The Effects of Temperature on Cardiac Pacing Thresholds

Background:  Human core body temperature can fluctuate between 36°C (sleep) and 42°C (intense exercise). Also, efforts are underway to develop implantable pacing systems that minimize heating during magnetic resonance imaging (MRI) scans (i.e., MRI safe). Concerns exist that ventricular pacing captu...

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Veröffentlicht in:Pacing and clinical electrophysiology 2010-07, Vol.33 (7), p.826-833
Hauptverfasser: MARSHALL, MARK T., LIAO, KENNETH K., LOUSHIN, MICHAEL K., IAIZZO, PAUL A.
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container_end_page 833
container_issue 7
container_start_page 826
container_title Pacing and clinical electrophysiology
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creator MARSHALL, MARK T.
LIAO, KENNETH K.
LOUSHIN, MICHAEL K.
IAIZZO, PAUL A.
description Background:  Human core body temperature can fluctuate between 36°C (sleep) and 42°C (intense exercise). Also, efforts are underway to develop implantable pacing systems that minimize heating during magnetic resonance imaging (MRI) scans (i.e., MRI safe). Concerns exist that ventricular pacing capture thresholds (VPCT) are modified by changing cardiac temperatures. This project was designed to assess the effects of temperature on VPCT of the mammalian heart. Methods:  Fresh ventricular specimens were obtained from healthy canine, healthy swine, and diseased human hearts. Isolated trabeculae were suspended in temperature‐controlled tissue baths containing oxygenated Krebs buffer. Small active fixation pacing leads delivered pacing pulses to each specimen. Baseline strength‐duration curves were determined at 37°C, then at randomized temperatures ranging from 35°C to 42°C. Final thresholds were repeated at 37°C to confirm baseline responses. All threshold data were normalized to a baseline average. Results:  Both canine and swine trabeculae elicited significant decreases in thresholds (10–14%) at pacing stimulus durations (pulsewidths) of 0.02 ms (P < 0.01) and 0.10 ms (P < 0.05) between the temperatures of 38°C and 41°C, compared to baseline. Thresholds at 42°C trended back to baseline for both canine (NS) and swine trabeculae (P < 0.05 compared to 38°C–41°C). Human trabeculae thresholds increased >35% (P < 0.05) at 42°C relative to baseline with no significant differences at other temperatures. Conclusions:  Temperature is a significant factor on pacing thresholds for mammalian ventricular myocardium. Our data for the diseased human trabeculae indicate that cases where cardiac heating may occur (e.g., radiofrequency energy due to MRI scans, febrile events), patients without adequate VPCT safety margin may be at higher risk of loss of proper function of an implanted pacing or defibrillation system. (PACE 2010; 826–833)
doi_str_mv 10.1111/j.1540-8159.2009.02681.x
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Also, efforts are underway to develop implantable pacing systems that minimize heating during magnetic resonance imaging (MRI) scans (i.e., MRI safe). Concerns exist that ventricular pacing capture thresholds (VPCT) are modified by changing cardiac temperatures. This project was designed to assess the effects of temperature on VPCT of the mammalian heart. Methods:  Fresh ventricular specimens were obtained from healthy canine, healthy swine, and diseased human hearts. Isolated trabeculae were suspended in temperature‐controlled tissue baths containing oxygenated Krebs buffer. Small active fixation pacing leads delivered pacing pulses to each specimen. Baseline strength‐duration curves were determined at 37°C, then at randomized temperatures ranging from 35°C to 42°C. Final thresholds were repeated at 37°C to confirm baseline responses. All threshold data were normalized to a baseline average. Results:  Both canine and swine trabeculae elicited significant decreases in thresholds (10–14%) at pacing stimulus durations (pulsewidths) of 0.02 ms (P &lt; 0.01) and 0.10 ms (P &lt; 0.05) between the temperatures of 38°C and 41°C, compared to baseline. Thresholds at 42°C trended back to baseline for both canine (NS) and swine trabeculae (P &lt; 0.05 compared to 38°C–41°C). Human trabeculae thresholds increased &gt;35% (P &lt; 0.05) at 42°C relative to baseline with no significant differences at other temperatures. Conclusions:  Temperature is a significant factor on pacing thresholds for mammalian ventricular myocardium. Our data for the diseased human trabeculae indicate that cases where cardiac heating may occur (e.g., radiofrequency energy due to MRI scans, febrile events), patients without adequate VPCT safety margin may be at higher risk of loss of proper function of an implanted pacing or defibrillation system. 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Also, efforts are underway to develop implantable pacing systems that minimize heating during magnetic resonance imaging (MRI) scans (i.e., MRI safe). Concerns exist that ventricular pacing capture thresholds (VPCT) are modified by changing cardiac temperatures. This project was designed to assess the effects of temperature on VPCT of the mammalian heart. Methods:  Fresh ventricular specimens were obtained from healthy canine, healthy swine, and diseased human hearts. Isolated trabeculae were suspended in temperature‐controlled tissue baths containing oxygenated Krebs buffer. Small active fixation pacing leads delivered pacing pulses to each specimen. Baseline strength‐duration curves were determined at 37°C, then at randomized temperatures ranging from 35°C to 42°C. Final thresholds were repeated at 37°C to confirm baseline responses. All threshold data were normalized to a baseline average. Results:  Both canine and swine trabeculae elicited significant decreases in thresholds (10–14%) at pacing stimulus durations (pulsewidths) of 0.02 ms (P &lt; 0.01) and 0.10 ms (P &lt; 0.05) between the temperatures of 38°C and 41°C, compared to baseline. Thresholds at 42°C trended back to baseline for both canine (NS) and swine trabeculae (P &lt; 0.05 compared to 38°C–41°C). Human trabeculae thresholds increased &gt;35% (P &lt; 0.05) at 42°C relative to baseline with no significant differences at other temperatures. Conclusions:  Temperature is a significant factor on pacing thresholds for mammalian ventricular myocardium. Our data for the diseased human trabeculae indicate that cases where cardiac heating may occur (e.g., radiofrequency energy due to MRI scans, febrile events), patients without adequate VPCT safety margin may be at higher risk of loss of proper function of an implanted pacing or defibrillation system. (PACE 2010; 826–833)</description><subject>Action Potentials - physiology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Body Temperature - physiology</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiac Pacing, Artificial - methods</subject><subject>Cardiology. Vascular system</subject><subject>defibrillators</subject><subject>Differential Threshold - physiology</subject><subject>Dogs</subject><subject>Heart</subject><subject>Heart Conduction System - physiology</subject><subject>Humans</subject><subject>imaging</subject><subject>implantable</subject><subject>magnetic resonance imaging</subject><subject>Medical sciences</subject><subject>pacemakers</subject><subject>Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. 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Vascular system</topic><topic>defibrillators</topic><topic>Differential Threshold - physiology</topic><topic>Dogs</topic><topic>Heart</topic><topic>Heart Conduction System - physiology</topic><topic>Humans</topic><topic>imaging</topic><topic>implantable</topic><topic>magnetic resonance imaging</topic><topic>Medical sciences</topic><topic>pacemakers</topic><topic>Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)</topic><topic>safety</topic><topic>Swine</topic><topic>Ventricular Function, Left - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MARSHALL, MARK T.</creatorcontrib><creatorcontrib>LIAO, KENNETH K.</creatorcontrib><creatorcontrib>LOUSHIN, MICHAEL K.</creatorcontrib><creatorcontrib>IAIZZO, PAUL A.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Pacing and clinical electrophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MARSHALL, MARK T.</au><au>LIAO, KENNETH K.</au><au>LOUSHIN, MICHAEL K.</au><au>IAIZZO, PAUL A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Effects of Temperature on Cardiac Pacing Thresholds</atitle><jtitle>Pacing and clinical electrophysiology</jtitle><addtitle>Pacing Clin Electrophysiol</addtitle><date>2010-07</date><risdate>2010</risdate><volume>33</volume><issue>7</issue><spage>826</spage><epage>833</epage><pages>826-833</pages><issn>0147-8389</issn><eissn>1540-8159</eissn><abstract>Background:  Human core body temperature can fluctuate between 36°C (sleep) and 42°C (intense exercise). Also, efforts are underway to develop implantable pacing systems that minimize heating during magnetic resonance imaging (MRI) scans (i.e., MRI safe). Concerns exist that ventricular pacing capture thresholds (VPCT) are modified by changing cardiac temperatures. This project was designed to assess the effects of temperature on VPCT of the mammalian heart. Methods:  Fresh ventricular specimens were obtained from healthy canine, healthy swine, and diseased human hearts. Isolated trabeculae were suspended in temperature‐controlled tissue baths containing oxygenated Krebs buffer. Small active fixation pacing leads delivered pacing pulses to each specimen. Baseline strength‐duration curves were determined at 37°C, then at randomized temperatures ranging from 35°C to 42°C. Final thresholds were repeated at 37°C to confirm baseline responses. All threshold data were normalized to a baseline average. Results:  Both canine and swine trabeculae elicited significant decreases in thresholds (10–14%) at pacing stimulus durations (pulsewidths) of 0.02 ms (P &lt; 0.01) and 0.10 ms (P &lt; 0.05) between the temperatures of 38°C and 41°C, compared to baseline. Thresholds at 42°C trended back to baseline for both canine (NS) and swine trabeculae (P &lt; 0.05 compared to 38°C–41°C). Human trabeculae thresholds increased &gt;35% (P &lt; 0.05) at 42°C relative to baseline with no significant differences at other temperatures. Conclusions:  Temperature is a significant factor on pacing thresholds for mammalian ventricular myocardium. Our data for the diseased human trabeculae indicate that cases where cardiac heating may occur (e.g., radiofrequency energy due to MRI scans, febrile events), patients without adequate VPCT safety margin may be at higher risk of loss of proper function of an implanted pacing or defibrillation system. (PACE 2010; 826–833)</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>20132492</pmid><doi>10.1111/j.1540-8159.2009.02681.x</doi><tpages>8</tpages></addata></record>
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subjects Action Potentials - physiology
Animals
Biological and medical sciences
Body Temperature - physiology
Cardiac dysrhythmias
Cardiac Pacing, Artificial - methods
Cardiology. Vascular system
defibrillators
Differential Threshold - physiology
Dogs
Heart
Heart Conduction System - physiology
Humans
imaging
implantable
magnetic resonance imaging
Medical sciences
pacemakers
Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)
safety
Swine
Ventricular Function, Left - physiology
title The Effects of Temperature on Cardiac Pacing Thresholds
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