Ivabradine ameliorates cardiomyopathy progression in a Duchenne muscular dystrophy model rat
Duchenne muscular dystrophy (DMD) is an X-linked recessive myopathy caused by dystrophin mutations. Inevitable progressive cardiomyopathy is a current leading cause of premature death although respiratory management has improved the prognosis of patients with DMD. Recent evidence shows that reducing...
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| Veröffentlicht in: | Experimental Animals 2024, Vol.73(2), pp.145-153 |
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| creator | Tochinai, Ryota Kimura, Koichi Saika, Takeru Fujii, Wataru Morita, Hiroyuki Nakanishi, Koki Tsuru, Yoshiharu Sekizawa, Shin-ichi Yamanouchi, Keitaro Kuwahara, Masayoshi |
| description | Duchenne muscular dystrophy (DMD) is an X-linked recessive myopathy caused by dystrophin mutations. Inevitable progressive cardiomyopathy is a current leading cause of premature death although respiratory management has improved the prognosis of patients with DMD. Recent evidence shows that reducing the heart rate is expected as one of the promising strategies for heart failure treatment, but administering a sufficient dose of β-blocker for patients with DMD with tachycardia is difficult because of their low blood pressure (BP). Thus, this study aimed to clarify the role of ivabradine, which suppresses cardiac sinus node pacemakers without decreasing BP, in ameliorating cardiomyopathy progression in a rat model with DMD. A trans-oral single ivabradine administration demonstrated a declined dose-dependent heart rate without any significant BP reduction. Trans-gastric repeated administrations of 5 mg/kg of ivabradine twice a day for 3 months showed ameliorated cardiomyopathy in DMD rats based on echocardiography and histopathological observations (left ventricular dysfunction, right ventricular dysfunction, and myocardial fibrosis) as compared with vehicle administration.Our finding indicates that ivabradine is expected as another treatment choice for patients with DMD having tachycardia. |
| doi_str_mv | 10.1538/expanim.23-0087 |
| format | Article |
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Inevitable progressive cardiomyopathy is a current leading cause of premature death although respiratory management has improved the prognosis of patients with DMD. Recent evidence shows that reducing the heart rate is expected as one of the promising strategies for heart failure treatment, but administering a sufficient dose of β-blocker for patients with DMD with tachycardia is difficult because of their low blood pressure (BP). Thus, this study aimed to clarify the role of ivabradine, which suppresses cardiac sinus node pacemakers without decreasing BP, in ameliorating cardiomyopathy progression in a rat model with DMD. A trans-oral single ivabradine administration demonstrated a declined dose-dependent heart rate without any significant BP reduction. Trans-gastric repeated administrations of 5 mg/kg of ivabradine twice a day for 3 months showed ameliorated cardiomyopathy in DMD rats based on echocardiography and histopathological observations (left ventricular dysfunction, right ventricular dysfunction, and myocardial fibrosis) as compared with vehicle administration.Our finding indicates that ivabradine is expected as another treatment choice for patients with DMD having tachycardia.</description><identifier>ISSN: 1341-1357</identifier><identifier>EISSN: 1881-7122</identifier><identifier>DOI: 10.1538/expanim.23-0087</identifier><identifier>PMID: 37914289</identifier><language>eng</language><publisher>Japan: Japanese Association for Laboratory Animal Science</publisher><subject>Animals ; Blood pressure ; Cardiac arrhythmia ; Cardiomyopathies - drug therapy ; Cardiomyopathies - etiology ; Cardiomyopathy ; Congestive heart failure ; Disease Models, Animal ; Disease Progression ; Duchenne's muscular dystrophy ; Dystrophin ; dystrophin deficiency ; Dystrophy ; Echocardiography ; Fibrosis ; heart ; Heart rate ; Heart Rate - drug effects ; hyperpolarization-activated cyclic nucleotide-gated (HCN) channel ; Ivabradine - administration & dosage ; Ivabradine - pharmacology ; Male ; Muscular dystrophy ; Muscular Dystrophy, Duchenne - drug therapy ; Muscular Dystrophy, Duchenne - physiopathology ; Myopathy ; Original ; Rats ; Rats, Sprague-Dawley ; Respiration ; Tachycardia ; Tachycardia - drug therapy ; Ventricle</subject><ispartof>Experimental Animals, 2024, Vol.73(2), pp.145-153</ispartof><rights>2024Japanese Association for Laboratory Animal Science</rights><rights>2024. This work is published under https://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 Japanese Association for Laboratory Animal Science 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c607t-fec142478ceb8e751974a05d9534acd1183a407cc875d8ce3054ac042426129f3</citedby><cites>FETCH-LOGICAL-c607t-fec142478ceb8e751974a05d9534acd1183a407cc875d8ce3054ac042426129f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11091361/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11091361/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,1877,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37914289$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tochinai, Ryota</creatorcontrib><creatorcontrib>Kimura, Koichi</creatorcontrib><creatorcontrib>Saika, Takeru</creatorcontrib><creatorcontrib>Fujii, Wataru</creatorcontrib><creatorcontrib>Morita, Hiroyuki</creatorcontrib><creatorcontrib>Nakanishi, Koki</creatorcontrib><creatorcontrib>Tsuru, Yoshiharu</creatorcontrib><creatorcontrib>Sekizawa, Shin-ichi</creatorcontrib><creatorcontrib>Yamanouchi, Keitaro</creatorcontrib><creatorcontrib>Kuwahara, Masayoshi</creatorcontrib><title>Ivabradine ameliorates cardiomyopathy progression in a Duchenne muscular dystrophy model rat</title><title>Experimental Animals</title><addtitle>Exp Anim</addtitle><description>Duchenne muscular dystrophy (DMD) is an X-linked recessive myopathy caused by dystrophin mutations. Inevitable progressive cardiomyopathy is a current leading cause of premature death although respiratory management has improved the prognosis of patients with DMD. Recent evidence shows that reducing the heart rate is expected as one of the promising strategies for heart failure treatment, but administering a sufficient dose of β-blocker for patients with DMD with tachycardia is difficult because of their low blood pressure (BP). Thus, this study aimed to clarify the role of ivabradine, which suppresses cardiac sinus node pacemakers without decreasing BP, in ameliorating cardiomyopathy progression in a rat model with DMD. A trans-oral single ivabradine administration demonstrated a declined dose-dependent heart rate without any significant BP reduction. Trans-gastric repeated administrations of 5 mg/kg of ivabradine twice a day for 3 months showed ameliorated cardiomyopathy in DMD rats based on echocardiography and histopathological observations (left ventricular dysfunction, right ventricular dysfunction, and myocardial fibrosis) as compared with vehicle administration.Our finding indicates that ivabradine is expected as another treatment choice for patients with DMD having tachycardia.</description><subject>Animals</subject><subject>Blood pressure</subject><subject>Cardiac arrhythmia</subject><subject>Cardiomyopathies - drug therapy</subject><subject>Cardiomyopathies - etiology</subject><subject>Cardiomyopathy</subject><subject>Congestive heart failure</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Duchenne's muscular dystrophy</subject><subject>Dystrophin</subject><subject>dystrophin deficiency</subject><subject>Dystrophy</subject><subject>Echocardiography</subject><subject>Fibrosis</subject><subject>heart</subject><subject>Heart rate</subject><subject>Heart Rate - drug effects</subject><subject>hyperpolarization-activated cyclic nucleotide-gated (HCN) channel</subject><subject>Ivabradine - administration & dosage</subject><subject>Ivabradine - pharmacology</subject><subject>Male</subject><subject>Muscular dystrophy</subject><subject>Muscular Dystrophy, Duchenne - drug therapy</subject><subject>Muscular Dystrophy, Duchenne - physiopathology</subject><subject>Myopathy</subject><subject>Original</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Respiration</subject><subject>Tachycardia</subject><subject>Tachycardia - drug therapy</subject><subject>Ventricle</subject><issn>1341-1357</issn><issn>1881-7122</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1r3DAQxUVJadK0596CIWcnGsleyacQ8tEGAr20t4KYlWd3tdiSI9kh-99HyW5Ne5GE5vfePHiMfQN-AbXUl_QyoHf9hZAl51p9YCegNZQKhDjKb1lBCbJWx-xzSlvOhVKi-cSOpWqgEro5YX8ennEZsXWeCuypcyHiSKmwGFsX-l0YcNzsiiGGdaSUXPCF8wUWt5PdkM-ifkp26jAW7S6NMQwZ7kNLXZF9vrCPK-wSfT3cp-z3_d2vmx_l48_vDzfXj6VdcDWWK7I5TaW0paUmVUOjKuR129SyQtsCaIkVV9ZqVbcZkrzO_zxLxAJEs5Kn7GrvO0zLnlpLfozYmSG6HuPOBHTm_4l3G7MOzwaANyAXkB3ODw4xPE2URrMNU_Q5tJFcc97omotMXe4pG0NKkVbzCuDmrQ9z6MMIad76yIqzf5PN_N8CMnC3B7ZpxDXNAMbR2Y5mQyWNeD_2xvPcbjAa8vIVSv-jgA</recordid><startdate>20240101</startdate><enddate>20240101</enddate><creator>Tochinai, Ryota</creator><creator>Kimura, Koichi</creator><creator>Saika, Takeru</creator><creator>Fujii, Wataru</creator><creator>Morita, Hiroyuki</creator><creator>Nakanishi, Koki</creator><creator>Tsuru, Yoshiharu</creator><creator>Sekizawa, Shin-ichi</creator><creator>Yamanouchi, Keitaro</creator><creator>Kuwahara, Masayoshi</creator><general>Japanese Association for Laboratory Animal Science</general><general>Japan Science and Technology Agency</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>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20240101</creationdate><title>Ivabradine ameliorates cardiomyopathy progression in a Duchenne muscular dystrophy model rat</title><author>Tochinai, Ryota ; Kimura, Koichi ; Saika, Takeru ; Fujii, Wataru ; Morita, Hiroyuki ; Nakanishi, Koki ; Tsuru, Yoshiharu ; Sekizawa, Shin-ichi ; Yamanouchi, Keitaro ; Kuwahara, Masayoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c607t-fec142478ceb8e751974a05d9534acd1183a407cc875d8ce3054ac042426129f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Blood pressure</topic><topic>Cardiac arrhythmia</topic><topic>Cardiomyopathies - drug therapy</topic><topic>Cardiomyopathies - etiology</topic><topic>Cardiomyopathy</topic><topic>Congestive heart failure</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Duchenne's muscular dystrophy</topic><topic>Dystrophin</topic><topic>dystrophin deficiency</topic><topic>Dystrophy</topic><topic>Echocardiography</topic><topic>Fibrosis</topic><topic>heart</topic><topic>Heart rate</topic><topic>Heart Rate - drug effects</topic><topic>hyperpolarization-activated cyclic nucleotide-gated (HCN) channel</topic><topic>Ivabradine - administration & dosage</topic><topic>Ivabradine - pharmacology</topic><topic>Male</topic><topic>Muscular dystrophy</topic><topic>Muscular Dystrophy, Duchenne - drug therapy</topic><topic>Muscular Dystrophy, Duchenne - physiopathology</topic><topic>Myopathy</topic><topic>Original</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Respiration</topic><topic>Tachycardia</topic><topic>Tachycardia - drug therapy</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tochinai, Ryota</creatorcontrib><creatorcontrib>Kimura, Koichi</creatorcontrib><creatorcontrib>Saika, Takeru</creatorcontrib><creatorcontrib>Fujii, Wataru</creatorcontrib><creatorcontrib>Morita, Hiroyuki</creatorcontrib><creatorcontrib>Nakanishi, Koki</creatorcontrib><creatorcontrib>Tsuru, Yoshiharu</creatorcontrib><creatorcontrib>Sekizawa, Shin-ichi</creatorcontrib><creatorcontrib>Yamanouchi, Keitaro</creatorcontrib><creatorcontrib>Kuwahara, Masayoshi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental Animals</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tochinai, Ryota</au><au>Kimura, Koichi</au><au>Saika, Takeru</au><au>Fujii, Wataru</au><au>Morita, Hiroyuki</au><au>Nakanishi, Koki</au><au>Tsuru, Yoshiharu</au><au>Sekizawa, Shin-ichi</au><au>Yamanouchi, Keitaro</au><au>Kuwahara, Masayoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ivabradine ameliorates cardiomyopathy progression in a Duchenne muscular dystrophy model rat</atitle><jtitle>Experimental Animals</jtitle><addtitle>Exp Anim</addtitle><date>2024-01-01</date><risdate>2024</risdate><volume>73</volume><issue>2</issue><spage>145</spage><epage>153</epage><pages>145-153</pages><artnum>23-0087</artnum><issn>1341-1357</issn><eissn>1881-7122</eissn><abstract>Duchenne muscular dystrophy (DMD) is an X-linked recessive myopathy caused by dystrophin mutations. Inevitable progressive cardiomyopathy is a current leading cause of premature death although respiratory management has improved the prognosis of patients with DMD. Recent evidence shows that reducing the heart rate is expected as one of the promising strategies for heart failure treatment, but administering a sufficient dose of β-blocker for patients with DMD with tachycardia is difficult because of their low blood pressure (BP). Thus, this study aimed to clarify the role of ivabradine, which suppresses cardiac sinus node pacemakers without decreasing BP, in ameliorating cardiomyopathy progression in a rat model with DMD. A trans-oral single ivabradine administration demonstrated a declined dose-dependent heart rate without any significant BP reduction. Trans-gastric repeated administrations of 5 mg/kg of ivabradine twice a day for 3 months showed ameliorated cardiomyopathy in DMD rats based on echocardiography and histopathological observations (left ventricular dysfunction, right ventricular dysfunction, and myocardial fibrosis) as compared with vehicle administration.Our finding indicates that ivabradine is expected as another treatment choice for patients with DMD having tachycardia.</abstract><cop>Japan</cop><pub>Japanese Association for Laboratory Animal Science</pub><pmid>37914289</pmid><doi>10.1538/expanim.23-0087</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Blood pressure Cardiac arrhythmia Cardiomyopathies - drug therapy Cardiomyopathies - etiology Cardiomyopathy Congestive heart failure Disease Models, Animal Disease Progression Duchenne's muscular dystrophy Dystrophin dystrophin deficiency Dystrophy Echocardiography Fibrosis heart Heart rate Heart Rate - drug effects hyperpolarization-activated cyclic nucleotide-gated (HCN) channel Ivabradine - administration & dosage Ivabradine - pharmacology Male Muscular dystrophy Muscular Dystrophy, Duchenne - drug therapy Muscular Dystrophy, Duchenne - physiopathology Myopathy Original Rats Rats, Sprague-Dawley Respiration Tachycardia Tachycardia - drug therapy Ventricle |
| title | Ivabradine ameliorates cardiomyopathy progression in a Duchenne muscular dystrophy model rat |
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