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  1. Article ; Online: Predicting Sudden Cardiac Death in Genetic Heart Disease.

    Cadrin-Tourigny, Julia / Tadros, Rafik

    The Canadian journal of cardiology

    2022  Volume 38, Issue 4, Page(s) 479–490

    Abstract: Genetic heart diseases are common causes of sudden cardiac death (SCD) in the young and are typically divided into inherited cardiomyopathies and primary electrical heart diseases. Cardiomyopathies associated with risk of SCD include hypertrophic ... ...

    Abstract Genetic heart diseases are common causes of sudden cardiac death (SCD) in the young and are typically divided into inherited cardiomyopathies and primary electrical heart diseases. Cardiomyopathies associated with risk of SCD include hypertrophic cardiomyopathy (HCM) and arrhythmogenic cardiomyopathy (ACM). The latter includes arrhythmogenic right ventricular cardiomyopathy (ARVC) as well as ACM primarily affecting the left ventricle, such as lamin cardiomyopathy. Primary electrical diseases more commonly seen in clinical practice include Brugada syndrome (BrS) and long QT syndrome (LQTS). Risk stratification of SCD is a central component of the management of patients with these genetic heart diseases. Numerous risk factors have been identified with variable degrees of scientific evidence. More recently, risk prediction models have been developed to estimate the absolute risk of sustained arrhythmias and SCD, to support clinicians and patients in decision making regarding prophylactic implantable cardioverter-defibrillators (ICDs). This paper provides a practical review of the current literature on risk stratification in ARVC and other ACMs, HCM, BrS, and LQTS, and summarises current recommendations for ICD use.
    MeSH term(s) Arrhythmias, Cardiac/etiology ; Arrhythmogenic Right Ventricular Dysplasia/complications ; Arrhythmogenic Right Ventricular Dysplasia/diagnosis ; Arrhythmogenic Right Ventricular Dysplasia/genetics ; Cardiomyopathy, Hypertrophic/complications ; Death, Sudden, Cardiac/epidemiology ; Death, Sudden, Cardiac/etiology ; Death, Sudden, Cardiac/prevention & control ; Defibrillators, Implantable/adverse effects ; Heart Diseases ; Humans ; Risk Assessment ; Risk Factors
    Language English
    Publishing date 2022-01-30
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 632813-1
    ISSN 1916-7075 ; 0828-282X
    ISSN (online) 1916-7075
    ISSN 0828-282X
    DOI 10.1016/j.cjca.2022.01.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A Primer on Inherited Cardiac Arrhythmias and Cardiomyopathies.

    Tadros, Rafik / Cadrin-Tourigny, Julia / Roberts, Jason D

    Cardiac electrophysiology clinics

    2023  Volume 15, Issue 3, Page(s) xv–xvi

    MeSH term(s) Humans ; Cardiomyopathies/genetics ; Arrhythmias, Cardiac/genetics
    Language English
    Publishing date 2023-06-20
    Publishing country United States
    Document type Editorial
    ISSN 1877-9190
    ISSN (online) 1877-9190
    DOI 10.1016/j.ccep.2023.06.006
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  3. Article ; Online: Clinical Genetic Testing for Atrial Fibrillation: Are We There Yet?

    Roberts, Jason D / Chalazan, Brandon / Andrade, Jason G / Macle, Laurent / Nattel, Stanley / Tadros, Rafik

    The Canadian journal of cardiology

    2024  Volume 40, Issue 4, Page(s) 540–553

    Abstract: Important progress has been made toward unravelling the complex genetics underlying atrial fibrillation (AF). Initial studies were aimed to identify monogenic causes; however, it has become increasingly clear that the most common predisposing genetic ... ...

    Abstract Important progress has been made toward unravelling the complex genetics underlying atrial fibrillation (AF). Initial studies were aimed to identify monogenic causes; however, it has become increasingly clear that the most common predisposing genetic substrate for AF is polygenic. Despite intensive investigations, there is robust evidence for rare variants for only a limited number of genes and cases. Although the current yield for genetic testing in early onset AF might be modest, there is an increasing appreciation that genetic culprits for potentially life-threatening ventricular cardiomyopathies and channelopathies might initially present with AF. The potential clinical significance of this recognition is highlighted by evidence that suggests that identification of a pathogenic or likely pathogenic rare variant in a patient with early onset AF is associated with an increased risk of death. These findings suggest that it might be warranted to screen patients with early onset AF for these potentially more sinister cardiac conditions. Beyond facilitating the early identification of genetic culprits associated with potentially malignant phenotypes, insight into underlying AF genetic substrates might improve the selection of patients for existing therapies and guide the development of novel ones. Herein, we review the evidence that links genetic factors to AF, then discuss an approach to using genetic testing for early onset AF patients in the present context, and finally consider the potential value of genetic testing in the foreseeable future. Although further work might be necessary before recommending uniform integration of genetic testing in cases of early onset AF, ongoing research increasingly highlights its potential contributions to clinical care.
    MeSH term(s) Humans ; Atrial Fibrillation/diagnosis ; Atrial Fibrillation/genetics ; Genetic Testing ; Risk Assessment
    Language English
    Publishing date 2024-03-28
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 632813-1
    ISSN 1916-7075 ; 0828-282X
    ISSN (online) 1916-7075
    ISSN 0828-282X
    DOI 10.1016/j.cjca.2023.11.022
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  4. Article ; Online: Hypertrophic Cardiomyopathy: Evolution to the Present, Ongoing Challenges, and Opportunities.

    McKenna, William J / Crean, Andrew / Greenway, Steven / Tadros, Rafik / Veselka, Josef / Woo, Anna

    The Canadian journal of cardiology

    2024  

    Language English
    Publishing date 2024-03-16
    Publishing country England
    Document type Editorial
    ZDB-ID 632813-1
    ISSN 1916-7075 ; 0828-282X
    ISSN (online) 1916-7075
    ISSN 0828-282X
    DOI 10.1016/j.cjca.2024.03.005
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  5. Article ; Online: Sudden Death Risk Assessment in Hypertrophic Cardiomyopathy Across the Lifespan: Reconciling the American and European Approaches.

    Al Samarraie, Ahmad / Petzl, Adrian / Cadrin-Tourigny, Julia / Tadros, Rafik

    Cardiac electrophysiology clinics

    2023  Volume 15, Issue 3, Page(s) 367–378

    Abstract: Hypertrophic cardiomyopathy (HCM) is the most prevalent inherited cardiac disease. Since the modern description of HCM more than seven decades ago, great focus has been placed on preventing its most catastrophic complication: sudden cardiac death (SCD). ... ...

    Abstract Hypertrophic cardiomyopathy (HCM) is the most prevalent inherited cardiac disease. Since the modern description of HCM more than seven decades ago, great focus has been placed on preventing its most catastrophic complication: sudden cardiac death (SCD). Implantable cardioverter-defibrillators (ICD) have been recognized to provide effective prophylactic therapy. Over the years, two leading societies, the European Society of Cardiology (ESC) and the American Heart Association/American College of Cardiology (AHA/ACC), have proposed risk stratification models to assess SCD in adults. European guidelines rely on a risk calculator, the HCM Risk-SCD, while American guidelines propose a stand-alone risk factor approach. Recently, risk prediction models were also developed in the pediatric population. This article reviews the latest recommendations on the risk stratification of SCD in HCM and summarises current indications for ICD use.
    MeSH term(s) Adult ; Humans ; Child ; United States/epidemiology ; Longevity ; Risk Assessment ; Risk Factors ; Defibrillators, Implantable/adverse effects ; Death, Sudden, Cardiac/etiology ; Cardiomyopathy, Hypertrophic/complications ; Cardiomyopathy, Hypertrophic/therapy
    Language English
    Publishing date 2023-06-17
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ISSN 1877-9190
    ISSN (online) 1877-9190
    DOI 10.1016/j.ccep.2023.04.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Use, misuse, and pitfalls of the drug challenge test in the diagnosis of the Brugada syndrome.

    Wilde, Arthur A M / Amin, Ahmad S / Morita, Hiroshi / Tadros, Rafik

    European heart journal

    2023  Volume 44, Issue 27, Page(s) 2427–2439

    Abstract: The diagnosis of Brugada syndrome (BrS) requires the presence of a coved (Type 1) ST segment elevation in the right precordial leads of the electrocardiogram (ECG). The dynamic nature of the ECG is well known, and in patients with suspected BrS but non- ... ...

    Abstract The diagnosis of Brugada syndrome (BrS) requires the presence of a coved (Type 1) ST segment elevation in the right precordial leads of the electrocardiogram (ECG). The dynamic nature of the ECG is well known, and in patients with suspected BrS but non-diagnostic ECG at baseline, a sodium channel blocker test (SCBT) is routinely used to unmask BrS. There is little doubt, however, that in asymptomatic patients, a drug-induced Brugada pattern is associated with a much better prognosis compared to a spontaneous Type 1 ECG. The SCBT is also increasingly used to delineate the arrhythmogenic substrate during ablation studies. In the absence of a "gold standard" for the diagnosis of BrS, sensitivity and specificity of the SCBT remain elusive. By studying patient groups with different underlying diseases, it has become clear that the specificity of the test may not be optimal. This review aims to discuss the pitfalls of the SCBT and provides some directions in whom and when to perform the test. It is concluded that because of the debated specificity and the overall very low risk for future events in asymptomatic individuals, patients should be properly selected and counseled before SCBT is performed and that SCBT should not be performed in asymptomatic patients with a Type 2 Brugada pattern and no family history of BrS or sudden death.
    MeSH term(s) Humans ; Brugada Syndrome/diagnosis ; Electrocardiography ; Sodium Channel Blockers ; Prognosis ; Death, Sudden
    Chemical Substances Sodium Channel Blockers
    Language English
    Publishing date 2023-06-21
    Publishing country England
    Document type Review ; Journal Article
    ZDB-ID 603098-1
    ISSN 1522-9645 ; 0195-668X
    ISSN (online) 1522-9645
    ISSN 0195-668X
    DOI 10.1093/eurheartj/ehad295
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  7. Article ; Online: Cardiomyopathy Genes and Idiopathic VF: A Known Unknown?

    Mellor, Greg J / Tadros, Rafik / Krahn, Andrew D

    Circulation. Genomic and precision medicine

    2022  Volume 15, Issue 1, Page(s) e003680

    MeSH term(s) Cardiomyopathies/genetics ; Death, Sudden, Cardiac ; Exome ; Humans ; Ventricular Fibrillation/genetics
    Language English
    Publishing date 2022-02-01
    Publishing country United States
    Document type Editorial ; Comment
    ISSN 2574-8300
    ISSN (online) 2574-8300
    DOI 10.1161/CIRCGEN.122.003680
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  8. Article ; Online: An integrated overview of AV node physiology.

    Billette, Jacques / Tadros, Rafik

    Pacing and clinical electrophysiology : PACE

    2019  Volume 42, Issue 7, Page(s) 805–820

    Abstract: The atrioventricular (AV) node generates half of the AV delay needed for blood pumping and filters atrial impulses that could otherwise induce life-threatening ventricular arrhythmias. It is also a pacemaker and a key target in the treatment of cardiac ... ...

    Abstract The atrioventricular (AV) node generates half of the AV delay needed for blood pumping and filters atrial impulses that could otherwise induce life-threatening ventricular arrhythmias. It is also a pacemaker and a key target in the treatment of cardiac arrhythmias. The special roles of the AV node primarily arise from its slow conduction, long refractory period, and cellular automaticity. However, efforts to establish the dynamics of these properties and their interaction led to many controversies. In fact, the AV node's behavior is so complex that it seems to escape broadly applicable rules. This review summarizes progresses made in resolving these issues and in integrating the multiple roles of the AV node within a common functional model. Presented evidence shows that the rate-dependent conduction and refractory properties of the AV node can be reliably characterized and reconciled from nodal responses to S
    MeSH term(s) Atrioventricular Node/physiology ; Heart Conduction System/physiology ; Humans
    Language English
    Publishing date 2019-06-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 424437-0
    ISSN 1540-8159 ; 0147-8389
    ISSN (online) 1540-8159
    ISSN 0147-8389
    DOI 10.1111/pace.13734
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  9. Article ; Online: Unraveling the Genetic Substrate and Phenotypic Variability of Hypertrophic Cardiomyopathy: A Role for Desmosome Gene Variants?

    Jordà, Paloma / Oudit, Gavin Y / Tadros, Rafik

    The Canadian journal of cardiology

    2021  Volume 38, Issue 1, Page(s) 3–5

    MeSH term(s) Biological Variation, Population ; Cardiomyopathy, Hypertrophic/diagnosis ; Cardiomyopathy, Hypertrophic/genetics ; Desmosomes ; Genetic Variation ; Humans
    Language English
    Publishing date 2021-12-01
    Publishing country England
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 632813-1
    ISSN 1916-7075 ; 0828-282X
    ISSN (online) 1916-7075
    ISSN 0828-282X
    DOI 10.1016/j.cjca.2021.11.013
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  10. Article ; Online: When genetic burden reaches threshold.

    Walsh, Roddy / Tadros, Rafik / Bezzina, Connie R

    European heart journal

    2020  Volume 41, Issue 39, Page(s) 3849–3855

    Abstract: Rare cardiac genetic diseases have generally been considered to be broadly Mendelian in nature, with clinical genetic testing for these conditions predicated on the detection of a primary causative rare pathogenic variant that will enable cascade genetic ...

    Abstract Rare cardiac genetic diseases have generally been considered to be broadly Mendelian in nature, with clinical genetic testing for these conditions predicated on the detection of a primary causative rare pathogenic variant that will enable cascade genetic screening in families. However, substantial variability in penetrance and disease severity among carriers of pathogenic variants, as well as the inability to detect rare Mendelian variants in considerable proportions of patients, indicates that more complex aetiologies are likely to underlie these diseases. Recent findings have suggested genetic variants across a range of population frequencies and effect sizes may combine, along with non-genetic factors, to determine whether the threshold for expression of disease is reached and the severity of the phenotype. The availability of increasingly large genetically characterized cohorts of patients with rare cardiac diseases is enabling the discovery of common genetic variation that may underlie both variable penetrance in Mendelian diseases and the genetic aetiology of apparently non-Mendelian rare cardiac conditions. It is likely that the genetic architecture of rare cardiac diseases will vary considerably between different conditions as well as between patients with similar phenotypes, ranging from near-Mendelian disease to models more akin to common, complex disease. Uncovering the broad range of genetic factors that predispose patients to rare cardiac diseases offers the promise of improved risk prediction and more focused clinical management in patients and their families.
    MeSH term(s) Genetic Predisposition to Disease ; Genetic Testing ; Genetic Variation/genetics ; Heterozygote ; Humans ; Phenotype ; Rare Diseases
    Language English
    Publishing date 2020-04-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603098-1
    ISSN 1522-9645 ; 0195-668X
    ISSN (online) 1522-9645
    ISSN 0195-668X
    DOI 10.1093/eurheartj/ehaa269
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