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Phenotyping of Cardiac Amyloidosis

Phenotyping of Cardiac Amyloidosis Circulation: Cardiovascular Imaging EDITORIAL Advancing From Macro to Micro? See Article by Khalique et al Sarah Cuddy, MB, BCh, BAO Michael Jerosch-Herold, myloidosis is the exemplar restrictive cardiomyopathy in which misfolded PhD proteins deposit as amyloid fibrils in the interstitial space of the myocar - Sharmila Dorbala, MD, Adium. The most common types of cardiac amyloidosis (CA) are transthyre- MPH tin (ATTR) amyloidosis and light chain amyloidosis (AL), due to misfolding of the amyloidogenic transthyretin protein in the former or immunoglobulin light chains in the setting of a plasma cell dyscrasia in the latter. CA manifests as heart failure from biventricular myocardial thickening, biatrial enlargement, diastolic dysfunc- tion and, in later stages, systolic dysfunction. Because there are no useful animal models of CA, much of our knowledge about this disease phenotype has been gained through cardiac magnetic resonance (CMR), echocardiography, and radio- nuclide imaging. A major focus of imaging studies of CA has been to distinguish left ventricular (LV) thickening of amyloid infiltration from LV myocyte hypertrophy of hypertrophic cardiomyopathy (HCM) or hypertensive heart disease. Cardiac structural and func- tional phenotype by echocardiography, including global longitudinal strain, can- not definitively distinguish LV hypertrophy from amyloidosis. The identification, initially by http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Circulation: Cardiovascular Imaging Wolters Kluwer Health

Phenotyping of Cardiac Amyloidosis

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Publisher
Wolters Kluwer Health
Copyright
© 2020 American Heart Association, Inc.
ISSN
1941-9651
eISSN
1942-0080
DOI
10.1161/CIRCIMAGING.120.010785
Publisher site
See Article on Publisher Site

Abstract

Circulation: Cardiovascular Imaging EDITORIAL Advancing From Macro to Micro? See Article by Khalique et al Sarah Cuddy, MB, BCh, BAO Michael Jerosch-Herold, myloidosis is the exemplar restrictive cardiomyopathy in which misfolded PhD proteins deposit as amyloid fibrils in the interstitial space of the myocar - Sharmila Dorbala, MD, Adium. The most common types of cardiac amyloidosis (CA) are transthyre- MPH tin (ATTR) amyloidosis and light chain amyloidosis (AL), due to misfolding of the amyloidogenic transthyretin protein in the former or immunoglobulin light chains in the setting of a plasma cell dyscrasia in the latter. CA manifests as heart failure from biventricular myocardial thickening, biatrial enlargement, diastolic dysfunc- tion and, in later stages, systolic dysfunction. Because there are no useful animal models of CA, much of our knowledge about this disease phenotype has been gained through cardiac magnetic resonance (CMR), echocardiography, and radio- nuclide imaging. A major focus of imaging studies of CA has been to distinguish left ventricular (LV) thickening of amyloid infiltration from LV myocyte hypertrophy of hypertrophic cardiomyopathy (HCM) or hypertensive heart disease. Cardiac structural and func- tional phenotype by echocardiography, including global longitudinal strain, can- not definitively distinguish LV hypertrophy from amyloidosis. The identification, initially by

Journal

Circulation: Cardiovascular Imaging – Wolters Kluwer Health

Published: May 1, 2020

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