF) inducibility was the highest in the HF-LAAC group (51 ± 5%,
p
< 0.001), followed by the LAAC group (30 ± 4%,
p
= 0.006) and the HF-LAAC+ARNi group (25 ± 5%,
p
= 0.11) when compared to the control group (18 ± 4%). Atrial and ventricular fibrosis were noted in all groups except the control group.
Conclusion
LAA closure decreased ANP, which in turn increased AF and VF inducibility. Atrial and ventricular arrhythmogenicity was suppressed by ARNi.</description><identifier>ISSN: 0920-3206</identifier><identifier>EISSN: 1573-7241</identifier><identifier>DOI: 10.1007/s10557-021-07174-2</identifier><identifier>PMID: 33818689</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aminobutyrates - pharmacology ; Angiotensin ; Angiotensin Receptor Antagonists - pharmacology ; Animal models ; Animals ; Arrhythmias, Cardiac - etiology ; Arrhythmias, Cardiac - prevention & control ; Atrial Appendage - surgery ; Atrial Natriuretic Factor - metabolism ; Atrial natriuretic peptide ; Biphenyl Compounds - pharmacology ; Cardiac arrhythmia ; Cardiology ; Congestive heart failure ; Drug Combinations ; Ejection fraction ; Electrophysiological recording ; Event-related potentials ; Fibrillation ; Fibrosis ; Heart Atria - surgery ; Heart failure ; Hospitals ; Inhibitors ; Medicine ; Medicine & Public Health ; Models, Animal ; Myocardium ; Neprilysin ; Neprilysin - antagonists & inhibitors ; Original Article ; Pacemakers ; Peptides ; Rabbits ; Receptors ; Refractory period ; Septal Occluder Device ; Stroke ; Treatment Outcome ; Valsartan - pharmacology ; Ventricle ; Ventricular fibrillation</subject><ispartof>Cardiovascular drugs and therapy, 2021-08, Vol.35 (4), p.759-768</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-25ab014d1e2540655a24eb534efd0ae70713f2afd386974086b97beb62372dae3</citedby><cites>FETCH-LOGICAL-c375t-25ab014d1e2540655a24eb534efd0ae70713f2afd386974086b97beb62372dae3</cites><orcidid>0000-0001-9102-227X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10557-021-07174-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10557-021-07174-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33818689$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheng, Wen-Han</creatorcontrib><creatorcontrib>Lugtu, Isaiah C.</creatorcontrib><creatorcontrib>Chang, Shih-Lin</creatorcontrib><creatorcontrib>Liu, Shin-Huei</creatorcontrib><creatorcontrib>Chen, Shih-Ann</creatorcontrib><creatorcontrib>Lo, Li-Wei</creatorcontrib><title>Effects of Angiotensin Receptor-Neprilysin Inhibitor in Arrhythmogenicity Following Left Atrial Appendage Closure in an Animal Model</title><title>Cardiovascular drugs and therapy</title><addtitle>Cardiovasc Drugs Ther</addtitle><addtitle>Cardiovasc Drugs Ther</addtitle><description>Purpose
Left atrial appendage (LAA) closure decreases atrial natriuretic peptide (ANP) levels, which indirectly increases the risk of arrhythmogenicity. We aimed to determine the effect of a combined angiotensin receptor-neprilysin inhibitor (ARNi) on arrhythmogenicity following LAA closure in an animal model.
Methods
Twenty-four rabbits were randomized into four groups: (1) control, (2) LAA closure (LAAC), (3) heart failure (HF)-LAAC, and (4) HF-LAAC with sacubitril/valsartan (+ARNi). HF models were developed in the HF-LAAC and HF-LAAC+ARNi groups. Epicardial LAA exclusion was performed in the LAAC, HF-LAAC, and HF-LAAC+ARNi groups. ANP levels were measured. An electrophysiological study was performed. The myocardium was harvested for histopathological analysis.
Results
The ANP level decreased in the LAAC group (785 ± 103 pg/mL,
p
= 0.03), failed to increase in the HF-LAAC group (917 ± 172 pg/mL,
p
= 0.3), and increased in the HF-LAAC+ARNi group (1524 ± 126 pg/mL,
p
< 0.01) compared to that in the control group (1014 ± 56 pg/mL). The atrial effective refractory period (ERP) was prolonged in the HF-LAAC group and restored to baseline in the HF-LAAC+ARNi group. Ventricular ERP was the longest in the HF-LAAC group. The atrial fibrillation window of vulnerability (AF WOV) was elevated in the LAAC, HF-LAAC, and HF-LAAC+ARNi groups, with the latter group having lower AF WOV than the two former groups. Ventricular fibrillation (VF) inducibility was the highest in the HF-LAAC group (51 ± 5%,
p
< 0.001), followed by the LAAC group (30 ± 4%,
p
= 0.006) and the HF-LAAC+ARNi group (25 ± 5%,
p
= 0.11) when compared to the control group (18 ± 4%). Atrial and ventricular fibrosis were noted in all groups except the control group.
Conclusion
LAA closure decreased ANP, which in turn increased AF and VF inducibility. Atrial and ventricular arrhythmogenicity was suppressed by ARNi.</description><subject>Aminobutyrates - pharmacology</subject><subject>Angiotensin</subject><subject>Angiotensin Receptor Antagonists - pharmacology</subject><subject>Animal models</subject><subject>Animals</subject><subject>Arrhythmias, Cardiac - etiology</subject><subject>Arrhythmias, Cardiac - prevention & control</subject><subject>Atrial Appendage - surgery</subject><subject>Atrial Natriuretic Factor - metabolism</subject><subject>Atrial natriuretic peptide</subject><subject>Biphenyl Compounds - pharmacology</subject><subject>Cardiac arrhythmia</subject><subject>Cardiology</subject><subject>Congestive heart failure</subject><subject>Drug Combinations</subject><subject>Ejection fraction</subject><subject>Electrophysiological recording</subject><subject>Event-related potentials</subject><subject>Fibrillation</subject><subject>Fibrosis</subject><subject>Heart Atria - surgery</subject><subject>Heart failure</subject><subject>Hospitals</subject><subject>Inhibitors</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Models, Animal</subject><subject>Myocardium</subject><subject>Neprilysin</subject><subject>Neprilysin - antagonists & inhibitors</subject><subject>Original Article</subject><subject>Pacemakers</subject><subject>Peptides</subject><subject>Rabbits</subject><subject>Receptors</subject><subject>Refractory period</subject><subject>Septal Occluder Device</subject><subject>Stroke</subject><subject>Treatment Outcome</subject><subject>Valsartan - pharmacology</subject><subject>Ventricle</subject><subject>Ventricular fibrillation</subject><issn>0920-3206</issn><issn>1573-7241</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kU1v1DAQhi1ERbeFP8ABReLCxdSfsXOMVv2SFpAQnC0nmWRdJXawE1V754fj7RaQOHAazczzvrbmRegtJR8pIeoqUSKlwoRRTBRVArMXaEOl4lgxQV-iDakYwZyR8hxdpPRAsqiq9Ct0zrmmutTVBv287ntol1SEvqj94MICPjlffIUW5iVE_Bnm6MbDcXbv965xeVjkpo5xf1j2UxjAu9Yth-ImjGN4dH4odtAvRb1EZ8einmfwnR2g2I4hrRGOYpv13k15_Sl0ML5GZ70dE7x5rpfo-831t-0d3n25vd_WO9xyJRfMpG0IFR0FJgUppbRMQCO5gL4jFlQ-Au-Z7Tuuy0oJosumUg00JeOKdRb4Jfpw8p1j-LFCWszkUgvjaD2ENRkmidYVUZpl9P0_6ENYo8-_y5SohKaEq0yxE9XGkFKE3uRjTTYeDCXmmJE5ZWRyRuYpI3O0fvdsvTYTdH8kv0PJAD8BKa_8APHv2_-x_QVoA51O</recordid><startdate>20210801</startdate><enddate>20210801</enddate><creator>Cheng, Wen-Han</creator><creator>Lugtu, Isaiah C.</creator><creator>Chang, Shih-Lin</creator><creator>Liu, Shin-Huei</creator><creator>Chen, Shih-Ann</creator><creator>Lo, Li-Wei</creator><general>Springer US</general><general>Springer Nature B.V</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9102-227X</orcidid></search><sort><creationdate>20210801</creationdate><title>Effects of Angiotensin Receptor-Neprilysin Inhibitor in Arrhythmogenicity Following Left Atrial Appendage Closure in an Animal Model</title><author>Cheng, Wen-Han ; Lugtu, Isaiah C. ; Chang, Shih-Lin ; Liu, Shin-Huei ; Chen, Shih-Ann ; Lo, Li-Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-25ab014d1e2540655a24eb534efd0ae70713f2afd386974086b97beb62372dae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Aminobutyrates - pharmacology</topic><topic>Angiotensin</topic><topic>Angiotensin Receptor Antagonists - pharmacology</topic><topic>Animal models</topic><topic>Animals</topic><topic>Arrhythmias, Cardiac - etiology</topic><topic>Arrhythmias, Cardiac - prevention & control</topic><topic>Atrial Appendage - surgery</topic><topic>Atrial Natriuretic Factor - metabolism</topic><topic>Atrial natriuretic peptide</topic><topic>Biphenyl Compounds - pharmacology</topic><topic>Cardiac arrhythmia</topic><topic>Cardiology</topic><topic>Congestive heart failure</topic><topic>Drug Combinations</topic><topic>Ejection fraction</topic><topic>Electrophysiological recording</topic><topic>Event-related potentials</topic><topic>Fibrillation</topic><topic>Fibrosis</topic><topic>Heart Atria - surgery</topic><topic>Heart failure</topic><topic>Hospitals</topic><topic>Inhibitors</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Models, Animal</topic><topic>Myocardium</topic><topic>Neprilysin</topic><topic>Neprilysin - antagonists & inhibitors</topic><topic>Original Article</topic><topic>Pacemakers</topic><topic>Peptides</topic><topic>Rabbits</topic><topic>Receptors</topic><topic>Refractory period</topic><topic>Septal Occluder Device</topic><topic>Stroke</topic><topic>Treatment Outcome</topic><topic>Valsartan - pharmacology</topic><topic>Ventricle</topic><topic>Ventricular fibrillation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheng, Wen-Han</creatorcontrib><creatorcontrib>Lugtu, Isaiah C.</creatorcontrib><creatorcontrib>Chang, Shih-Lin</creatorcontrib><creatorcontrib>Liu, Shin-Huei</creatorcontrib><creatorcontrib>Chen, Shih-Ann</creatorcontrib><creatorcontrib>Lo, Li-Wei</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular drugs and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheng, Wen-Han</au><au>Lugtu, Isaiah C.</au><au>Chang, Shih-Lin</au><au>Liu, Shin-Huei</au><au>Chen, Shih-Ann</au><au>Lo, Li-Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Angiotensin Receptor-Neprilysin Inhibitor in Arrhythmogenicity Following Left Atrial Appendage Closure in an Animal Model</atitle><jtitle>Cardiovascular drugs and therapy</jtitle><stitle>Cardiovasc Drugs Ther</stitle><addtitle>Cardiovasc Drugs Ther</addtitle><date>2021-08-01</date><risdate>2021</risdate><volume>35</volume><issue>4</issue><spage>759</spage><epage>768</epage><pages>759-768</pages><issn>0920-3206</issn><eissn>1573-7241</eissn><abstract>Purpose
Left atrial appendage (LAA) closure decreases atrial natriuretic peptide (ANP) levels, which indirectly increases the risk of arrhythmogenicity. We aimed to determine the effect of a combined angiotensin receptor-neprilysin inhibitor (ARNi) on arrhythmogenicity following LAA closure in an animal model.
Methods
Twenty-four rabbits were randomized into four groups: (1) control, (2) LAA closure (LAAC), (3) heart failure (HF)-LAAC, and (4) HF-LAAC with sacubitril/valsartan (+ARNi). HF models were developed in the HF-LAAC and HF-LAAC+ARNi groups. Epicardial LAA exclusion was performed in the LAAC, HF-LAAC, and HF-LAAC+ARNi groups. ANP levels were measured. An electrophysiological study was performed. The myocardium was harvested for histopathological analysis.
Results
The ANP level decreased in the LAAC group (785 ± 103 pg/mL,
p
= 0.03), failed to increase in the HF-LAAC group (917 ± 172 pg/mL,
p
= 0.3), and increased in the HF-LAAC+ARNi group (1524 ± 126 pg/mL,
p
< 0.01) compared to that in the control group (1014 ± 56 pg/mL). The atrial effective refractory period (ERP) was prolonged in the HF-LAAC group and restored to baseline in the HF-LAAC+ARNi group. Ventricular ERP was the longest in the HF-LAAC group. The atrial fibrillation window of vulnerability (AF WOV) was elevated in the LAAC, HF-LAAC, and HF-LAAC+ARNi groups, with the latter group having lower AF WOV than the two former groups. Ventricular fibrillation (VF) inducibility was the highest in the HF-LAAC group (51 ± 5%,
p
< 0.001), followed by the LAAC group (30 ± 4%,
p
= 0.006) and the HF-LAAC+ARNi group (25 ± 5%,
p
= 0.11) when compared to the control group (18 ± 4%). Atrial and ventricular fibrosis were noted in all groups except the control group.
Conclusion
LAA closure decreased ANP, which in turn increased AF and VF inducibility. Atrial and ventricular arrhythmogenicity was suppressed by ARNi.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33818689</pmid><doi>10.1007/s10557-021-07174-2</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-9102-227X</orcidid></addata></record> |
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| ispartof | Cardiovascular drugs and therapy, 2021-08, Vol.35 (4), p.759-768 |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Aminobutyrates - pharmacology Angiotensin Angiotensin Receptor Antagonists - pharmacology Animal models Animals Arrhythmias, Cardiac - etiology Arrhythmias, Cardiac - prevention & control Atrial Appendage - surgery Atrial Natriuretic Factor - metabolism Atrial natriuretic peptide Biphenyl Compounds - pharmacology Cardiac arrhythmia Cardiology Congestive heart failure Drug Combinations Ejection fraction Electrophysiological recording Event-related potentials Fibrillation Fibrosis Heart Atria - surgery Heart failure Hospitals Inhibitors Medicine Medicine & Public Health Models, Animal Myocardium Neprilysin Neprilysin - antagonists & inhibitors Original Article Pacemakers Peptides Rabbits Receptors Refractory period Septal Occluder Device Stroke Treatment Outcome Valsartan - pharmacology Ventricle Ventricular fibrillation |
| title | Effects of Angiotensin Receptor-Neprilysin Inhibitor in Arrhythmogenicity Following Left Atrial Appendage Closure in an Animal Model |
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