Identification of Undetected Monogenic Cardiovascular Disorders.


Journal

Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365

Informations de publication

Date de publication:
18 08 2020
Historique:
received: 27 03 2020
revised: 14 06 2020
accepted: 15 06 2020
entrez: 15 8 2020
pubmed: 15 8 2020
medline: 23 1 2021
Statut: ppublish

Résumé

Monogenic diseases are individually rare but collectively common, and are likely underdiagnosed. The purpose of this study was to estimate the prevalence of monogenic cardiovascular diseases (MCVDs) and potentially missed diagnoses in a cardiovascular cohort. Exomes from 8,574 individuals referred for cardiac catheterization were analyzed. Pathogenic/likely pathogenic (P/LP) variants associated with MCVD (cardiomyopathies, arrhythmias, connective tissue disorders, and familial hypercholesterolemia were identified. Electronic health records (EHRs) were reviewed for individuals harboring P/LP variants who were predicted to develop disease (G+). G+ individuals who did not have a documented relevant diagnosis were classified into groups of whether they may represent missed diagnoses (unknown, unlikely, possible, probable, or definite) based on relevant diagnostic criteria/features for that disease. In total, 159 P/LP variants were identified; 2,361 individuals harbored at least 1 P/LP variant, of whom 389 G+ individuals (4.5% of total cohort) were predicted to have at least 1 MCVD. EHR review of 342 G+ individuals predicted to have 1 MCVD with sufficient EHR data revealed that 52 had been given the relevant clinical diagnosis. The remaining 290 individuals were classified as potentially having an MCVD as follows: 193 unlikely (66.6%), 50 possible (17.2%), 30 probable (10.3%), and 17 definite (5.9%). Grouping possible, probable, definite, and known diagnoses, 149 were considered to have an MCVD. Novel MCVD pathogenic variants were identified in 16 individuals. Overall, 149 individuals (1.7% of cohort) had MCVDs, but only 35% were diagnosed. These patients represents a "missed opportunity," which could be addressed by greater use of genetic testing of patients seen by cardiologists.

Sections du résumé

BACKGROUND
Monogenic diseases are individually rare but collectively common, and are likely underdiagnosed.
OBJECTIVES
The purpose of this study was to estimate the prevalence of monogenic cardiovascular diseases (MCVDs) and potentially missed diagnoses in a cardiovascular cohort.
METHODS
Exomes from 8,574 individuals referred for cardiac catheterization were analyzed. Pathogenic/likely pathogenic (P/LP) variants associated with MCVD (cardiomyopathies, arrhythmias, connective tissue disorders, and familial hypercholesterolemia were identified. Electronic health records (EHRs) were reviewed for individuals harboring P/LP variants who were predicted to develop disease (G+). G+ individuals who did not have a documented relevant diagnosis were classified into groups of whether they may represent missed diagnoses (unknown, unlikely, possible, probable, or definite) based on relevant diagnostic criteria/features for that disease.
RESULTS
In total, 159 P/LP variants were identified; 2,361 individuals harbored at least 1 P/LP variant, of whom 389 G+ individuals (4.5% of total cohort) were predicted to have at least 1 MCVD. EHR review of 342 G+ individuals predicted to have 1 MCVD with sufficient EHR data revealed that 52 had been given the relevant clinical diagnosis. The remaining 290 individuals were classified as potentially having an MCVD as follows: 193 unlikely (66.6%), 50 possible (17.2%), 30 probable (10.3%), and 17 definite (5.9%). Grouping possible, probable, definite, and known diagnoses, 149 were considered to have an MCVD. Novel MCVD pathogenic variants were identified in 16 individuals.
CONCLUSIONS
Overall, 149 individuals (1.7% of cohort) had MCVDs, but only 35% were diagnosed. These patients represents a "missed opportunity," which could be addressed by greater use of genetic testing of patients seen by cardiologists.

Identifiants

pubmed: 32792077
pii: S0735-1097(20)35733-8
doi: 10.1016/j.jacc.2020.06.037
pmc: PMC7428466
mid: NIHMS1613641
pii:
doi:

Substances chimiques

HFE protein, human 0
Hemochromatosis Protein 0
GAA protein, human EC 3.2.1.20
alpha-Glucosidases EC 3.2.1.20

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

797-808

Subventions

Organisme : NHLBI NIH HHS
ID : P01 HL036587
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002553
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

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Auteurs

Jawan W Abdulrahim (JW)

Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, North Carolina.

Lydia Coulter Kwee (LC)

Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, North Carolina.

Fawaz Alenezi (F)

Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.

Albert Y Sun (AY)

Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.

Aris Baras (A)

Regeneron Genetics Center, Regeneron Pharmaceuticals Inc., Tarrytown, New York.

Teminioluwa A Ajayi (TA)

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Ricardo Henao (R)

Center for Applied Genomics and Precision Medicine, Duke University, Durham, North Carolina.

Christopher L Holley (CL)

Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.

Robert W McGarrah (RW)

Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, North Carolina; Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.

James P Daubert (JP)

Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.

Lauren K Truby (LK)

Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.

Sreekanth Vemulapalli (S)

Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.

Andrew Wang (A)

Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.

Michel G Khouri (MG)

Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina.

Svati H Shah (SH)

Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, North Carolina; Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina. Electronic address: svati.shah@duke.edu.

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