The effect of the heart rate lowering drug Ivabradine on hemodynamics in atherosclerotic mice
The heart rate lowering drug Ivabradine was shown to improve cardiac outcome in patients with previous heart failure. However, in patients without heart failure, no beneficial effect of Ivabradine was observed. Animal studies suggested a preventive effect of Ivabradine on atherosclerosis which was d...
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| creator | Xing, R. Moerman, A. M. Ridwan, R. Y. Gaalen, K. van Meester, E. J. van der Steen, A. F. W. Evans, P. C. Gijsen, F. J. H. Van der Heiden, K. |
| description | The heart rate lowering drug Ivabradine was shown to improve cardiac outcome in patients with previous heart failure. However, in patients without heart failure, no beneficial effect of Ivabradine was observed. Animal studies suggested a preventive effect of Ivabradine on atherosclerosis which was due to an increase in wall shear stress (WSS), the blood flow-induced frictional force exerted on the endothelium, triggering anti-inflammatory responses. However, data on the effect of Ivabradine on WSS is sparse. We aim to study the effect of Ivabradine on (i) the 3D WSS distribution over a growing plaque and (ii) plaque composition. We induced atherosclerosis in ApoE
−/−
mice by placing a tapered cast around the right common carotid artery (RCCA). Five weeks after cast placement, Ivabradine was administered via drinking water (15 mg/kg/day) for 2 weeks, after which the RCCA was excised for histology analyses. Before and after Ivabradine treatment, animals were imaged with Doppler Ultrasound to measure blood velocity. Vessel geometry was obtained using contrast-enhanced micro-CT. Time-averaged WSS during systole, diastole and peak WSS was subsequently computed. Ivabradine significantly decreased heart rate (459 ± 28 bpm vs. 567 ± 32 bpm, p |
| doi_str_mv | 10.1038/s41598-018-32458-3 |
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−/−
mice by placing a tapered cast around the right common carotid artery (RCCA). Five weeks after cast placement, Ivabradine was administered via drinking water (15 mg/kg/day) for 2 weeks, after which the RCCA was excised for histology analyses. Before and after Ivabradine treatment, animals were imaged with Doppler Ultrasound to measure blood velocity. Vessel geometry was obtained using contrast-enhanced micro-CT. Time-averaged WSS during systole, diastole and peak WSS was subsequently computed. Ivabradine significantly decreased heart rate (459 ± 28 bpm vs. 567 ± 32 bpm, p < 0.001). Normalized peak flow significantly increased in the Ivabradine group (124.2% ± 40.5% vs. 87.3% ± 25.4%, p < 0.05), reflected by an increased normalized WSS level during systole (110.7% ± 18.4% vs. 75.4% ± 24.6%, p < 0.05). However, plaque size or composition including plaque area, relative necrotic core area and macrophage content were not altered in mice treated with Ivabradine compared to controls. We conclude that increased WSS in response to Ivabradine treatment did not affect plaque progression in a murine model.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-32458-3</identifier><identifier>PMID: 30228313</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 59 ; 639/766/189 ; 64/60 ; 692/4019/592/75/593/2100 ; Animal models ; Animals ; Apolipoprotein E ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - drug therapy ; Atherosclerosis - pathology ; Blood flow ; Cardiovascular Agents - pharmacology ; Carotid artery ; Circulatory system ; Computed tomography ; Disease Models, Animal ; Doppler effect ; Drinking water ; Endothelium ; Heart diseases ; Heart failure ; Heart rate ; Heart Rate - drug effects ; Heart Rate - physiology ; Hemodynamics ; Histology ; Humanities and Social Sciences ; Inflammation ; Ivabradine - pharmacology ; Macrophages ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout, ApoE ; multidisciplinary ; Patients ; Plaque, Atherosclerotic - pathology ; Plaque, Atherosclerotic - prevention & control ; Science ; Science (multidisciplinary) ; Shear stress ; Stress, Mechanical ; Ultrasound</subject><ispartof>Scientific reports, 2018-09, Vol.8 (1), p.14014-7, Article 14014</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-c7ec5905b20131c20992c0a3f89d89f25ea17a489d8bd7ab9f3c9ef1b585a8f73</citedby><cites>FETCH-LOGICAL-c474t-c7ec5905b20131c20992c0a3f89d89f25ea17a489d8bd7ab9f3c9ef1b585a8f73</cites><orcidid>0000-0003-2680-5117</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6143553/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6143553/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30228313$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xing, R.</creatorcontrib><creatorcontrib>Moerman, A. M.</creatorcontrib><creatorcontrib>Ridwan, R. Y.</creatorcontrib><creatorcontrib>Gaalen, K. van</creatorcontrib><creatorcontrib>Meester, E. J.</creatorcontrib><creatorcontrib>van der Steen, A. F. W.</creatorcontrib><creatorcontrib>Evans, P. C.</creatorcontrib><creatorcontrib>Gijsen, F. J. H.</creatorcontrib><creatorcontrib>Van der Heiden, K.</creatorcontrib><title>The effect of the heart rate lowering drug Ivabradine on hemodynamics in atherosclerotic mice</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>The heart rate lowering drug Ivabradine was shown to improve cardiac outcome in patients with previous heart failure. However, in patients without heart failure, no beneficial effect of Ivabradine was observed. Animal studies suggested a preventive effect of Ivabradine on atherosclerosis which was due to an increase in wall shear stress (WSS), the blood flow-induced frictional force exerted on the endothelium, triggering anti-inflammatory responses. However, data on the effect of Ivabradine on WSS is sparse. We aim to study the effect of Ivabradine on (i) the 3D WSS distribution over a growing plaque and (ii) plaque composition. We induced atherosclerosis in ApoE
−/−
mice by placing a tapered cast around the right common carotid artery (RCCA). Five weeks after cast placement, Ivabradine was administered via drinking water (15 mg/kg/day) for 2 weeks, after which the RCCA was excised for histology analyses. Before and after Ivabradine treatment, animals were imaged with Doppler Ultrasound to measure blood velocity. Vessel geometry was obtained using contrast-enhanced micro-CT. Time-averaged WSS during systole, diastole and peak WSS was subsequently computed. Ivabradine significantly decreased heart rate (459 ± 28 bpm vs. 567 ± 32 bpm, p < 0.001). Normalized peak flow significantly increased in the Ivabradine group (124.2% ± 40.5% vs. 87.3% ± 25.4%, p < 0.05), reflected by an increased normalized WSS level during systole (110.7% ± 18.4% vs. 75.4% ± 24.6%, p < 0.05). However, plaque size or composition including plaque area, relative necrotic core area and macrophage content were not altered in mice treated with Ivabradine compared to controls. We conclude that increased WSS in response to Ivabradine treatment did not affect plaque progression in a murine model.</description><subject>13/51</subject><subject>59</subject><subject>639/766/189</subject><subject>64/60</subject><subject>692/4019/592/75/593/2100</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apolipoprotein E</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - drug therapy</subject><subject>Atherosclerosis - pathology</subject><subject>Blood flow</subject><subject>Cardiovascular Agents - pharmacology</subject><subject>Carotid artery</subject><subject>Circulatory system</subject><subject>Computed tomography</subject><subject>Disease Models, Animal</subject><subject>Doppler effect</subject><subject>Drinking water</subject><subject>Endothelium</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart rate</subject><subject>Heart Rate - drug effects</subject><subject>Heart Rate - physiology</subject><subject>Hemodynamics</subject><subject>Histology</subject><subject>Humanities and Social Sciences</subject><subject>Inflammation</subject><subject>Ivabradine - pharmacology</subject><subject>Macrophages</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout, ApoE</subject><subject>multidisciplinary</subject><subject>Patients</subject><subject>Plaque, Atherosclerotic - pathology</subject><subject>Plaque, Atherosclerotic - prevention & control</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Shear stress</subject><subject>Stress, Mechanical</subject><subject>Ultrasound</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc9vFSEQx4nR2Kb2H_BgSLx4WYUBunAxMY0_mjTxUo-GsOzwHs0uPGG3Tf97eb5aqwc5DAx8ZpiZLyEvOXvLmdDvquTK6I5x3QmQqtkn5BiYVB0IgKePzkfktNZr1pYCI7l5To4EA9CCi2Py_WqLFENAv9Ac6NK8Lbqy0OIWpFO-xRLTho5l3dCLGzcUN8aENKeGzXm8S26OvtKYqGuxJVc_NbtET9s9viDPgpsqnt7vJ-Tbp49X51-6y6-fL84_XHZe9nLpfI9eGaYGYFxwD8wY8MyJoM2oTQCFjvdO7r1h7N1ggvAGAx-UVk6HXpyQ94e8u3WYcfSYluImuytxduXOZhft3y8pbu0m39gzLoVSoiV4c5-g5B8r1sXOsXqcJpcwr9UC58DNGYBs6Ot_0Ou8ltTaaxTTbaxSq0bBgfJtJrVgeCiGM7sX0B4EtE1A-0tAu6_i1eM2HkJ-y9UAcQDqbi8Llj9__yftT0jKpx4</recordid><startdate>20180918</startdate><enddate>20180918</enddate><creator>Xing, R.</creator><creator>Moerman, A. 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M. ; Ridwan, R. Y. ; Gaalen, K. van ; Meester, E. J. ; van der Steen, A. F. W. ; Evans, P. C. ; Gijsen, F. J. 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M.</au><au>Ridwan, R. Y.</au><au>Gaalen, K. van</au><au>Meester, E. J.</au><au>van der Steen, A. F. W.</au><au>Evans, P. C.</au><au>Gijsen, F. J. H.</au><au>Van der Heiden, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effect of the heart rate lowering drug Ivabradine on hemodynamics in atherosclerotic mice</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-09-18</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>14014</spage><epage>7</epage><pages>14014-7</pages><artnum>14014</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The heart rate lowering drug Ivabradine was shown to improve cardiac outcome in patients with previous heart failure. However, in patients without heart failure, no beneficial effect of Ivabradine was observed. Animal studies suggested a preventive effect of Ivabradine on atherosclerosis which was due to an increase in wall shear stress (WSS), the blood flow-induced frictional force exerted on the endothelium, triggering anti-inflammatory responses. However, data on the effect of Ivabradine on WSS is sparse. We aim to study the effect of Ivabradine on (i) the 3D WSS distribution over a growing plaque and (ii) plaque composition. We induced atherosclerosis in ApoE
−/−
mice by placing a tapered cast around the right common carotid artery (RCCA). Five weeks after cast placement, Ivabradine was administered via drinking water (15 mg/kg/day) for 2 weeks, after which the RCCA was excised for histology analyses. Before and after Ivabradine treatment, animals were imaged with Doppler Ultrasound to measure blood velocity. Vessel geometry was obtained using contrast-enhanced micro-CT. Time-averaged WSS during systole, diastole and peak WSS was subsequently computed. Ivabradine significantly decreased heart rate (459 ± 28 bpm vs. 567 ± 32 bpm, p < 0.001). Normalized peak flow significantly increased in the Ivabradine group (124.2% ± 40.5% vs. 87.3% ± 25.4%, p < 0.05), reflected by an increased normalized WSS level during systole (110.7% ± 18.4% vs. 75.4% ± 24.6%, p < 0.05). However, plaque size or composition including plaque area, relative necrotic core area and macrophage content were not altered in mice treated with Ivabradine compared to controls. We conclude that increased WSS in response to Ivabradine treatment did not affect plaque progression in a murine model.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30228313</pmid><doi>10.1038/s41598-018-32458-3</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0003-2680-5117</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/51 59 639/766/189 64/60 692/4019/592/75/593/2100 Animal models Animals Apolipoprotein E Arteriosclerosis Atherosclerosis Atherosclerosis - drug therapy Atherosclerosis - pathology Blood flow Cardiovascular Agents - pharmacology Carotid artery Circulatory system Computed tomography Disease Models, Animal Doppler effect Drinking water Endothelium Heart diseases Heart failure Heart rate Heart Rate - drug effects Heart Rate - physiology Hemodynamics Histology Humanities and Social Sciences Inflammation Ivabradine - pharmacology Macrophages Male Mice Mice, Inbred C57BL Mice, Knockout, ApoE multidisciplinary Patients Plaque, Atherosclerotic - pathology Plaque, Atherosclerotic - prevention & control Science Science (multidisciplinary) Shear stress Stress, Mechanical Ultrasound |
| title | The effect of the heart rate lowering drug Ivabradine on hemodynamics in atherosclerotic mice |
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