Cardiac crises: Cardiac arrhythmias and cardiomyopathy during TANGO2 deficiency related metabolic crises.


Journal

Heart rhythm
ISSN: 1556-3871
Titre abrégé: Heart Rhythm
Pays: United States
ID NLM: 101200317

Informations de publication

Date de publication:
10 2022
Historique:
received: 26 03 2022
revised: 05 05 2022
accepted: 06 05 2022
pubmed: 15 5 2022
medline: 5 10 2022
entrez: 14 5 2022
Statut: ppublish

Résumé

TANGO2 deficiency disorder (TDD) is an autosomal recessive disease associated with metabolic crisis, lethal cardiac arrhythmias, and cardiomyopathy. Data regarding treatment, management, and outcomes of cardiac manifestations of TDD are lacking. The purpose of this study was to describe TDD-related cardiac crises. Retrospective multicenter chart review was made of TDD patients admitted with cardiac crises, defined as development of ventricular tachycardia (VT), cardiomyopathy, or cardiac arrest during metabolic crises. Twenty-seven children were admitted for 43 cardiac crises (median age 6.4 years; interquartile range [IQR] 2.4-9.8 years) at 14 centers. During crisis, QTc prolongation occurred in all (median 547 ms; IQR 504-600 ms) and a type I Brugada pattern in 8 (26%). Arrhythmias included VT in 21 (78%), supraventricular tachycardia in 3 (11%), and heart block in 1 (4%). Nineteen patients (70%) developed cardiomyopathy, and 20 (74%) experienced a cardiac arrest. There were 10 deaths (37%), 6 related to arrhythmias. In 5 patients, recalcitrant VT occurred despite use of antiarrhythmic drugs. In 6 patients, arrhythmias were controlled after extracorporeal membrane oxygenation (ECMO) support; 5 of these patients survived. Among 10 patients who survived VT without ECMO, successful treatment included intravenous magnesium, isoproterenol, and atrial pacing in multiple cases and verapamil in 1 patient. Initiation of feeds seemed to decrease VT events. TDD-related cardiac crises are associated with a high risk of arrhythmias, cardiomyopathy, cardiac arrest, and death. Although further studies are needed, early recognition and appropriate treatment are critical. Acutely, intravenous magnesium, isoproterenol, atrial pacing, and ECMO as a last resort seem to be the best current treatment options, and early initiation of feeds may prevent VT events.

Sections du résumé

BACKGROUND
TANGO2 deficiency disorder (TDD) is an autosomal recessive disease associated with metabolic crisis, lethal cardiac arrhythmias, and cardiomyopathy. Data regarding treatment, management, and outcomes of cardiac manifestations of TDD are lacking.
OBJECTIVE
The purpose of this study was to describe TDD-related cardiac crises.
METHODS
Retrospective multicenter chart review was made of TDD patients admitted with cardiac crises, defined as development of ventricular tachycardia (VT), cardiomyopathy, or cardiac arrest during metabolic crises.
RESULTS
Twenty-seven children were admitted for 43 cardiac crises (median age 6.4 years; interquartile range [IQR] 2.4-9.8 years) at 14 centers. During crisis, QTc prolongation occurred in all (median 547 ms; IQR 504-600 ms) and a type I Brugada pattern in 8 (26%). Arrhythmias included VT in 21 (78%), supraventricular tachycardia in 3 (11%), and heart block in 1 (4%). Nineteen patients (70%) developed cardiomyopathy, and 20 (74%) experienced a cardiac arrest. There were 10 deaths (37%), 6 related to arrhythmias. In 5 patients, recalcitrant VT occurred despite use of antiarrhythmic drugs. In 6 patients, arrhythmias were controlled after extracorporeal membrane oxygenation (ECMO) support; 5 of these patients survived. Among 10 patients who survived VT without ECMO, successful treatment included intravenous magnesium, isoproterenol, and atrial pacing in multiple cases and verapamil in 1 patient. Initiation of feeds seemed to decrease VT events.
CONCLUSION
TDD-related cardiac crises are associated with a high risk of arrhythmias, cardiomyopathy, cardiac arrest, and death. Although further studies are needed, early recognition and appropriate treatment are critical. Acutely, intravenous magnesium, isoproterenol, atrial pacing, and ECMO as a last resort seem to be the best current treatment options, and early initiation of feeds may prevent VT events.

Identifiants

pubmed: 35568137
pii: S1547-5271(22)01966-X
doi: 10.1016/j.hrthm.2022.05.009
pmc: PMC10642301
mid: NIHMS1937449
pii:
doi:

Substances chimiques

Anti-Arrhythmia Agents 0
Verapamil CJ0O37KU29
Magnesium I38ZP9992A
Isoproterenol L628TT009W

Types de publication

Journal Article Multicenter Study Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1673-1681

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL147108
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL130554
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL163277
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL136932
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL136389
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022. Published by Elsevier Inc.

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Auteurs

Christina Y Miyake (CY)

Department of Pediatrics, Division of Pediatric Cardiology, Texas Children's Hospital and Baylor College of Medicine, Houston, Texas; Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston Texas. Electronic address: cymiyake@bcm.org.

Erica J Lay (EJ)

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.

Cheyenne M Beach (CM)

Yale University School of Medicine, New Haven, Connecticut.

Scott R Ceresnak (SR)

Lucile Packard Children's Hospital, Stanford University, Palo Alto, California.

Caridad M Delauz (CM)

John's Hopkins Medicine, Baltimore, Maryland.

Taylor S Howard (TS)

Department of Pediatrics, Division of Pediatric Cardiology, Texas Children's Hospital and Baylor College of Medicine, Houston, Texas.

Christopher M Janson (CM)

Children's Hospital Philadelphia, Philadelphia, Pennsylvania.

Kate Jardine (K)

John Hunter Children's Hospital, Newcastle, New South Wales, Australia.

Prince J Kannankeril (PJ)

Vanderbilt University Medical Center, Nashville, Tennessee.

Maina Kava (M)

Department of Neurology and Metabolic Medicine, Perth Children's Hospital, Perth, Western Australia.

Jeffrey J Kim (JJ)

Department of Pediatrics, Division of Pediatric Cardiology, Texas Children's Hospital and Baylor College of Medicine, Houston, Texas.

Leonardo Liberman (L)

New York Presbyterian, Morgan Stanley Children's Hospital, New York, New York.

Scott L Macicek (SL)

Ochsner Medical Center, New Orleans, Louisiana.

Tam Dam Pham (TD)

Department of Pediatrics, Division of Pediatric Cardiology, Texas Children's Hospital and Baylor College of Medicine, Houston, Texas.

Terry Robertson (T)

Women and Children's Hospital, Adelaide, Australia.

Santiago O Valdes (SO)

Department of Pediatrics, Division of Pediatric Cardiology, Texas Children's Hospital and Baylor College of Medicine, Houston, Texas.

Gregory Webster (G)

Lurie Children's Hospital, Chicago, Illinois.

Sara B Stephens (SB)

Department of Pediatrics, Division of Pediatric Cardiology, Texas Children's Hospital and Baylor College of Medicine, Houston, Texas.

Diana M Milewicz (DM)

Department of Internal Medicine, McGovern Medical School, University of Texas Health Center at Houston, Houston, Texas.

Mahshid Azamian (M)

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.

Saad A Ehsan (SA)

Baylor College School of Medicine, Houston, Texas.

Kimberly M Houck (KM)

Department of Pediatrics, Division of Neurology, Texas Children's Hospital and Baylor College of Medicine, Houston, Texas.

Claudia Soler-Alfonso (C)

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.

Kevin E Glinton (KE)

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.

Mustafa Tosur (M)

Department of Pediatrics, Division of Endocrinology, Texas Children's Hospital and Baylor College of Medicine, Houston, Texas.

Na Li (N)

Department of Internal Medicine, McGovern Medical School, University of Texas Health Center at Houston, Houston, Texas.

Weiyi Xu (W)

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.

Seema R Lalani (SR)

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.

Lilei Zhang (L)

Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston Texas; Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.

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Classifications MeSH