<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nakano T</submitter><funding>AMED, Practical Research Project for Rare/Intractable Diseases</funding><funding>MEXT KAKENHI, Grants-in-aid from the Ministry of Education, Culture, Sports, Science</funding><funding>AMED, Practical Research Project for Life-Style related Diseases including Cardiovascular Diseases and Diabetes Mellitus</funding><funding>Health Labour Sciences Research, Technology and the Ministry of Health, Labor, and Welfare of Japan</funding><funding>AMED, Platform Program for Promotion of Genome Medicine</funding><pagination>792</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9147607</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(5)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Transthyretin (TTR) amyloid cardiomyopathy (ATTR-CM) is increasingly being recognized as a cause of left ventricular (LV) hypertrophy (LVH) and progressive heart failure in elderly patients. However, little is known about the cardiac morphology of ATTR-CM and the association between the degree of TTR amyloid deposition and cardiac dysfunction in these patients.&lt;h4>Methods&lt;/h4>We studied 28 consecutive patients with ATTR-CM and analyzed the relationship between echocardiographic parameters and pathological features using endomyocardial biopsy samples.&lt;h4>Results&lt;/h4>The cardiac geometries of patients with ATTR-CM were mainly classified as concentric LVH (96.4%). The relative wall thickness, a marker of LVH, tended to be positively correlated with the degree of non-cardiom</pubmed_abstract><journal>Journal of personalized medicine</journal><pubmed_title>Transthyretin Amyloid Cardiomyopathy: Impact of Transthyretin Amyloid Deposition in Myocardium on Cardiac Morphology and Function.</pubmed_title><pmcid>PMC9147607</pmcid><funding_grant_id>JP19km0405009</funding_grant_id><funding_grant_id>JP19ek0109367, JP19ek0109406</funding_grant_id><funding_grant_id>JP19ek0210080, JP19ek0210118, JP19ek0210121, JP19ek0210115</funding_grant_id><funding_grant_id>19189094, 17933459</funding_grant_id><funding_grant_id>JP19155855</funding_grant_id><pubmed_authors>Hoshii Y</pubmed_authors><pubmed_authors>Terada C</pubmed_authors><pubmed_authors>Saito Y</pubmed_authors><pubmed_authors>Nakano T</pubmed_authors><pubmed_authors>Nakada Y</pubmed_authors><pubmed_authors>Ueda T</pubmed_authors><pubmed_authors>Hatakeyama K</pubmed_authors><pubmed_authors>Hashimoto Y</pubmed_authors><pubmed_authors>Nakagawa H</pubmed_authors><pubmed_authors>Seno A</pubmed_authors><pubmed_authors>Watanabe M</pubmed_authors><pubmed_authors>Sakaguchi Y</pubmed_authors><pubmed_authors>Nishida T</pubmed_authors><pubmed_authors>Ohbayashi C</pubmed_authors><pubmed_authors>Ishihara S</pubmed_authors><pubmed_authors>Terasaki S</pubmed_authors><pubmed_authors>Onoue K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transthyretin Amyloid Cardiomyopathy: Impact of Transthyretin Amyloid Deposition in Myocardium on Cardiac Morphology and Function.</name><description>&lt;h4>Background&lt;/h4>Transthyretin (TTR) amyloid cardiomyopathy (ATTR-CM) is increasingly being recognized as a cause of left ventricular (LV) hypertrophy (LVH) and progressive heart failure in elderly patients. However, little is known about the cardiac morphology of ATTR-CM and the association between the degree of TTR amyloid deposition and cardiac dysfunction in these patients.&lt;h4>Methods&lt;/h4>We studied 28 consecutive patients with ATTR-CM and analyzed the relationship between echocardiographic parameters and pathological features using endomyocardial biopsy samples.&lt;h4>Results&lt;/h4>The cardiac geometries of patients with ATTR-CM were mainly classified as concentric LVH (96.4%). The relative wall thickness, a marker of LVH, tended to be positively correlated with the degree of non-cardiom</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 May</publication><modification>2025-05-29T14:36:21.096Z</modification><creation>2025-02-19T02:16:19.215Z</creation></dates><accession>S-EPMC9147607</accession><cross_references><pubmed>35629214</pubmed><doi>10.3390/jpm12050792</doi></cross_references></HashMap>