Body Temperature Circadian Rhythm Variability Corresponds to Left Ventricular Systolic Dysfunction in Decompensated Cardiomyopathic Hamsters

Abstract Background A declining amplitude of body temperature circadian rhythm (BTCR) predicts decompensation or death in cardiomyopathic hamsters. We tested the hypothesis that changes in BTCR amplitude accompany significant changes in left ventricular (LV) size and function. Methods and Results Us...

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Veröffentlicht in:Journal of cardiac failure 2011-11, Vol.17 (11), p.937-943
Hauptverfasser: Ahmed, Amany, MD, Gondi, Sreedevi, MD, Cox, Casey, BSc, Zheng, Minjuan, MD, Mohammed, Anwarullah, MD, Stupin, Igor V., MD, PhD, Wang, Suwei, PhD, Vela, Deborah, MD, Brewer, Alan, MBA, BSc, Elayda, Macarthur A., MD, PhD, Maximilian Buja, L., MD, Ward Casscells, S., MD, Wilson, James M., MD
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container_end_page 943
container_issue 11
container_start_page 937
container_title Journal of cardiac failure
container_volume 17
creator Ahmed, Amany, MD
Gondi, Sreedevi, MD
Cox, Casey, BSc
Zheng, Minjuan, MD
Mohammed, Anwarullah, MD
Stupin, Igor V., MD, PhD
Wang, Suwei, PhD
Vela, Deborah, MD
Brewer, Alan, MBA, BSc
Elayda, Macarthur A., MD, PhD
Maximilian Buja, L., MD
Ward Casscells, S., MD
Wilson, James M., MD
description Abstract Background A declining amplitude of body temperature circadian rhythm (BTCR) predicts decompensation or death in cardiomyopathic hamsters. We tested the hypothesis that changes in BTCR amplitude accompany significant changes in left ventricular (LV) size and function. Methods and Results Using intraperitoneal transmitters, we continuously monitored the temperature of 30 male BIO TO-2 Syrian dilated cardiomyopathic hamsters. Cosinor analysis was used to detect significant changes—defined as changes >1 standard deviation from the baseline amplitude for 3 consecutive days—in BTCR amplitude over each hamster’s lifespan. The Student t -test was used to compare BTCR variability and LV size and function (as assessed by 2D echocardiography) between baseline and the time that BTCR amplitude declined. All hamsters received 10 mg/kg furosemide daily. At the time of BTCR amplitude decline, functional parameters had changed significantly ( P < .0001) from baseline: ejection fraction (0.31 ± 0.09% vs. 0.52 ± 0.08%), LV end-systolic volume (0.11 ± 0.03 vs. 0.05 ± 0.02 cm3 ), and LV end-diastolic volume (0.16 ± 0.04 vs. 0.10 ± 0.03 cm3 ). Conclusions In decompensated cardiomyopathic hamsters, a decline in BTCR amplitude was associated with progression of heart failure and cardiac decompensation. Variation in BTCR warrants further investigation because of its potential implications for the diagnosis and treatment of cardiovascular disorders.
doi_str_mv 10.1016/j.cardfail.2011.07.004
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We tested the hypothesis that changes in BTCR amplitude accompany significant changes in left ventricular (LV) size and function. Methods and Results Using intraperitoneal transmitters, we continuously monitored the temperature of 30 male BIO TO-2 Syrian dilated cardiomyopathic hamsters. Cosinor analysis was used to detect significant changes—defined as changes &gt;1 standard deviation from the baseline amplitude for 3 consecutive days—in BTCR amplitude over each hamster’s lifespan. The Student t -test was used to compare BTCR variability and LV size and function (as assessed by 2D echocardiography) between baseline and the time that BTCR amplitude declined. All hamsters received 10 mg/kg furosemide daily. At the time of BTCR amplitude decline, functional parameters had changed significantly ( P &lt; .0001) from baseline: ejection fraction (0.31 ± 0.09% vs. 0.52 ± 0.08%), LV end-systolic volume (0.11 ± 0.03 vs. 0.05 ± 0.02 cm3 ), and LV end-diastolic volume (0.16 ± 0.04 vs. 0.10 ± 0.03 cm3 ). Conclusions In decompensated cardiomyopathic hamsters, a decline in BTCR amplitude was associated with progression of heart failure and cardiac decompensation. Variation in BTCR warrants further investigation because of its potential implications for the diagnosis and treatment of cardiovascular disorders.</description><identifier>ISSN: 1071-9164</identifier><identifier>EISSN: 1532-8414</identifier><identifier>DOI: 10.1016/j.cardfail.2011.07.004</identifier><identifier>PMID: 22041331</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Body Temperature ; Cardiovascular ; Circadian Rhythm - physiology ; Cricetinae ; Disease Models, Animal ; Heart failure ; Heart Failure - diagnostic imaging ; Heart Failure - pathology ; Linear Models ; Male ; Risk Assessment ; Systole ; Ultrasonography ; Ventricular Dysfunction, Left - diagnostic imaging ; Ventricular Dysfunction, Left - pathology</subject><ispartof>Journal of cardiac failure, 2011-11, Vol.17 (11), p.937-943</ispartof><rights>2011</rights><rights>Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-901f28f94897cef9644e150b3ccbd9a3d611602eb4ce8461edb2af7b350c36bf3</citedby><cites>FETCH-LOGICAL-c422t-901f28f94897cef9644e150b3ccbd9a3d611602eb4ce8461edb2af7b350c36bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.cardfail.2011.07.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22041331$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ahmed, Amany, MD</creatorcontrib><creatorcontrib>Gondi, Sreedevi, MD</creatorcontrib><creatorcontrib>Cox, Casey, BSc</creatorcontrib><creatorcontrib>Zheng, Minjuan, MD</creatorcontrib><creatorcontrib>Mohammed, Anwarullah, MD</creatorcontrib><creatorcontrib>Stupin, Igor V., MD, PhD</creatorcontrib><creatorcontrib>Wang, Suwei, PhD</creatorcontrib><creatorcontrib>Vela, Deborah, MD</creatorcontrib><creatorcontrib>Brewer, Alan, MBA, BSc</creatorcontrib><creatorcontrib>Elayda, Macarthur A., MD, PhD</creatorcontrib><creatorcontrib>Maximilian Buja, L., MD</creatorcontrib><creatorcontrib>Ward Casscells, S., MD</creatorcontrib><creatorcontrib>Wilson, James M., MD</creatorcontrib><title>Body Temperature Circadian Rhythm Variability Corresponds to Left Ventricular Systolic Dysfunction in Decompensated Cardiomyopathic Hamsters</title><title>Journal of cardiac failure</title><addtitle>J Card Fail</addtitle><description>Abstract Background A declining amplitude of body temperature circadian rhythm (BTCR) predicts decompensation or death in cardiomyopathic hamsters. We tested the hypothesis that changes in BTCR amplitude accompany significant changes in left ventricular (LV) size and function. Methods and Results Using intraperitoneal transmitters, we continuously monitored the temperature of 30 male BIO TO-2 Syrian dilated cardiomyopathic hamsters. Cosinor analysis was used to detect significant changes—defined as changes &gt;1 standard deviation from the baseline amplitude for 3 consecutive days—in BTCR amplitude over each hamster’s lifespan. The Student t -test was used to compare BTCR variability and LV size and function (as assessed by 2D echocardiography) between baseline and the time that BTCR amplitude declined. All hamsters received 10 mg/kg furosemide daily. At the time of BTCR amplitude decline, functional parameters had changed significantly ( P &lt; .0001) from baseline: ejection fraction (0.31 ± 0.09% vs. 0.52 ± 0.08%), LV end-systolic volume (0.11 ± 0.03 vs. 0.05 ± 0.02 cm3 ), and LV end-diastolic volume (0.16 ± 0.04 vs. 0.10 ± 0.03 cm3 ). Conclusions In decompensated cardiomyopathic hamsters, a decline in BTCR amplitude was associated with progression of heart failure and cardiac decompensation. Variation in BTCR warrants further investigation because of its potential implications for the diagnosis and treatment of cardiovascular disorders.</description><subject>Animals</subject><subject>Body Temperature</subject><subject>Cardiovascular</subject><subject>Circadian Rhythm - physiology</subject><subject>Cricetinae</subject><subject>Disease Models, Animal</subject><subject>Heart failure</subject><subject>Heart Failure - diagnostic imaging</subject><subject>Heart Failure - pathology</subject><subject>Linear Models</subject><subject>Male</subject><subject>Risk Assessment</subject><subject>Systole</subject><subject>Ultrasonography</subject><subject>Ventricular Dysfunction, Left - diagnostic imaging</subject><subject>Ventricular Dysfunction, Left - pathology</subject><issn>1071-9164</issn><issn>1532-8414</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk1v1DAQhiMEoh_wFyrfOG0Yf2w-LghIoUVaCYmWXi3Hnmi9JHawHaT8B340Xm3LgQunmcMz887MO0VxRaGkQKu3h1KrYAZlx5IBpSXUJYB4VpzTLWebRlDxPOdQ001LK3FWXMR4AIBGQP2yOGMMBOWcnhe_P3qzknucZgwqLQFJZ4NWxipHvu3XtJ_IgwpW9Xa0aSWdDwHj7J2JJHmywyGRB3QpWL2MKpC7NSY_Wk2u1zgsTifrHbGOXKP2WcJFldCQLo9u_bT6WaV9hm_VFBOG-Kp4Magx4uvHeFl8__zpvrvd7L7efOk-7DZaMJY2LdCBNUMrmrbWOLSVEEi30HOte9MqbipKK2DYC42NqCianqmh7vkWNK_6gV8Wb0595-B_LhiTnGzUOI7KoV-izAKV4KytM1mdSB18jAEHOQc7qbBKCvJohDzIJyPk0QgJtcxG5MKrR4mln9D8LXu6fAbenwDMi_6yGGTUFp1GYwPqJI23_9d4908LPVpntRp_4Irx4Jfg8hkllZFJkHfHdzh-A6UAbc1a_gejYbWQ</recordid><startdate>20111101</startdate><enddate>20111101</enddate><creator>Ahmed, Amany, MD</creator><creator>Gondi, Sreedevi, MD</creator><creator>Cox, Casey, BSc</creator><creator>Zheng, Minjuan, MD</creator><creator>Mohammed, Anwarullah, MD</creator><creator>Stupin, Igor V., MD, PhD</creator><creator>Wang, Suwei, PhD</creator><creator>Vela, Deborah, MD</creator><creator>Brewer, Alan, MBA, BSc</creator><creator>Elayda, Macarthur A., MD, PhD</creator><creator>Maximilian Buja, L., MD</creator><creator>Ward Casscells, S., MD</creator><creator>Wilson, James M., MD</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>20111101</creationdate><title>Body Temperature Circadian Rhythm Variability Corresponds to Left Ventricular Systolic Dysfunction in Decompensated Cardiomyopathic Hamsters</title><author>Ahmed, Amany, MD ; Gondi, Sreedevi, MD ; Cox, Casey, BSc ; Zheng, Minjuan, MD ; Mohammed, Anwarullah, MD ; Stupin, Igor V., MD, PhD ; Wang, Suwei, PhD ; Vela, Deborah, MD ; Brewer, Alan, MBA, BSc ; Elayda, Macarthur A., MD, PhD ; Maximilian Buja, L., MD ; Ward Casscells, S., MD ; Wilson, James M., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-901f28f94897cef9644e150b3ccbd9a3d611602eb4ce8461edb2af7b350c36bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Body Temperature</topic><topic>Cardiovascular</topic><topic>Circadian Rhythm - physiology</topic><topic>Cricetinae</topic><topic>Disease Models, Animal</topic><topic>Heart failure</topic><topic>Heart Failure - diagnostic imaging</topic><topic>Heart Failure - pathology</topic><topic>Linear Models</topic><topic>Male</topic><topic>Risk Assessment</topic><topic>Systole</topic><topic>Ultrasonography</topic><topic>Ventricular Dysfunction, Left - diagnostic imaging</topic><topic>Ventricular Dysfunction, Left - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ahmed, Amany, MD</creatorcontrib><creatorcontrib>Gondi, Sreedevi, MD</creatorcontrib><creatorcontrib>Cox, Casey, BSc</creatorcontrib><creatorcontrib>Zheng, Minjuan, MD</creatorcontrib><creatorcontrib>Mohammed, Anwarullah, MD</creatorcontrib><creatorcontrib>Stupin, Igor V., MD, PhD</creatorcontrib><creatorcontrib>Wang, Suwei, PhD</creatorcontrib><creatorcontrib>Vela, Deborah, MD</creatorcontrib><creatorcontrib>Brewer, Alan, MBA, BSc</creatorcontrib><creatorcontrib>Elayda, Macarthur A., MD, PhD</creatorcontrib><creatorcontrib>Maximilian Buja, L., MD</creatorcontrib><creatorcontrib>Ward Casscells, S., MD</creatorcontrib><creatorcontrib>Wilson, James M., MD</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>Journal of cardiac failure</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ahmed, Amany, MD</au><au>Gondi, Sreedevi, MD</au><au>Cox, Casey, BSc</au><au>Zheng, Minjuan, MD</au><au>Mohammed, Anwarullah, MD</au><au>Stupin, Igor V., MD, PhD</au><au>Wang, Suwei, PhD</au><au>Vela, Deborah, MD</au><au>Brewer, Alan, MBA, BSc</au><au>Elayda, Macarthur A., MD, PhD</au><au>Maximilian Buja, L., MD</au><au>Ward Casscells, S., MD</au><au>Wilson, James M., MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Body Temperature Circadian Rhythm Variability Corresponds to Left Ventricular Systolic Dysfunction in Decompensated Cardiomyopathic Hamsters</atitle><jtitle>Journal of cardiac failure</jtitle><addtitle>J Card Fail</addtitle><date>2011-11-01</date><risdate>2011</risdate><volume>17</volume><issue>11</issue><spage>937</spage><epage>943</epage><pages>937-943</pages><issn>1071-9164</issn><eissn>1532-8414</eissn><abstract>Abstract Background A declining amplitude of body temperature circadian rhythm (BTCR) predicts decompensation or death in cardiomyopathic hamsters. We tested the hypothesis that changes in BTCR amplitude accompany significant changes in left ventricular (LV) size and function. Methods and Results Using intraperitoneal transmitters, we continuously monitored the temperature of 30 male BIO TO-2 Syrian dilated cardiomyopathic hamsters. Cosinor analysis was used to detect significant changes—defined as changes &gt;1 standard deviation from the baseline amplitude for 3 consecutive days—in BTCR amplitude over each hamster’s lifespan. The Student t -test was used to compare BTCR variability and LV size and function (as assessed by 2D echocardiography) between baseline and the time that BTCR amplitude declined. All hamsters received 10 mg/kg furosemide daily. At the time of BTCR amplitude decline, functional parameters had changed significantly ( P &lt; .0001) from baseline: ejection fraction (0.31 ± 0.09% vs. 0.52 ± 0.08%), LV end-systolic volume (0.11 ± 0.03 vs. 0.05 ± 0.02 cm3 ), and LV end-diastolic volume (0.16 ± 0.04 vs. 0.10 ± 0.03 cm3 ). Conclusions In decompensated cardiomyopathic hamsters, a decline in BTCR amplitude was associated with progression of heart failure and cardiac decompensation. Variation in BTCR warrants further investigation because of its potential implications for the diagnosis and treatment of cardiovascular disorders.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22041331</pmid><doi>10.1016/j.cardfail.2011.07.004</doi><tpages>7</tpages></addata></record>
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subjects Animals
Body Temperature
Cardiovascular
Circadian Rhythm - physiology
Cricetinae
Disease Models, Animal
Heart failure
Heart Failure - diagnostic imaging
Heart Failure - pathology
Linear Models
Male
Risk Assessment
Systole
Ultrasonography
Ventricular Dysfunction, Left - diagnostic imaging
Ventricular Dysfunction, Left - pathology
title Body Temperature Circadian Rhythm Variability Corresponds to Left Ventricular Systolic Dysfunction in Decompensated Cardiomyopathic Hamsters
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