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Can echocardiograph...
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Gustavsson, SandraUmeå universitet,Klinisk fysiologi,Kardiologi,Heart Centre
(author)
Can echocardiography and ECG discriminate hereditary transthyretin V30M amyloidosis from hypertrophic cardiomyopathy?
- Article/chapterEnglish2015
Publisher, publication year, extent ...
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2015-06-24
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Informa UK Limited,2015
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:umu-109962
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https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-109962URI
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https://doi.org/10.3109/13506129.2015.1037831DOI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Objective: Hereditary transthyretin (ATTR) amyloidosis with increased left ventricular wall thickness could easily be misdiagnosed by echocardiography as hypertrophic cardiomyopathy (HCM). Our aim was to create a diagnostic tool based on echocardiography and ECG that could optimise identification of ATTR amyloidosis. Methods: Data were analysed from 33 patients with biopsy proven ATTR amyloidosis and 30 patients with diagnosed HCM. Conventional features from ECG were acquired as well as two dimensional and Doppler echocardiography, speckle tracking derived strain and tissue characterisation analysis. Classification trees were used to select the most important variables for differentiation between ATTR amyloidosis and HCM. Results: The best classification was obtained using both ECG and echocardiographic features, where a QRS voltage >30 mm was diagnostic for HCM, whereas in patients with QRS voltage <30 mm, an interventricular septal/posterior wall thickness ratio (IVSt/PWt) >1.6 was consistent with HCM and a ratio <1.6 supported the diagnosis of ATTR amyloidosis. This classification presented both high sensitivity (0.939) and specificity (0.833). Conclusion: Our study proposes an easily interpretable classification method for the differentiation between HCM and increased left ventricular myocardial thickness due to ATTR amyloidosis. Our combined echocardiographic and ECG model could increase the ability to identify ATTR cardiac amyloidosis in clinical practice.
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Added entries (persons, corporate bodies, meetings, titles ...)
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Granåsen, GabrielUmeå universitet,Institutionen för strålningsvetenskaper(Swepub:umu)galgrn00
(author)
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Grönlund, ChristerUmeå universitet,Institutionen för strålningsvetenskaper,Centrum för medicinsk teknik och fysik (CMTF)(Swepub:umu)chgr0009
(author)
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Wiklund, UrbanUmeå universitet,Institutionen för strålningsvetenskaper(Swepub:umu)urwi0001
(author)
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Mörner, StellanUmeå universitet,Kardiologi(Swepub:umu)stmo0005
(author)
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Henein, MichaelUmeå universitet,Kardiologi(Swepub:umu)mihe0015
(author)
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Suhr, Ole BUmeå universitet,Medicin(Swepub:umu)olsu0002
(author)
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Lindqvist, PerUmeå universitet,Klinisk fysiologi,Kardiologi(Swepub:umu)peli0011
(author)
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Umeå universitetKlinisk fysiologi
(creator_code:org_t)
Related titles
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In:Amyloid: Informa UK Limited22:3, s. 163-1701350-61291744-2818
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