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Article ; Online: COVID-19 does not only disturb our social rhythm.

Wilde, Arthur A M / Offerhaus, Joost Allard

2021 Volume 18, Issue 4, Page(s) 510–511

MeSH term(s)	Atrial Fibrillation ; COVID-19 ; Circadian Rhythm ; Hospital Mortality ; Humans ; SARS-CoV-2
Language	English
Publishing date	2021-04-01
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2229357-7
ISSN	1556-3871 ; 1547-5271
ISSN (online)	1556-3871
ISSN	1547-5271
DOI	10.1016/j.hrthm.2021.02.007
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Article ; Online: Cardiac Repolarization in Health and Disease.

Krijger Juárez, Christian / Amin, Ahmad S / Offerhaus, Joost A / Bezzina, Connie R / Boukens, Bastiaan J

JACC. Clinical electrophysiology

2022 Volume 9, Issue 1, Page(s) 124–138

Abstract: Abnormal cardiac repolarization is at the basis of life-threatening arrhythmias in various congenital and acquired cardiac diseases. Dysfunction of ion channels involved in repolarization at the cellular level are often the underlying cause of the ... ...

Abstract	Abnormal cardiac repolarization is at the basis of life-threatening arrhythmias in various congenital and acquired cardiac diseases. Dysfunction of ion channels involved in repolarization at the cellular level are often the underlying cause of the repolarization abnormality. The expression pattern of the gene encoding the affected ion channel dictates its impact on the shape of the T-wave and duration of the QT interval, thereby setting the stage for both the occurrence of the trigger and the substrate for maintenance of the arrhythmia. Here we discuss how research into the genetic and electrophysiological basis of repolarization has provided us with insights into cardiac repolarization in health and disease and how this in turn may provide the basis for future improved patient-specific management.
MeSH term(s)	Humans ; Heart ; Arrhythmias, Cardiac/genetics ; Electrophysiological Phenomena
Language	English
Publishing date	2022-11-30
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2846739-5
ISSN	2405-5018 ; 2405-500X ; 2405-500X
ISSN (online)	2405-5018 ; 2405-500X
ISSN	2405-500X
DOI	10.1016/j.jacep.2022.09.017
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Article ; Online: Prophylactic (hydroxy)chloroquine in COVID-19: Potential relevance for cardiac arrhythmia risk.

Offerhaus, Joost A / Wilde, Arthur A M / Remme, Carol Ann

Heart rhythm

2020 Volume 17, Issue 9, Page(s) 1480–1486

Abstract: Hydroxy)chloroquine ((H)CQ) is being investigated as a treatment for COVID-19, but studies have so far demonstrated either no or a small benefit. However, these studies have been mostly performed in patients admitted to the hospital and hence likely ... ...

Abstract	(Hydroxy)chloroquine ((H)CQ) is being investigated as a treatment for COVID-19, but studies have so far demonstrated either no or a small benefit. However, these studies have been mostly performed in patients admitted to the hospital and hence likely already (severely) affected. Another suggested approach uses prophylactic (H)CQ treatment aimed at preventing either severe acute respiratory syndrome coronavirus 2 infection or the development of disease. A substantial number of clinical trials are planned or underway aimed at assessing the prophylactic benefit of (H)CQ. However, (H)CQ may lead to QT prolongation and potentially induce life-threatening arrhythmias. This may be of particular relevance to patients with preexisting cardiovascular disease and those taking other QT-prolonging drugs. In addition, it is known that a certain percentage of the population carries genetic variant(s) that reduces their repolarization reserve, predisposing them to (H)CQ-induced QT prolongation, and this may be more relevant to female patients who already have a longer QT interval to start with. This review provides an overview of the current evidence on (H)CQ therapy in patients with COVID-19 and discusses different strategies for prophylactic (H)CQ therapy (ie, preinfection, postexposure, and postinfection). In particular, the potential cardiac effects, including QT prolongation and arrhythmias, will be addressed. Based on these insights, recommendations will be presented as to which preventive measures should be taken when giving (H)CQ prophylactically, including electrocardiographic monitoring.
MeSH term(s)	Antimalarials/therapeutic use ; Arrhythmias, Cardiac/epidemiology ; Betacoronavirus ; COVID-19 ; Coronavirus Infections/complications ; Coronavirus Infections/drug therapy ; Coronavirus Infections/prevention & control ; Humans ; Hydroxychloroquine/therapeutic use ; Pandemics/prevention & control ; Pneumonia, Viral/complications ; Pneumonia, Viral/prevention & control ; SARS-CoV-2 ; COVID-19 Drug Treatment
Chemical Substances	Antimalarials ; Hydroxychloroquine (4QWG6N8QKH)
Keywords	covid19
Language	English
Publishing date	2020-07-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2229357-7
ISSN	1556-3871 ; 1547-5271
ISSN (online)	1556-3871
ISSN	1547-5271
DOI	10.1016/j.hrthm.2020.07.001
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Article ; Online: Minor hypertrophic cardiomyopathy genes, major insights into the genetics of cardiomyopathies.

Walsh, Roddy / Offerhaus, Joost A / Tadros, Rafik / Bezzina, Connie R

Nature reviews. Cardiology

2021 Volume 19, Issue 3, Page(s) 151–167

Abstract: Hypertrophic cardiomyopathy (HCM) was traditionally described as an autosomal dominant Mendelian disease but is now increasingly recognized as having a complex genetic aetiology. Although eight core genes encoding sarcomeric proteins account for >90% of ... ...

Abstract	Hypertrophic cardiomyopathy (HCM) was traditionally described as an autosomal dominant Mendelian disease but is now increasingly recognized as having a complex genetic aetiology. Although eight core genes encoding sarcomeric proteins account for >90% of the pathogenic variants in patients with HCM, variants in several additional genes (ACTN2, ALPK3, CSRP3, FHOD3, FLNC, JPH2, KLHL24, PLN and TRIM63), encoding non-sarcomeric proteins with diverse functions, have been shown to be disease-causing in a small number of patients. Genome-wide association studies (GWAS) have identified numerous loci in cardiomyopathy case-control studies and biobank investigations of left ventricular functional traits. Genes associated with Mendelian cardiomyopathy are enriched in the putative causal gene lists at these loci. Intriguingly, many loci are associated with both HCM and dilated cardiomyopathy but with opposite directions of effect on left ventricular traits, highlighting a genetic basis underlying the contrasting pathophysiological effects observed in each condition. This overlap extends to rare Mendelian variants with distinct variant classes in several genes associated with HCM and dilated cardiomyopathy. In this Review, we appraise the complex contribution of the non-sarcomeric, HCM-associated genes to cardiomyopathies across a range of variant classes (from common non-coding variants of individually low effect size to complete gene knockouts), which provides insights into the genetic basis of cardiomyopathies, causal genes at GWAS loci and the application of clinical genetic testing.
MeSH term(s)	Cardiomyopathies/genetics ; Cardiomyopathy, Dilated/genetics ; Cardiomyopathy, Hypertrophic/genetics ; Genetic Testing ; Genome-Wide Association Study ; Humans ; Mutation
Language	English
Publishing date	2021-09-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2490375-9
ISSN	1759-5010 ; 1759-5002
ISSN (online)	1759-5010
ISSN	1759-5002
DOI	10.1038/s41569-021-00608-2
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Article ; Online: Epidemiology of inherited arrhythmias.

Offerhaus, Joost A / Bezzina, Connie R / Wilde, Arthur A M

Nature reviews. Cardiology

2019 Volume 17, Issue 4, Page(s) 205–215

Abstract: The primary electrical disorders are a group of inherited cardiac ventricular arrhythmias that are a major cause of sudden cardiac death in young individuals. Inherited ventricular arrhythmias result from mutations in genes encoding cardiac ion channels ... ...

Abstract	The primary electrical disorders are a group of inherited cardiac ventricular arrhythmias that are a major cause of sudden cardiac death in young individuals. Inherited ventricular arrhythmias result from mutations in genes encoding cardiac ion channels or their modulatory subunits. Advances in genetic screening in the past three decades have led to the assembly of large patient cohorts with these disorders. Studies in these patients, as well as in the general population, have striven to define the prevalence of these inherited arrhythmias and the characteristics of patients with different genetic subtypes of the disease. In this Review, we provide a comprehensive update on the epidemiology of inherited ventricular arrhythmias, focusing on natural history, prevalence and patient demographics. In addition, we summarize the various founder populations (groups of individuals with a disease that is caused by a genetic defect inherited from a common ancestor) that have been identified for some of these disorders and which lead to increased prevalence in some geographical regions. To date, although numerous studies have markedly increased our understanding of the epidemiology of these disorders, demographic data, especially from non-Western countries, remain scarce. Furthermore, defining the true prevalence of these disorders remains challenging. International collaboration will undoubtedly accelerate the collection of demographic information and improve the accuracy of prevalence data.
MeSH term(s)	Arrhythmias, Cardiac/diagnosis ; Arrhythmias, Cardiac/epidemiology ; Arrhythmias, Cardiac/genetics ; Female ; Humans ; Male ; Prevalence
Language	English
Publishing date	2019-10-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2490375-9
ISSN	1759-5010 ; 1759-5002
ISSN (online)	1759-5010
ISSN	1759-5002
DOI	10.1038/s41569-019-0266-2
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Article ; Online: Prophylactic (hydroxy)chloroquine in COVID-19

Offerhaus, Joost A. / Wilde, Arthur A.M. / Remme, Carol Ann

Heart Rhythm

Potential relevance for cardiac arrhythmia risk

2020 Volume 17, Issue 9, Page(s) 1480–1486

Keywords	Physiology (medical) ; Cardiology and Cardiovascular Medicine ; covid19
Language	English
Publisher	Elsevier BV
Publishing country	us
Document type	Article ; Online
ZDB-ID	2229357-7
ISSN	1556-3871 ; 1547-5271
ISSN (online)	1556-3871
ISSN	1547-5271
DOI	10.1016/j.hrthm.2020.07.001
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Article: Prophylactic (hydroxy)chloroquine in COVID-19: Potential relevance for cardiac arrhythmia risk

Offerhaus, Joost A / Wilde, Arthur A M / Remme, Carol Ann

Heart Rhythm

Abstract	(Hydroxy)chloroquine ((H)CQ) is being investigated as a treatment for COVID-19, but studies have so far demonstrated either no or a small benefit. However, these studies have been mostly performed in patients admitted to the hospital and hence likely already (severely) affected. Another suggested approach uses prophylactic (H)CQ treatment aimed at preventing either severe acute respiratory syndrome coronavirus 2 infection or the development of disease. A substantial number of clinical trials are planned or underway aimed at assessing the prophylactic benefit of (H)CQ. However, (H)CQ may lead to QT prolongation and potentially induce life-threatening arrhythmias. This may be of particular relevance to patients with preexisting cardiovascular disease and those taking other QT-prolonging drugs. In addition, it is known that a certain percentage of the population carries genetic variant(s) that reduces their repolarization reserve, predisposing them to (H)CQ-induced QT prolongation, and this may be more relevant to female patients who already have a longer QT interval to start with. This review provides an overview of the current evidence on (H)CQ therapy in patients with COVID-19 and discusses different strategies for prophylactic (H)CQ therapy (ie, preinfection, postexposure, and postinfection). In particular, the potential cardiac effects, including QT prolongation and arrhythmias, will be addressed. Based on these insights, recommendations will be presented as to which preventive measures should be taken when giving (H)CQ prophylactically, including electrocardiographic monitoring.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #627200
Database	COVID19

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Article ; Online: High heart rate associated early repolarization causes J-waves in both zebra finch and mouse.

Offerhaus, Joost A / Snelderwaard, Peter C / Algül, Sila / Faber, Jaeike W / Riebel, Katharina / Jensen, Bjarke / Boukens, Bastiaan J

Physiological reports

2021 Volume 9, Issue 5, Page(s) e14775

Abstract: High heart rates are a feature of small endothermic-or warm-blooded-mammals and birds. In small mammals, the QT interval is short, and local ventricular recordings reveal early repolarization that coincides with the J-wave on the ECG, a positive ... ...

Abstract	High heart rates are a feature of small endothermic-or warm-blooded-mammals and birds. In small mammals, the QT interval is short, and local ventricular recordings reveal early repolarization that coincides with the J-wave on the ECG, a positive deflection following the QRS complex. Early repolarization contributes to short QT-intervals thereby enabling brief cardiac cycles and high heart rates. We therefore hypothesized high hearts rates associate with early repolarization and J-waves on the ECG of endothermic birds. We tested this hypothesis by comparing isolated hearts of zebra finches and mice and recorded pseudo-ECGs and optical action potentials (zebra finch, n = 8; mouse, n = 8). In both species, heart rate exceeded 300 beats per min, and total ventricular activation was fast (QRS < 10 ms). Ventricular activation progressed from the left to the right ventricle in zebra finch, whereas it progressed from apex-to-base in mouse. In both species, the early repolarization front followed the activation front, causing a positive J-wave in the pseudo-ECG. Inhibition of early repolarization by 4-aminopyridine reduced J-wave amplitude in both species. Action potential duration was similar between ventricles in zebra finch, whereas in mouse the left ventricular action potential was longer. Accordingly, late repolarization had opposite directions in zebra finch (left-right) and mouse (right-left). This caused a similar direction for the zebra finch J-wave and T-wave, whereas in the mouse they were discordant. Our findings demonstrate that early repolarization and the associated J-wave may have evolved by convergence in association with high heart rates.
MeSH term(s)	Action Potentials/physiology ; Animals ; Arrhythmias, Cardiac/physiopathology ; Electrocardiography/methods ; Finches/physiology ; Heart/physiology ; Heart Conduction System/physiology ; Heart Rate/physiology ; Heart Ventricles/physiopathology ; Mice
Language	English
Publishing date	2021-03-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.14775
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Article: Sex- and age specific association of new-onset atrial fibrillation with in-hospital mortality in hospitalised COVID-19 patients.

Offerhaus, Joost A / Joosten, Linda P T / van Smeden, Maarten / Linschoten, Marijke / Bleijendaal, Hidde / Tieleman, Robert / Wilde, Arthur A M / Rutten, Frans H / Geersing, Geert-Jan / Remme, Carol Ann

International journal of cardiology. Heart & vasculature

2022 Volume 39, Page(s) 100970

Abstract: Background: Coronavirus disease 2019 (COVID-19) is a systemic disease with cardiovascular involvement, including cardiac arrhythmias. Notably, new-onset atrial fibrillation (AF) and atrial flutter (AFL) during hospitalisation in COVID-19 patients has ... ...

Abstract	Background: Coronavirus disease 2019 (COVID-19) is a systemic disease with cardiovascular involvement, including cardiac arrhythmias. Notably, new-onset atrial fibrillation (AF) and atrial flutter (AFL) during hospitalisation in COVID-19 patients has been associated with increased mortality. However, how this risk is impacted by age and sex is still poorly understood. Methods: For this multicentre cohort study, we extracted demographics, medical history, occurrence of electrical disorders and in-hospital mortality from the large international patient registry CAPACITY-COVID. For each electrical disorder, prevalence during hospitalisation was calculated. Subsequently, we analysed the incremental prognostic effect of developing AF/AFL on in-hospital mortality, using multivariable logistic regression analyses, stratified for sex and age. Results: In total, 5782 patients (64% male; median age 67) were included. Of all patients 11.0% (95% CI 10.2-11.8) experienced AF and 1.6% (95% CI 1.3-1.9) experienced AFL during hospitalisation. Ventricular arrhythmias were rare (<0.8% (95% CI 0.6-1.0)) and a conduction disorder was observed in 6.3% (95% CI 5.7-7.0). An event of AF/AFL appeared to occur more often in patients with pre-existing heart failure. After multivariable adjustment for age and sex, new-onset AF/AFL was significantly associated with a poorer prognosis, exemplified by a two- to three-fold increased risk of in-hospital mortality in males aged 60-72 years, whereas this effect was largely attenuated in older male patients and not observed in female patients. Conclusion: In this large COVID-19 cohort, new-onset AF/AFL was associated with increased in-hospital mortality, yet this increased risk was restricted to males aged 60-72 years.
Language	English
Publishing date	2022-02-04
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	2818464-6
ISSN	2352-9067
ISSN	2352-9067
DOI	10.1016/j.ijcha.2022.100970
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Article ; Online: Variant Intronic Enhancer Controls

Man, Joyce C K / Bosada, Fernanda M / Scholman, Koen T / Offerhaus, Joost A / Walsh, Roddy / van Duijvenboden, Karel / van Eif, Vincent W W / Bezzina, Connie R / Verkerk, Arie O / Boukens, Bastiaan J / Barnett, Phil / Christoffels, Vincent M

Circulation

2021 Volume 144, Issue 3, Page(s) 229–242

Abstract: Background: Genetic variants in : Methods: The expression of : Results: We found that cardiomyocytes of the atria, sinoatrial node, and ventricular conduction system express a short transcript comprising the last 7 exons of the gene (: ... ...

Abstract	Background: Genetic variants in Methods: The expression of Results: We found that cardiomyocytes of the atria, sinoatrial node, and ventricular conduction system express a short transcript comprising the last 7 exons of the gene ( Conclusions: Genetic variants in and around
MeSH term(s)	Action Potentials/genetics ; Animals ; Biomarkers ; Cardiac Conduction System Disease/diagnosis ; Cardiac Conduction System Disease/genetics ; Cardiac Conduction System Disease/physiopathology ; Cardiac Electrophysiology ; Disease Susceptibility ; Electrocardiography ; Enhancer Elements, Genetic ; Female ; Gene Expression Regulation ; Genetic Association Studies ; Heart Conduction System/physiology ; Introns ; Male ; Mice ; NAV1.5 Voltage-Gated Sodium Channel/genetics ; NAV1.8 Voltage-Gated Sodium Channel/genetics ; Quantitative Trait Loci ; Quantitative Trait, Heritable
Chemical Substances	Biomarkers ; NAV1.5 Voltage-Gated Sodium Channel ; NAV1.8 Voltage-Gated Sodium Channel ; Scn10a protein, mouse ; Scn5a protein, mouse
Language	English
Publishing date	2021-04-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.121.054083
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