Transient swallowing‐induced atrial tachycardia in a patient with genotyped hypertrophic cardiomyopathy

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Abstract

Most cases of swallowing‐induced atrial tachycardia require radiofrequency catheter ablation for a permanent cure; however, the arrhythmia subsided after temporary prescription of verapamil in a patient with genotyped hypertrophic cardiomyopathy.

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Lifelong left ventricular remodeling of hypertrophic cardiomyopathy caused by a founder frameshift deletion mutation in the cardiac Myosin-binding protein C gene among Japanese.

Masanori Nishinaga, Akinori Kimura, M. Okawa … (2005)

We studied the longitudinal evolution of hypertrophic cardiomyopathy (HCM) caused by a founder frameshift mutation in the cardiac myosin-binding protein C (MyBPC) gene. Mutations in the MyBPC gene have been associated with delayed expression of HCM and a good prognosis. Few studies, however, demonstrated the phenotype-genotype correlations in the longitudinal study. We studied long-term evolution of clinical features of 15 unrelated families who were found to have an identical frameshift mutation in the MyBPC gene: a one-base deletion of a thymidine at nucleotide 11645 (V592fs/8). Thirty-nine individuals in 15 families were genotype-positive. Thirty of the 39 individuals with the mutation were phenotype-positive. The disease penetrance was 100% in subjects > or =50 years and 65% in those <50 years. "End-stage" HCM (ejection fraction <50%) was observed in 7 (18%) of the 39 genotype-positive individuals (7 [23%] of the 30 phenotype-positive patients); 6 of them were 60 years or older. Seven patients were hospitalized for treatment of repeated congestive heart failure, and four patients died or had implantable cardioverter-defibrillator discharge (13%; incidence, 1.4%/year) during a mean follow-up period of 9.2 +/- 5.5 years. Elderly patients with a V592fs/8 mutation in the MyBPC gene may evolve into the "end-stage" HCM, characterized by left ventricular systolic dysfunction, cavity dilation, and irreversible heart failure. The clinical course in patients with this mutation is not benign in the long run, with progressive left ventricular remodeling with advancing age.

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Structural interpretation of the mutations in the beta-cardiac myosin that have been implicated in familial hypertrophic cardiomyopathy.

L Fananapazir, Rachel M Holden, Paul Epstein … (1995)

In 10-30% of hypertrophic cardiomyopathy kindreds, the disease is caused by > 29 missense mutations in the cardiac beta-myosin heavy chain (MYH7) gene. The amino acid sequence similarity between chicken skeletal muscle and human beta-cardiac myosin and the three-dimensional structure of the chicken skeletal muscle myosin head have provided the opportunity to examine the structural consequences of these naturally occurring mutations in human beta-cardiac myosin. This study demonstrates that the mutations are related to distinct structural and functional domains. Twenty-four are clustered around four specific locations in the myosin head that are (i) associated with the actin binding interface, (ii) around the nucleotide binding site, (iii) adjacent to the region that connects the two reactive cysteine residues, and (iv) in close proximity to the interface of the heavy chain with the essential light chain. The remaining five mutations are in the myosin rod. The locations of these mutations provide insight into the way they impair the functioning of this molecular motor and also into the mechanism of energy transduction.

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Supraventricular tachycardia induced by swallowing: a case report and review of the literature.

Gary W Cline, F Morady, B. Smieja-Król … (1986)

A 64-year-old man who complained of palpitations brought on by swallowing was found to have short runs of paroxysmal supraventricular tachycardia (SVT) induced by swallowing. Electrophysiology studies suggested that the SVT was an automatic atrial tachycardia. An esophageal manometric study demonstrated that the tachycardia was coincident with relaxation of the upper esophageal spincter and preceded peristaltic activity in the esophageal body. Atropine and bethanechol did not affect the swallow-induced tachycardia. The patient's symptoms were controlled by verapamil and quinidine. After five months, these medications were discontinued, with no recurrence of symptoms. Based on analysis of ten prior cases and the present case, it appears that swallow-induced SVT generally occurs in men between the ages of 45-75 years who have no evidence of structural heart disease or an esophageal disorder. The SVT is usually either a nonsustained automatic atrial tachycardia or atrial fibrillation. The mechanism is conjectural, but the most likely possibility is a vagally-mediated neural reflex, probably involving a neurotransmitter other than acetylcholine.

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Contributors

Kenshi Hayashi:

ORCID: https://orcid.org/0000-0002-8219-7729

kenshi@med.kanazawa-u.ac.jp

Journal

Journal ID (nlm-ta): Clin Case Rep

Journal ID (iso-abbrev): Clin Case Rep

Journal ID (doi): 10.1002/(ISSN)2050-0904

Journal ID (publisher-id): CCR3

Title: Clinical Case Reports

Publisher: John Wiley and Sons Inc. (Hoboken )

ISSN (Electronic): 2050-0904

Publication date (Electronic): 08 June 2020

Publication date Collection: September 2020

Volume: 8

Issue: 9 ( doiID: 10.1002/ccr3.v8.9 )

Pages: 1809-1813

Affiliations

[ ¹ ] Department of Cardiovascular Medicine Kanazawa University Graduate School of Medical Sciences Kanazawa Japan

[ ² ] Division of Cardiology Toyohashi Heart Center Toyohashi Japan

Author notes

[*] [* ] Correspondence

Kenshi Hayashi, Department of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Sciences, 13‐1 Takara‐machi, Kanazawa, Ishikawa 920‐8641, Japan.

Email: kenshi@ 123456med.kanazawa-u.ac.jp

Author information

Noboru Fujino https://orcid.org/0000-0003-2695-5748

Kenshi Hayashi https://orcid.org/0000-0002-8219-7729

Article

Publisher ID: CCR33015

DOI: 10.1002/ccr3.3015

PMC ID: 7495763

SO-VID: dd694e21-e005-425f-af98-e1d699a3a589

License:

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

History

Date received : 03 February 2020

Date revision received : 07 April 2020

Date accepted : 15 May 2020

Page count

Figures: 3, Tables: 0, Pages: 5, Words: 2306

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source-schema-version-number 2.0

cover-date September 2020

details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.9.1 mode:remove_FC converted:17.09.2020

Keywords: cardiac beta‐myosin heavy chain gene,hypertrophic cardiomyopathy,mutation,swallowing‐induced atrial tachycardia

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Keywords: cardiac beta‐myosin heavy chain gene, hypertrophic cardiomyopathy, mutation, swallowing‐induced atrial tachycardia

Transient swallowing‐induced atrial tachycardia in a patient with genotyped hypertrophic cardiomyopathy

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Most cited references 9

Lifelong left ventricular remodeling of hypertrophic cardiomyopathy caused by a founder frameshift deletion mutation in the cardiac Myosin-binding protein C gene among Japanese.

Structural interpretation of the mutations in the beta-cardiac myosin that have been implicated in familial hypertrophic cardiomyopathy.

Supraventricular tachycardia induced by swallowing: a case report and review of the literature.

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