Aborted sudden cardiac death in a young soldier with concomitant hypertrophic cardiomyopathy and Wolff-Parkinson-White syndrome.

Cardiol Young

Division of Cardiology, Department of Internal Medicine, The Armed Forces Capital Hospital, Seongnam, Republic of Korea.

Published: February 2019

We present a young soldier presenting with aborted sudden cardiac death, who was found to have concomitant hypertrophic cardiomyopathy and Wolff-Parkinson-White syndrome. Along with pathological haemodynamic features of hypertrophic cardiomyopathy, an easily-inducible re-entrant tachycardia was clearly documented in our patient. Given the fatal potential of supraventricular tachycardia in hypertrophic cardiomyopathy, we postulated that his tachyarrhythmia could potentially trigger the event. Upon his refusal to receive implantable cardioverter/defibrillator therapy, we ablated anatomical arrhythmogenic substrate instead, and he remained uneventfully over 3 years on β-blocker.

Download full-text PDF

Source
http://dx.doi.org/10.1017/S1047951118002123DOI Listing

Publication Analysis

Top Keywords

hypertrophic cardiomyopathy
16
aborted sudden
8
sudden cardiac
8
cardiac death
8
young soldier
8
concomitant hypertrophic
8
cardiomyopathy wolff-parkinson-white
8
wolff-parkinson-white syndrome
8
death young
4
soldier concomitant
4

Similar Publications

Background: Cardiomyopathy is a disease that affects the myocardium and can be classified as dilated, restrictive, or hypertrophic cardiomyopathy. Among the subtypes, restrictive cardiomyopathy is characterized by restriction of ventricular filling and its uncommon cause is a disease due to mutation on Filamin C (FLNC) gene. Filamin C is an actin-binding protein encoded by FLNC gene and participates in sarcomere stability maintenance, which is expressed on the striated muscle.

View Article and Find Full Text PDF

We describe a case of novel use of trametinib in treating arrythmia without concomitant cardiomyopathy. Our patient is a two-year-old female born with Costello syndrome due to heterozygous mutations in the HRAS gene c34 G > T p (G12C). Shortly after birth, she was diagnosed with multifocal atrial tachyarrhythmia.

View Article and Find Full Text PDF

Myocyte disarray and fibrosis are underlying pathologies of hypertrophic cardiomyopathy (HCM) caused by genetic mutations. However, the extent of their contributions has not been extensively evaluated. In this study, we investigated the effects of genetic mutations on myofiber function and fibrosis patterns in HCM.

View Article and Find Full Text PDF

Background: Although many studies have demonstrated a lower incidence of sudden cardiac arrest or death (SCA/D) in female athletes than in male, there is limited understanding of the specific underlying causes.

Objective: This systematic review aimed to assess the disparities in SCA/D incidence between male and female competitive athletes and explore the associated etiologies.

Methods: A comprehensive search was conducted for retrospective and prospective studies examining SCA/D incidence in male and female athletes.

View Article and Find Full Text PDF

We presented a case of a 49-year-old presenting with atypical chest pain and hypertrophic phenotype cardiomyopathy without coronary artery disease. At cardiac magnetic resonance (CMR), the left ventricle was of normal volumes and preserved global ejection fraction with an asymmetric wall hypertrophy. The evaluation of native myocardial T1 has been calculated at an average global value of 924 ms, compatible with hypertrophic phenotype cardiomyopathy with reduced native T1 values as observed in Anderson-Fabry disease.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!