CMR derived left ventricular septal convexity in carriers of the hypertrophic cardiomyopathy-causing MYBPC3-Q1061X mutation
This manuscript has not been published before and is not currently being considered for publication elsewhere. Increased septal convexity of left ventricle has been described in subjects with hypertrophic cardiomyopathy (HCM) -causing mutations without left ventricular hypertrophy (LVH). Our objecti...
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| description | This manuscript has not been published before and is not currently being considered for publication elsewhere. Increased septal convexity of left ventricle has been described in subjects with hypertrophic cardiomyopathy (HCM) -causing mutations without left ventricular hypertrophy (LVH). Our objective was to study septal convexity by cardiac magnetic resonance (CMR) in subjects with the Finnish founder mutation Q1016X in the myosin-binding protein C gene (
MYBPC3)
. Septal convexity was measured in end-diastolic 4-chamber CMR image in 67 study subjects (47 subjects with the
MYBPC3
-Q1061X mutation and 20 healthy relatives without the mutation). Septal convexity was significantly increased in subjects with the
MYBPC3
-Q1061X mutation and LVH (n = 32) compared to controls (11.4 ± 4.3 vs 2.7 ± 3.2 mm,
P
|
| doi_str_mv | 10.1038/s41598-019-42376-7 |
| format | Article |
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MYBPC3)
. Septal convexity was measured in end-diastolic 4-chamber CMR image in 67 study subjects (47 subjects with the
MYBPC3
-Q1061X mutation and 20 healthy relatives without the mutation). Septal convexity was significantly increased in subjects with the
MYBPC3
-Q1061X mutation and LVH (n = 32) compared to controls (11.4 ± 4.3 vs 2.7 ± 3.2 mm,
P
< 0.001). In mutation carriers without LVH, there was a trend for increased septal convexity compared to controls (4.9 ± 2.5 vs 2.7 ± 3.2 mm,
P
= 0.074). When indexed for BSA, septal convexity in mutation carriers without LVH was 2.8 ± 1.4 mm/m
2
and 1.5 ± 1.6 mm/m
2
in controls (
P
= 0.036). In all mutation carriers, septal convexity correlated significantly with body surface area, age, maximal LV wall thickness, LV mass, and late gadolinium enhancement. Subjects with the
MYBPC3
–Q10961X mutation have increased septal convexity irrespective of the presence of LVH. Septal convexity appears to reflect septal remodeling, and could be useful in recognizing LVH negative mutation carriers.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-42376-7</identifier><identifier>PMID: 30976029</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/4019 ; 692/4019/592/1540 ; 692/698 ; Adult ; C gene ; Cardiomyopathy ; Cardiomyopathy, Hypertrophic - complications ; Cardiomyopathy, Hypertrophic - epidemiology ; Cardiomyopathy, Hypertrophic - genetics ; Carrier Proteins - genetics ; Case-Control Studies ; Echocardiography ; Electrocardiography ; Female ; Finland - epidemiology ; Gadolinium ; Genetic Predisposition to Disease ; Heart ; Heart Septum - diagnostic imaging ; Heart Septum - pathology ; Humanities and Social Sciences ; Humans ; Hypertrophy ; Hypertrophy, Left Ventricular - diagnostic imaging ; Hypertrophy, Left Ventricular - etiology ; Hypertrophy, Left Ventricular - pathology ; Magnetic Resonance Imaging, Cine - methods ; Male ; Middle Aged ; multidisciplinary ; Mutation ; Myosin ; Myosin-binding protein C ; Phenotype ; Protein C ; Science ; Science (multidisciplinary) ; Ventricle</subject><ispartof>Scientific reports, 2019-04, Vol.9 (1), p.5960-5960, Article 5960</ispartof><rights>The Author(s) 2019</rights><rights>The Author(s) 2019. 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-d59fa6ae787d91def19f4c0a0f20549a2131b68db0169c660bd5e108f17a35fb3</citedby><cites>FETCH-LOGICAL-c474t-d59fa6ae787d91def19f4c0a0f20549a2131b68db0169c660bd5e108f17a35fb3</cites><orcidid>0000-0001-5409-3300</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/PMC6459818/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6459818/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,41099,42168,51554,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30976029$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tarkiainen, Mika</creatorcontrib><creatorcontrib>Sipola, Petri</creatorcontrib><creatorcontrib>Jalanko, Mikko</creatorcontrib><creatorcontrib>Heliö, Tiina</creatorcontrib><creatorcontrib>Jääskeläinen, Pertti</creatorcontrib><creatorcontrib>Kivelä, Kati</creatorcontrib><creatorcontrib>Laine, Mika</creatorcontrib><creatorcontrib>Lauerma, Kirsi</creatorcontrib><creatorcontrib>Kuusisto, Johanna</creatorcontrib><title>CMR derived left ventricular septal convexity in carriers of the hypertrophic cardiomyopathy-causing MYBPC3-Q1061X mutation</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>This manuscript has not been published before and is not currently being considered for publication elsewhere. Increased septal convexity of left ventricle has been described in subjects with hypertrophic cardiomyopathy (HCM) -causing mutations without left ventricular hypertrophy (LVH). Our objective was to study septal convexity by cardiac magnetic resonance (CMR) in subjects with the Finnish founder mutation Q1016X in the myosin-binding protein C gene (
MYBPC3)
. Septal convexity was measured in end-diastolic 4-chamber CMR image in 67 study subjects (47 subjects with the
MYBPC3
-Q1061X mutation and 20 healthy relatives without the mutation). Septal convexity was significantly increased in subjects with the
MYBPC3
-Q1061X mutation and LVH (n = 32) compared to controls (11.4 ± 4.3 vs 2.7 ± 3.2 mm,
P
< 0.001). In mutation carriers without LVH, there was a trend for increased septal convexity compared to controls (4.9 ± 2.5 vs 2.7 ± 3.2 mm,
P
= 0.074). When indexed for BSA, septal convexity in mutation carriers without LVH was 2.8 ± 1.4 mm/m
2
and 1.5 ± 1.6 mm/m
2
in controls (
P
= 0.036). In all mutation carriers, septal convexity correlated significantly with body surface area, age, maximal LV wall thickness, LV mass, and late gadolinium enhancement. Subjects with the
MYBPC3
–Q10961X mutation have increased septal convexity irrespective of the presence of LVH. Septal convexity appears to reflect septal remodeling, and could be useful in recognizing LVH negative mutation carriers.</description><subject>692/4019</subject><subject>692/4019/592/1540</subject><subject>692/698</subject><subject>Adult</subject><subject>C gene</subject><subject>Cardiomyopathy</subject><subject>Cardiomyopathy, Hypertrophic - complications</subject><subject>Cardiomyopathy, Hypertrophic - epidemiology</subject><subject>Cardiomyopathy, Hypertrophic - genetics</subject><subject>Carrier Proteins - genetics</subject><subject>Case-Control Studies</subject><subject>Echocardiography</subject><subject>Electrocardiography</subject><subject>Female</subject><subject>Finland - epidemiology</subject><subject>Gadolinium</subject><subject>Genetic Predisposition to Disease</subject><subject>Heart</subject><subject>Heart Septum - diagnostic imaging</subject><subject>Heart Septum - pathology</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Hypertrophy, Left Ventricular - diagnostic imaging</subject><subject>Hypertrophy, Left Ventricular - etiology</subject><subject>Hypertrophy, Left Ventricular - pathology</subject><subject>Magnetic Resonance Imaging, Cine - methods</subject><subject>Male</subject><subject>Middle Aged</subject><subject>multidisciplinary</subject><subject>Mutation</subject><subject>Myosin</subject><subject>Myosin-binding protein C</subject><subject>Phenotype</subject><subject>Protein C</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Ventricle</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kUtv1TAUhCNERau2f4AFssSGjYsfSRxvkOCKl9SKh0CCleU4xzeukji1nSui_nmS3rYUFnhjS_OdsceTZU8pOaOEVy9jTgtZYUIlzhkXJRaPsiNG8gIzztjjB-fD7DTGS7KsgsmcyifZISdSlITJo-x6c_EVNRDcDhrUgU1oB0MKzkydDijCmHSHjB928MulGbkBGR2CgxCRtyi1gNp5hJCCH1tnVrFxvp_9qFM7Y6On6IYtuvj55vOG4y-UlPQH6qekk_PDSXZgdRfh9HY_zr6_e_tt8wGff3r_cfP6HJtc5Ak3hbS61CAq0UjagKXS5oZoYhkpcqkZ5bQuq6YmtJSmLEndFEBJZanQvLA1P85e7X3Hqe6hMWtA3akxuF6HWXnt1N_K4Fq19TtV5ssX02oxeHFrEPzVBDGp3kUDXacH8FNUjBFZSFEIvqDP_0Ev_RSGJd5KCVkxwVaK7SkTfIwB7P1jKFFrvWpfr1rqVTf1KrEMPXsY437krswF4HsgLtKwhfDn7v_Y_gahFrIZ</recordid><startdate>20190411</startdate><enddate>20190411</enddate><creator>Tarkiainen, Mika</creator><creator>Sipola, Petri</creator><creator>Jalanko, Mikko</creator><creator>Heliö, Tiina</creator><creator>Jääskeläinen, Pertti</creator><creator>Kivelä, Kati</creator><creator>Laine, Mika</creator><creator>Lauerma, Kirsi</creator><creator>Kuusisto, Johanna</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5409-3300</orcidid></search><sort><creationdate>20190411</creationdate><title>CMR derived left ventricular septal convexity in carriers of the hypertrophic cardiomyopathy-causing MYBPC3-Q1061X mutation</title><author>Tarkiainen, Mika ; Sipola, Petri ; Jalanko, Mikko ; Heliö, Tiina ; Jääskeläinen, Pertti ; Kivelä, Kati ; Laine, Mika ; Lauerma, Kirsi ; Kuusisto, Johanna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-d59fa6ae787d91def19f4c0a0f20549a2131b68db0169c660bd5e108f17a35fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>692/4019</topic><topic>692/4019/592/1540</topic><topic>692/698</topic><topic>Adult</topic><topic>C gene</topic><topic>Cardiomyopathy</topic><topic>Cardiomyopathy, Hypertrophic - complications</topic><topic>Cardiomyopathy, Hypertrophic - epidemiology</topic><topic>Cardiomyopathy, Hypertrophic - genetics</topic><topic>Carrier Proteins - genetics</topic><topic>Case-Control Studies</topic><topic>Echocardiography</topic><topic>Electrocardiography</topic><topic>Female</topic><topic>Finland - epidemiology</topic><topic>Gadolinium</topic><topic>Genetic Predisposition to Disease</topic><topic>Heart</topic><topic>Heart Septum - diagnostic imaging</topic><topic>Heart Septum - pathology</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Hypertrophy</topic><topic>Hypertrophy, Left Ventricular - diagnostic imaging</topic><topic>Hypertrophy, Left Ventricular - etiology</topic><topic>Hypertrophy, Left Ventricular - pathology</topic><topic>Magnetic Resonance Imaging, Cine - methods</topic><topic>Male</topic><topic>Middle Aged</topic><topic>multidisciplinary</topic><topic>Mutation</topic><topic>Myosin</topic><topic>Myosin-binding protein C</topic><topic>Phenotype</topic><topic>Protein C</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tarkiainen, Mika</creatorcontrib><creatorcontrib>Sipola, Petri</creatorcontrib><creatorcontrib>Jalanko, Mikko</creatorcontrib><creatorcontrib>Heliö, Tiina</creatorcontrib><creatorcontrib>Jääskeläinen, Pertti</creatorcontrib><creatorcontrib>Kivelä, Kati</creatorcontrib><creatorcontrib>Laine, Mika</creatorcontrib><creatorcontrib>Lauerma, Kirsi</creatorcontrib><creatorcontrib>Kuusisto, Johanna</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tarkiainen, Mika</au><au>Sipola, Petri</au><au>Jalanko, Mikko</au><au>Heliö, Tiina</au><au>Jääskeläinen, Pertti</au><au>Kivelä, Kati</au><au>Laine, Mika</au><au>Lauerma, Kirsi</au><au>Kuusisto, Johanna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CMR derived left ventricular septal convexity in carriers of the hypertrophic cardiomyopathy-causing MYBPC3-Q1061X mutation</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-04-11</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>5960</spage><epage>5960</epage><pages>5960-5960</pages><artnum>5960</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>This manuscript has not been published before and is not currently being considered for publication elsewhere. Increased septal convexity of left ventricle has been described in subjects with hypertrophic cardiomyopathy (HCM) -causing mutations without left ventricular hypertrophy (LVH). Our objective was to study septal convexity by cardiac magnetic resonance (CMR) in subjects with the Finnish founder mutation Q1016X in the myosin-binding protein C gene (
MYBPC3)
. Septal convexity was measured in end-diastolic 4-chamber CMR image in 67 study subjects (47 subjects with the
MYBPC3
-Q1061X mutation and 20 healthy relatives without the mutation). Septal convexity was significantly increased in subjects with the
MYBPC3
-Q1061X mutation and LVH (n = 32) compared to controls (11.4 ± 4.3 vs 2.7 ± 3.2 mm,
P
< 0.001). In mutation carriers without LVH, there was a trend for increased septal convexity compared to controls (4.9 ± 2.5 vs 2.7 ± 3.2 mm,
P
= 0.074). When indexed for BSA, septal convexity in mutation carriers without LVH was 2.8 ± 1.4 mm/m
2
and 1.5 ± 1.6 mm/m
2
in controls (
P
= 0.036). In all mutation carriers, septal convexity correlated significantly with body surface area, age, maximal LV wall thickness, LV mass, and late gadolinium enhancement. Subjects with the
MYBPC3
–Q10961X mutation have increased septal convexity irrespective of the presence of LVH. Septal convexity appears to reflect septal remodeling, and could be useful in recognizing LVH negative mutation carriers.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30976029</pmid><doi>10.1038/s41598-019-42376-7</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-5409-3300</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Nature Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; Springer Nature OA/Free Journals; Free Full-Text Journals in Chemistry |
| subjects | 692/4019 692/4019/592/1540 692/698 Adult C gene Cardiomyopathy Cardiomyopathy, Hypertrophic - complications Cardiomyopathy, Hypertrophic - epidemiology Cardiomyopathy, Hypertrophic - genetics Carrier Proteins - genetics Case-Control Studies Echocardiography Electrocardiography Female Finland - epidemiology Gadolinium Genetic Predisposition to Disease Heart Heart Septum - diagnostic imaging Heart Septum - pathology Humanities and Social Sciences Humans Hypertrophy Hypertrophy, Left Ventricular - diagnostic imaging Hypertrophy, Left Ventricular - etiology Hypertrophy, Left Ventricular - pathology Magnetic Resonance Imaging, Cine - methods Male Middle Aged multidisciplinary Mutation Myosin Myosin-binding protein C Phenotype Protein C Science Science (multidisciplinary) Ventricle |
| title | CMR derived left ventricular septal convexity in carriers of the hypertrophic cardiomyopathy-causing MYBPC3-Q1061X mutation |
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