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Text
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Citation List Month
November 2017 List
Notes
<p>1524-4571<br />Lee, Teresa M<br />Hsu, Daphne T<br />Kantor, Paul<br />Towbin, Jeffrey A<br />Ware, Stephanie M<br />Colan, Steven D<br />Chung, Wendy K<br />Jefferies, John L<br />Rossano, Joseph W<br />Castleberry, Chesney D<br />Addonizio, Linda J<br />Lal, Ashwin K<br />Lamour, Jacqueline M<br />Miller, Erin M<br />Thrush, Philip T<br />Czachor, Jason D<br />Razoky, Hiedy<br />Hill, Ashley<br />Lipshultz, Steven E<br />Journal Article<br />Review<br />United States<br />Circ Res. 2017 Sep 15;121(7):855-873. doi: 10.1161/CIRCRESAHA.116.309386.</p>
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Title
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Pediatric Cardiomyopathies
Publisher
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Circulation Research
Date
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2017
Subject
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Epidemiology; Genetics; Pediatrics
Creator
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Lee TM; Hsu DT; Kantor P; Towbin JA; Ware SM; Colan SD; Chung WK; Jefferies JL; Rossano JW; Castleberry CD; Addonizio LJ; Lal AK; Lamour JM; Miller EM; Thrush PT; Czachor JD; Razoky H; Hill A; Lipshultz SE
Description
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Pediatric cardiomyopathies are rare diseases with an annual incidence of 1.1 to 1.5 per 100 000. Dilated and hypertrophic cardiomyopathies are the most common; restrictive, noncompaction, and mixed cardiomyopathies occur infrequently; and arrhythmogenic right ventricular cardiomyopathy is rare. Pediatric cardiomyopathies can result from coronary artery abnormalities, tachyarrhythmias, exposure to infection or toxins, or secondary to other underlying disorders. Increasingly, the importance of genetic mutations in the pathogenesis of isolated or syndromic pediatric cardiomyopathies is becoming apparent. Pediatric cardiomyopathies often occur in the absence of comorbidities, such as atherosclerosis, hypertension, renal dysfunction, and diabetes mellitus; as a result, they offer insights into the primary pathogenesis of myocardial dysfunction. Large international registries have characterized the epidemiology, cause, and outcomes of pediatric cardiomyopathies. Although adult and pediatric cardiomyopathies have similar morphological and clinical manifestations, their outcomes differ significantly. Within 2 years of presentation, normalization of function occurs in 20% of children with dilated cardiomyopathy, and 40% die or undergo transplantation. Infants with hypertrophic cardiomyopathy have a 2-year mortality of 30%, whereas death is rare in older children. Sudden death is rare. Molecular evidence indicates that gene expression differs between adult and pediatric cardiomyopathies, suggesting that treatment response may differ as well. Clinical trials to support evidence-based treatments and the development of disease-specific therapies for pediatric cardiomyopathies are in their infancy. This compendium summarizes current knowledge of the genetic and molecular origins, clinical course, and outcomes of the most common phenotypic presentations of pediatric cardiomyopathies and highlights key areas where additional research is required. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifiers: NCT02549664 and NCT01912534.
Identifier
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10.1161/circresaha.116.309386
Rights
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Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Addonizio LJ
Castleberry CD
Chung WK
Circulation Research
Colan SD
Czachor JD
Epidemiology
Genetics
Hill A
Hsu DT
Jefferies JL
Kantor P
Lal AK
Lamour JM
Lee TM
Lipshultz SE
Miller EM
November 2017 List
Pediatrics
Razoky H
Rossano JW
Thrush PT
Towbin JA
Ware SM