Literature DB >> 31170290

Calmodulin mutations and life-threatening cardiac arrhythmias: insights from the International Calmodulinopathy Registry.

Lia Crotti1,2,3,4,5, Carla Spazzolini1,5, David J Tester6,7,8, Alice Ghidoni1,2,5, Alban-Elouen Baruteau5,9,10, Britt-Maria Beckmann11, Elijah R Behr5,10, Jeffrey S Bennett12, Connie R Bezzina5,13, Zahurul A Bhuiyan14, Alpay Celiker15, Marina Cerrone16, Federica Dagradi1,5, Gaetano M De Ferrari17,18, Susan P Etheridge19, Meena Fatah20, Pablo Garcia-Pavia5,21,22, Saleh Al-Ghamdi23, Robert M Hamilton20, Zuhair N Al-Hassnan24, Minoru Horie25, Juan Jimenez-Jaimez26, Ronald J Kanter27, Juan P Kaski5,28,29, Maria-Christina Kotta1,2,5, Najim Lahrouchi5,13, Naomasa Makita30, Gabrielle Norrish28,29, Hans H Odland31, Seiko Ohno25,32, John Papagiannis33, Gianfranco Parati3,4, Nicole Sekarski34, Kristian Tveten35, Matteo Vatta36,37,38, Gregory Webster39, Arthur A M Wilde5,13, Julianne Wojciak40, Alfred L George41, Michael J Ackerman6, Peter J Schwartz1,2,5.   

Abstract

AIMS: Calmodulinopathies are rare life-threatening arrhythmia syndromes which affect mostly young individuals and are, caused by mutations in any of the three genes (CALM 1-3) that encode identical calmodulin proteins. We established the International Calmodulinopathy Registry (ICalmR) to understand the natural history, clinical features, and response to therapy of patients with a CALM-mediated arrhythmia syndrome. METHODS AND
RESULTS: A dedicated Case Report File was created to collect demographic, clinical, and genetic information. ICalmR has enrolled 74 subjects, with a variant in the CALM1 (n = 36), CALM2 (n = 23), or CALM3 (n = 15) genes. Sixty-four (86.5%) were symptomatic and the 10-year cumulative mortality was 27%. The two prevalent phenotypes are long QT syndrome (LQTS; CALM-LQTS, n = 36, 49%) and catecholaminergic polymorphic ventricular tachycardia (CPVT; CALM-CPVT, n = 21, 28%). CALM-LQTS patients have extremely prolonged QTc intervals (594 ± 73 ms), high prevalence (78%) of life-threatening arrhythmias with median age at onset of 1.5 years [interquartile range (IQR) 0.1-5.5 years] and poor response to therapies. Most electrocardiograms (ECGs) show late onset peaked T waves. All CALM-CPVT patients were symptomatic with median age of onset of 6.0 years (IQR 3.0-8.5 years). Basal ECG frequently shows prominent U waves. Other CALM-related phenotypes are idiopathic ventricular fibrillation (IVF, n = 7), sudden unexplained death (SUD, n = 4), overlapping features of CPVT/LQTS (n = 3), and predominant neurological phenotype (n = 1). Cardiac structural abnormalities and neurological features were present in 18 and 13 patients, respectively.
CONCLUSION: Calmodulinopathies are largely characterized by adrenergically-induced life-threatening arrhythmias. Available therapies are disquietingly insufficient, especially in CALM-LQTS. Combination therapy with drugs, sympathectomy, and devices should be considered. Published on behalf of the European Society of Cardiology. All rights reserved.
© The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.

Entities:  

Keywords:  Calmodulin ; Cathecolaminergic polymorphic ventricular tachycardia ; Idiopathic ventricular fibrillation ; Long QT syndrome ; Sudden death

Mesh:

Substances:

Year:  2019        PMID: 31170290      PMCID: PMC6748747          DOI: 10.1093/eurheartj/ehz311

Source DB:  PubMed          Journal:  Eur Heart J        ISSN: 0195-668X            Impact factor:   29.983


  44 in total

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9.  Left cardiac sympathetic denervation in the management of high-risk patients affected by the long-QT syndrome.

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Journal:  Circulation       Date:  2004-03-29       Impact factor: 29.690

10.  Left cardiac sympathetic denervation for the treatment of long QT syndrome and catecholaminergic polymorphic ventricular tachycardia using video-assisted thoracic surgery.

Authors:  Christopher A Collura; Jonathan N Johnson; Christopher Moir; Michael J Ackerman
Journal:  Heart Rhythm       Date:  2009-03-19       Impact factor: 6.343

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2.  The arrhythmogenic N53I variant subtly changes the structure and dynamics in the calmodulin N-terminal domain, altering its interaction with the cardiac ryanodine receptor.

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3.  L51P, a novel mutation in the PAS domain of hERG channel, confers long QT syndrome by impairing channel activation.

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4.  Genetic Mosaicism in Calmodulinopathy.

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Journal:  Circ Genom Precis Med       Date:  2019-08-27

5.  Disruption of protein quality control of the human ether-à-go-go related gene K+ channel results in profound long QT syndrome.

Authors:  Hannah A Ledford; Lu Ren; Phung N Thai; Seojin Park; Valeriy Timofeyev; Padmini Sirish; Wilson Xu; Aiyana M Emigh; James R Priest; Marco V Perez; Euan A Ashley; Vladimir Yarov-Yarovoy; Ebenezer N Yamoah; Xiao-Dong Zhang; Nipavan Chiamvimonvat
Journal:  Heart Rhythm       Date:  2021-10-09       Impact factor: 6.343

6.  European Heart Rhythm Association (EHRA)/Heart Rhythm Society (HRS)/Asia Pacific Heart Rhythm Society (APHRS)/Latin American Heart Rhythm Society (LAHRS) Expert Consensus Statement on the state of genetic testing for cardiac diseases.

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