Effect of altering the left ventricular pressure on epicardial activation time in dogs with and without pacing-induced heart failure
The influence of an increased left ventricular end-diastolic pressure (LVEDP) on the development of lethal arrhythmias in chronic heart failure is unclear. We investigated the effect of chronic and acute LVEDP increase on the epicardial activation time of sinus (SB) and paced (PB) beats. Six dogs un...
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| creator | FOTUHI, Parwis C NIPON CHATTIPAKORN ROLLINS, Dennis L BICKNELL, Jeanette L SREENAN, Catherine M KILLINGSWORTH, Cheryl R WALCOTT, Gregory P IDEKER, Raymond E |
| description | The influence of an increased left ventricular end-diastolic pressure (LVEDP) on the development of lethal arrhythmias in chronic heart failure is unclear. We investigated the effect of chronic and acute LVEDP increase on the epicardial activation time of sinus (SB) and paced (PB) beats.
Six dogs underwent rapid ventricular pacing at 220-280[emsp4 ]beats/min for 6-14 weeks for induction of heart failure. On the study day, baseline (ba) LVEDP was determined for the surviving heart failure animals (HF-ba), and for seven control animals (C-ba). The epicardial activation time (EAT, time between the earliest and latest epicardial activation) for five consecutive SB and five ventricular PB during the baseline hemodynamic state were recorded using a 504 electrode mapping-sock. In the control animals a 2-litre volume (vl) was infused over 10[emsp4 ]min to acutely increase the LVEDP (C-vl) to a level comparable to the chronic increased LVEDP of the HF-ba. The same volume challenge was performed in two HF animals (HF-vl) and the EAT for SB and PB was redetermined.
Three of six HF animals died during induction of heart failure. In the three remaining HF animals, chronic LVEDP increased from 6+/-1 to 17+/-10.8[emsp4 ]mmHg (P=0.07), EAT for SB increased by 68 % compared to control animals (HF-ba vs. C-ba, P |
| doi_str_mv | 10.1023/A:1026549112331 |
| format | Article |
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Six dogs underwent rapid ventricular pacing at 220-280[emsp4 ]beats/min for 6-14 weeks for induction of heart failure. On the study day, baseline (ba) LVEDP was determined for the surviving heart failure animals (HF-ba), and for seven control animals (C-ba). The epicardial activation time (EAT, time between the earliest and latest epicardial activation) for five consecutive SB and five ventricular PB during the baseline hemodynamic state were recorded using a 504 electrode mapping-sock. In the control animals a 2-litre volume (vl) was infused over 10[emsp4 ]min to acutely increase the LVEDP (C-vl) to a level comparable to the chronic increased LVEDP of the HF-ba. The same volume challenge was performed in two HF animals (HF-vl) and the EAT for SB and PB was redetermined.
Three of six HF animals died during induction of heart failure. In the three remaining HF animals, chronic LVEDP increased from 6+/-1 to 17+/-10.8[emsp4 ]mmHg (P=0.07), EAT for SB increased by 68 % compared to control animals (HF-ba vs. C-ba, P<0.05). In contrast, in the control animals the acute rise in LVEDP from 6.8+/-4.5 to 14.7+/-6.2 mmHg P<0.05), shortened the EAT for SB (C-ba vs. C-vl, P<0.05). A similar decrease in EAT for SB caused by acute volume load was seen in the HF animals, but did not reach significance due to the small sample size (one of the three remaining HF animals died of spontaneous ventricular fibrillation before the volume load). Chronic LVEDP elevation significantly prolonged the EAT for PB from 72+/-11 to 120+/-31[emsp4 ]ms (C-ba vs. HF-ba) while acute LVEDP increase had no significant effect on EAT for PB.
Chronic HF increases LVEDP and prolongs EAT, while an acute increase in LVEDP shortens the EAT for sinus beats. A prolongation of EAT in heart failure may make the heart more susceptible to ventricular arrhythmias and electromechanical dissociation.</description><identifier>ISSN: 1383-875X</identifier><identifier>EISSN: 1572-8595</identifier><identifier>DOI: 10.1023/A:1026549112331</identifier><identifier>PMID: 11141200</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Acute Disease ; Animals ; Biological and medical sciences ; Cardiac Pacing, Artificial - methods ; Cardiology. Vascular system ; Chronic Disease ; Disease Models, Animal ; Dogs ; Echocardiography - methods ; Heart ; Heart Failure - diagnostic imaging ; Heart Failure - mortality ; Heart Failure - therapy ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Hemodynamics - physiology ; Medical sciences ; Pressure ; Reference Values ; Survival Rate ; Time Factors ; Treatment Outcome ; Ventricular Dysfunction, Left - diagnostic imaging ; Ventricular Dysfunction, Left - mortality ; Ventricular Dysfunction, Left - therapy</subject><ispartof>Journal of interventional cardiac electrophysiology, 2000-12, Vol.4 (4), p.561-568</ispartof><rights>2001 INIST-CNRS</rights><rights>Copyright Kluwer Academic Publishers Dec 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1011430$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11141200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FOTUHI, Parwis C</creatorcontrib><creatorcontrib>NIPON CHATTIPAKORN</creatorcontrib><creatorcontrib>ROLLINS, Dennis L</creatorcontrib><creatorcontrib>BICKNELL, Jeanette L</creatorcontrib><creatorcontrib>SREENAN, Catherine M</creatorcontrib><creatorcontrib>KILLINGSWORTH, Cheryl R</creatorcontrib><creatorcontrib>WALCOTT, Gregory P</creatorcontrib><creatorcontrib>IDEKER, Raymond E</creatorcontrib><title>Effect of altering the left ventricular pressure on epicardial activation time in dogs with and without pacing-induced heart failure</title><title>Journal of interventional cardiac electrophysiology</title><addtitle>J Interv Card Electrophysiol</addtitle><description>The influence of an increased left ventricular end-diastolic pressure (LVEDP) on the development of lethal arrhythmias in chronic heart failure is unclear. We investigated the effect of chronic and acute LVEDP increase on the epicardial activation time of sinus (SB) and paced (PB) beats.
Six dogs underwent rapid ventricular pacing at 220-280[emsp4 ]beats/min for 6-14 weeks for induction of heart failure. On the study day, baseline (ba) LVEDP was determined for the surviving heart failure animals (HF-ba), and for seven control animals (C-ba). The epicardial activation time (EAT, time between the earliest and latest epicardial activation) for five consecutive SB and five ventricular PB during the baseline hemodynamic state were recorded using a 504 electrode mapping-sock. In the control animals a 2-litre volume (vl) was infused over 10[emsp4 ]min to acutely increase the LVEDP (C-vl) to a level comparable to the chronic increased LVEDP of the HF-ba. The same volume challenge was performed in two HF animals (HF-vl) and the EAT for SB and PB was redetermined.
Three of six HF animals died during induction of heart failure. In the three remaining HF animals, chronic LVEDP increased from 6+/-1 to 17+/-10.8[emsp4 ]mmHg (P=0.07), EAT for SB increased by 68 % compared to control animals (HF-ba vs. C-ba, P<0.05). In contrast, in the control animals the acute rise in LVEDP from 6.8+/-4.5 to 14.7+/-6.2 mmHg P<0.05), shortened the EAT for SB (C-ba vs. C-vl, P<0.05). A similar decrease in EAT for SB caused by acute volume load was seen in the HF animals, but did not reach significance due to the small sample size (one of the three remaining HF animals died of spontaneous ventricular fibrillation before the volume load). Chronic LVEDP elevation significantly prolonged the EAT for PB from 72+/-11 to 120+/-31[emsp4 ]ms (C-ba vs. HF-ba) while acute LVEDP increase had no significant effect on EAT for PB.
Chronic HF increases LVEDP and prolongs EAT, while an acute increase in LVEDP shortens the EAT for sinus beats. A prolongation of EAT in heart failure may make the heart more susceptible to ventricular arrhythmias and electromechanical dissociation.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiac Pacing, Artificial - methods</subject><subject>Cardiology. Vascular system</subject><subject>Chronic Disease</subject><subject>Disease Models, Animal</subject><subject>Dogs</subject><subject>Echocardiography - methods</subject><subject>Heart</subject><subject>Heart Failure - diagnostic imaging</subject><subject>Heart Failure - mortality</subject><subject>Heart Failure - therapy</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Hemodynamics - physiology</subject><subject>Medical sciences</subject><subject>Pressure</subject><subject>Reference Values</subject><subject>Survival Rate</subject><subject>Time Factors</subject><subject>Treatment Outcome</subject><subject>Ventricular Dysfunction, Left - diagnostic imaging</subject><subject>Ventricular Dysfunction, Left - mortality</subject><subject>Ventricular Dysfunction, Left - therapy</subject><issn>1383-875X</issn><issn>1572-8595</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpd0M9rFTEQB_Agiv2hZ28SRLytZpKX3ay3UmotFLxU8LbMSyZ9KXnZNclWeu8fbtAnQk_zZfjwZRjG3oD4CEKqT2ef2-j1ZgSQSsEzdgx6kJ3Ro37esjKqM4P-ccROSrkTQoxNv2RHALABKcQxe7zwnmzls-cYK-WQbnndEY_kK7-nVHOwa8TMl0ylrJn4nDgtwWJ2ASNHW8M91tC2NeyJh8TdfFv4r1B3HJP7E-a18gVt6-5Ccqslx3eEuXKPIbbOV-yFx1jo9WGesu9fLm7Ov3bX3y6vzs-uu0X2qnZyGI3pATx4Rbq3UqOl7XYE67feEY3SeW-MASOxH7xpKzcYLeTGQa9QqlP24W_vkuefK5U67UOxFCMmmtcyDVIrMwjd4Lsn8G5ec2q3TRLM2IvRDA29PaB1uyc3LTnsMT9M_57bwPsDwGIx-ozJhvLfiQaVUL8BqreKgw</recordid><startdate>20001201</startdate><enddate>20001201</enddate><creator>FOTUHI, Parwis C</creator><creator>NIPON CHATTIPAKORN</creator><creator>ROLLINS, Dennis L</creator><creator>BICKNELL, Jeanette L</creator><creator>SREENAN, Catherine M</creator><creator>KILLINGSWORTH, Cheryl R</creator><creator>WALCOTT, Gregory P</creator><creator>IDEKER, Raymond E</creator><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QO</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>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20001201</creationdate><title>Effect of altering the left ventricular pressure on epicardial activation time in dogs with and without pacing-induced heart failure</title><author>FOTUHI, Parwis C ; NIPON CHATTIPAKORN ; ROLLINS, Dennis L ; BICKNELL, Jeanette L ; SREENAN, Catherine M ; KILLINGSWORTH, Cheryl R ; WALCOTT, Gregory P ; IDEKER, Raymond E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p263t-27988611f1f3e56c25acebb91cfbfdee92dff888182a67f8deed785024d163a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiac Pacing, Artificial - methods</topic><topic>Cardiology. Vascular system</topic><topic>Chronic Disease</topic><topic>Disease Models, Animal</topic><topic>Dogs</topic><topic>Echocardiography - methods</topic><topic>Heart</topic><topic>Heart Failure - diagnostic imaging</topic><topic>Heart Failure - mortality</topic><topic>Heart Failure - therapy</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Hemodynamics - physiology</topic><topic>Medical sciences</topic><topic>Pressure</topic><topic>Reference Values</topic><topic>Survival Rate</topic><topic>Time Factors</topic><topic>Treatment Outcome</topic><topic>Ventricular Dysfunction, Left - diagnostic imaging</topic><topic>Ventricular Dysfunction, Left - mortality</topic><topic>Ventricular Dysfunction, Left - therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FOTUHI, Parwis C</creatorcontrib><creatorcontrib>NIPON CHATTIPAKORN</creatorcontrib><creatorcontrib>ROLLINS, Dennis L</creatorcontrib><creatorcontrib>BICKNELL, Jeanette L</creatorcontrib><creatorcontrib>SREENAN, Catherine M</creatorcontrib><creatorcontrib>KILLINGSWORTH, Cheryl R</creatorcontrib><creatorcontrib>WALCOTT, Gregory P</creatorcontrib><creatorcontrib>IDEKER, Raymond E</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</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>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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of interventional cardiac electrophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FOTUHI, Parwis C</au><au>NIPON CHATTIPAKORN</au><au>ROLLINS, Dennis L</au><au>BICKNELL, Jeanette L</au><au>SREENAN, Catherine M</au><au>KILLINGSWORTH, Cheryl R</au><au>WALCOTT, Gregory P</au><au>IDEKER, Raymond E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of altering the left ventricular pressure on epicardial activation time in dogs with and without pacing-induced heart failure</atitle><jtitle>Journal of interventional cardiac electrophysiology</jtitle><addtitle>J Interv Card Electrophysiol</addtitle><date>2000-12-01</date><risdate>2000</risdate><volume>4</volume><issue>4</issue><spage>561</spage><epage>568</epage><pages>561-568</pages><issn>1383-875X</issn><eissn>1572-8595</eissn><abstract>The influence of an increased left ventricular end-diastolic pressure (LVEDP) on the development of lethal arrhythmias in chronic heart failure is unclear. We investigated the effect of chronic and acute LVEDP increase on the epicardial activation time of sinus (SB) and paced (PB) beats.
Six dogs underwent rapid ventricular pacing at 220-280[emsp4 ]beats/min for 6-14 weeks for induction of heart failure. On the study day, baseline (ba) LVEDP was determined for the surviving heart failure animals (HF-ba), and for seven control animals (C-ba). The epicardial activation time (EAT, time between the earliest and latest epicardial activation) for five consecutive SB and five ventricular PB during the baseline hemodynamic state were recorded using a 504 electrode mapping-sock. In the control animals a 2-litre volume (vl) was infused over 10[emsp4 ]min to acutely increase the LVEDP (C-vl) to a level comparable to the chronic increased LVEDP of the HF-ba. The same volume challenge was performed in two HF animals (HF-vl) and the EAT for SB and PB was redetermined.
Three of six HF animals died during induction of heart failure. In the three remaining HF animals, chronic LVEDP increased from 6+/-1 to 17+/-10.8[emsp4 ]mmHg (P=0.07), EAT for SB increased by 68 % compared to control animals (HF-ba vs. C-ba, P<0.05). In contrast, in the control animals the acute rise in LVEDP from 6.8+/-4.5 to 14.7+/-6.2 mmHg P<0.05), shortened the EAT for SB (C-ba vs. C-vl, P<0.05). A similar decrease in EAT for SB caused by acute volume load was seen in the HF animals, but did not reach significance due to the small sample size (one of the three remaining HF animals died of spontaneous ventricular fibrillation before the volume load). Chronic LVEDP elevation significantly prolonged the EAT for PB from 72+/-11 to 120+/-31[emsp4 ]ms (C-ba vs. HF-ba) while acute LVEDP increase had no significant effect on EAT for PB.
Chronic HF increases LVEDP and prolongs EAT, while an acute increase in LVEDP shortens the EAT for sinus beats. A prolongation of EAT in heart failure may make the heart more susceptible to ventricular arrhythmias and electromechanical dissociation.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>11141200</pmid><doi>10.1023/A:1026549112331</doi><tpages>8</tpages></addata></record> |
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| subjects | Acute Disease Animals Biological and medical sciences Cardiac Pacing, Artificial - methods Cardiology. Vascular system Chronic Disease Disease Models, Animal Dogs Echocardiography - methods Heart Heart Failure - diagnostic imaging Heart Failure - mortality Heart Failure - therapy Heart failure, cardiogenic pulmonary edema, cardiac enlargement Hemodynamics - physiology Medical sciences Pressure Reference Values Survival Rate Time Factors Treatment Outcome Ventricular Dysfunction, Left - diagnostic imaging Ventricular Dysfunction, Left - mortality Ventricular Dysfunction, Left - therapy |
| title | Effect of altering the left ventricular pressure on epicardial activation time in dogs with and without pacing-induced heart failure |
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