Syncope in patients with inherited arrhythmias

Nakano, Yukiko; Shimizu, Wataru

doi:10.1016/j.joa.2017.07.007

Cited by 8 publications

(3 citation statements)

References 46 publications

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“…Individuals with CPVT may exhibit two distinct types of polymorphic VT. The first type (typical polymorphic VT) is characterized by constantly changing QRS morphology ( Figure 1 ) [ 39 ]. The second type (bidirectional tachycardia) is marked by a 180° rotation of the QRS complex from one beat to the next ( Figure 2 ) [ 40 ].…”

Section: Diagnosismentioning

confidence: 99%

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Catecholaminergic Polymorphic Ventricular Tachycardia: Clinical Characteristics, Diagnostic Evaluation and Therapeutic Strategies

Aggarwal,

Stolear,

Alam

et al. 2024

JCM

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Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a severe hereditary arrhythmia syndrome predominantly affecting children and young adults. It manifests through bidirectional or polymorphic ventricular arrhythmia, often culminating in syncope triggered by physical exertion or emotional stress which can lead to sudden cardiac death. Most cases stem from mutations in the gene responsible for encoding the cardiac ryanodine receptor (RyR2), or in the Calsequestrin 2 gene (CASQ2), disrupting the handling of calcium ions within the cardiac myocyte sarcoplasmic reticulum. Diagnosing CPVT typically involves unmasking the arrhythmia through exercise stress testing. This diagnosis emerges in the absence of structural heart disease by cardiac imaging and with a normal baseline electrocardiogram. Traditional first-line treatment primarily involves β-blocker therapy, significantly reducing CPVT-associated mortality. Adjunctive therapies such as moderate exercise training, flecainide, left cardiac sympathetic denervation and implantable cardioverter-defibrillators have been utilized with reasonable success. However, the spectrum of options for managing CPVT has expanded over time, demonstrating decreased rates of arrhythmic events. Furthermore, ongoing research into potential new therapies including gene therapies has the potential to further enhance treatment paradigms. This review aims to succinctly encapsulate the contemporary understanding of the clinical characteristics, diagnostic approach, established therapeutic interventions and the promising future directions in managing CPVT.

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Section: Diagnosismentioning

confidence: 99%

“… Polymorphic ventricular tachycardia (VT) during exercise test in adolescent female patient diagnosed with CPVT. Image reproduced from [ 39 ] under a creative commons [CC BY-NC-ND 4.0] license. …”

Section: Figurementioning

confidence: 99%

Catecholaminergic Polymorphic Ventricular Tachycardia: Clinical Characteristics, Diagnostic Evaluation and Therapeutic Strategies

Aggarwal,

Stolear,

Alam

et al. 2024

JCM

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“…The QT interval is measured from the beginning of the QRS complex to the end of the T wave and it refers to ventricular depolarization and repolarization (1,2). LQTS is an arrhythmogenic disease characterized with QT prolongation that can cause syncope and sudden cardiac death secondary to cardiac arrhythmias (3). LQTS is usually caused by mutations in genes that encode ion channels in the heart, however, some drugs, like selective serotonin reuptake inhibitors (SSRIs) can also lead to LOTS (4,5).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the Citalopram levels on QTc Interval in Rats using with Radio-telemetry

HARMANCI¹,

TOPRAK²,

KALTUŞ³

et al. 2022

Osmangazi̇ Journal of Medicine

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Long QT syndrome is an arrhythmogenic disease characterized by prolonged QT interval. Citalopram (CIT) was reported to prolong QT interval dose-dependently. Omeprazole (OMP), inhibits CIT metabolizing enzyme CYP2C19, thereby increases serum concentrations which may increase the risk of QT prolongation. These are commonly co-prescribed and recent studies have raised the safety concerns about. We aimed to investigate the dose dependent effects of citalopram alone and in combination with OMP. Forty male, Sprague Dawley rats were divided into 5 groups (n=8). CIT (10 mg/kg or 30 mg/kg) was given for 2 weeks alone or in combination with OMP (100 mg/kg) starting from the 2nd week. ECG recordings and blood samples were collected. QT interval significantly increased in all groups compared to control. The plasma level of CIT in the CIT30 group was significantly higher than CIT10 group (p<0.01) and was significantly higher in the CIT10+OMP group than that of the CIT10 group (p<0.01). In treatment groups, the increase in plasma citalopram level correlated positively with the increase in QT (r=0.844, r2=0.713). It was determined that CIT caused prolongation of QT interval, the addition of OMP increased QT interval more, and these increases correlated positively with CIT plasma concentration. Therefore, it would be appropriate to routinely measure CIT plasma levels in addition to ECG, particularly in patients with additional risk factors for QT prolongation.

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Syncope Management Protocol

Al-Harbi,

Al-Ghamdi

2024

Manual of Pediatric Cardiac Care

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Syncope in patients with inherited arrhythmias

Cited by 8 publications

References 46 publications

Catecholaminergic Polymorphic Ventricular Tachycardia: Clinical Characteristics, Diagnostic Evaluation and Therapeutic Strategies

Catecholaminergic Polymorphic Ventricular Tachycardia: Clinical Characteristics, Diagnostic Evaluation and Therapeutic Strategies

Evaluation of the Citalopram levels on QTc Interval in Rats using with Radio-telemetry

Syncope Management Protocol

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