ATTR Epidemiology, Genetics, and Prognostic Factors

Transthyretin amyloid cardiomyopathy (ATTR-CM) is an underdiagnosed disease and an underestimated cause of both heart failure and conduction abnormalities. It is characterized by pathologic accumulation of extracellular protein arising from unstable transthyretin (TTR) tetramers, which dissociate in...

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Main Authors: Chukwuemeka A. Obi, William C. Mostertz, Jan M. Griffin, Daniel P. Judge
Format: Article
Language:English
Published: Houston Methodist DeBakey Heart & Vascular Center 2022-03-01
Series:Methodist DeBakey Cardiovascular Journal
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Online Access:https://account.journal.houstonmethodist.org/index.php/up-j-mdbcj/article/view/1066
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author Chukwuemeka A. Obi
William C. Mostertz
Jan M. Griffin
Daniel P. Judge
author_facet Chukwuemeka A. Obi
William C. Mostertz
Jan M. Griffin
Daniel P. Judge
author_sort Chukwuemeka A. Obi
collection DOAJ
description Transthyretin amyloid cardiomyopathy (ATTR-CM) is an underdiagnosed disease and an underestimated cause of both heart failure and conduction abnormalities. It is characterized by pathologic accumulation of extracellular protein arising from unstable transthyretin (TTR) tetramers, which dissociate into monomers that misfold, aggregate, and form insoluble fibrils that are resistant to proteolysis. Cardiac amyloidosis appears in two distinct forms: hereditary and wild-type. There is considerable heterogeneity in the clinical presentation of ATTR, ranging from primarily cardiac, primarily neuropathic, or mixed cardiac and neuropathic disease. Pathogenic variants in the TTR gene that predominantly involve the heart include Val122Ile, Leu111Met, and Ile68Leu. The wild-type form of ATTR is also predominantly cardiac. Phenotypic heterogeneity is linked to differences among specific pathogenic TTR variants, geography, and the subtype of endemic versus nonendemic disease. Factors contributing to wild-type ATTR are largely unknown, but similar factors likely influence the penetrance of hereditary ATTR. Recognition of ATTR-CM is improving due to the increased use of cardiac scintigraphy as a noninvasive diagnostic tool, and early recognition of cardiac infiltration is crucial to optimize long-term prognosis.
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series Methodist DeBakey Cardiovascular Journal
spelling doaj-art-cf50307cb3a34e7eaec74e23ec0fdc612025-08-20T02:22:19ZengHouston Methodist DeBakey Heart & Vascular CenterMethodist DeBakey Cardiovascular Journal1947-61082022-03-01182172610.14797/mdcvj.1066326ATTR Epidemiology, Genetics, and Prognostic FactorsChukwuemeka A. Obi0https://orcid.org/0000-0003-0637-1614William C. Mostertz1https://orcid.org/0000-0001-7001-3956Jan M. Griffin2https://orcid.org/0000-0003-1729-7464Daniel P. Judge3https://orcid.org/0000-0002-3407-0248Division of Cardiology, Medical University of South Carolina, Charleston, South CarolinaDivision of Cardiology, Medical University of South Carolina, Charleston, South CarolinaDivision of Cardiology, Medical University of South Carolina, Charleston, South Carolina; Division of Cardiology, Columbia University Irving Medical Center, New York, New YorkDivision of Cardiology, Medical University of South Carolina, Charleston, South CarolinaTransthyretin amyloid cardiomyopathy (ATTR-CM) is an underdiagnosed disease and an underestimated cause of both heart failure and conduction abnormalities. It is characterized by pathologic accumulation of extracellular protein arising from unstable transthyretin (TTR) tetramers, which dissociate into monomers that misfold, aggregate, and form insoluble fibrils that are resistant to proteolysis. Cardiac amyloidosis appears in two distinct forms: hereditary and wild-type. There is considerable heterogeneity in the clinical presentation of ATTR, ranging from primarily cardiac, primarily neuropathic, or mixed cardiac and neuropathic disease. Pathogenic variants in the TTR gene that predominantly involve the heart include Val122Ile, Leu111Met, and Ile68Leu. The wild-type form of ATTR is also predominantly cardiac. Phenotypic heterogeneity is linked to differences among specific pathogenic TTR variants, geography, and the subtype of endemic versus nonendemic disease. Factors contributing to wild-type ATTR are largely unknown, but similar factors likely influence the penetrance of hereditary ATTR. Recognition of ATTR-CM is improving due to the increased use of cardiac scintigraphy as a noninvasive diagnostic tool, and early recognition of cardiac infiltration is crucial to optimize long-term prognosis.https://account.journal.houstonmethodist.org/index.php/up-j-mdbcj/article/view/1066transthyretinmisfoldingattr amyloidosismutationprognosis
spellingShingle Chukwuemeka A. Obi
William C. Mostertz
Jan M. Griffin
Daniel P. Judge
ATTR Epidemiology, Genetics, and Prognostic Factors
Methodist DeBakey Cardiovascular Journal
transthyretin
misfolding
attr amyloidosis
mutation
prognosis
title ATTR Epidemiology, Genetics, and Prognostic Factors
title_full ATTR Epidemiology, Genetics, and Prognostic Factors
title_fullStr ATTR Epidemiology, Genetics, and Prognostic Factors
title_full_unstemmed ATTR Epidemiology, Genetics, and Prognostic Factors
title_short ATTR Epidemiology, Genetics, and Prognostic Factors
title_sort attr epidemiology genetics and prognostic factors
topic transthyretin
misfolding
attr amyloidosis
mutation
prognosis
url https://account.journal.houstonmethodist.org/index.php/up-j-mdbcj/article/view/1066
work_keys_str_mv AT chukwuemekaaobi attrepidemiologygeneticsandprognosticfactors
AT williamcmostertz attrepidemiologygeneticsandprognosticfactors
AT janmgriffin attrepidemiologygeneticsandprognosticfactors
AT danielpjudge attrepidemiologygeneticsandprognosticfactors