Publications by authors named "Corinna Brunckhorst"

153 Publications

[CME ECG 68/Answers: Gender Specificities in Heart Rhythm Disorders].

Praxis (Bern 1994) 2021 ;110(4):189-191

Klinik für Kardiologie, Universitäres Herzzentrum, Universitätsspital Zürich.

CME ECG 68/Answers: Gender Specificities in Heart Rhythm Disorders Sex differences in heart rhythm disorders have been described, especially due to differences of hormone status in women and men. In general, women do have a higher baseline heart rate than men and shorter refractory periods of most structures in the conduction system, except the ventricles. This is particularly apparent in paroxysmal supraventricular tachycardias. The incidence of a dual AV nodal physiology is the same in both sexes. However, an AV-nodal reentry tachycardia is much more frequent in women than in men. The embryonal disposition for an accessory pathway, as well as the resultant AV reentry tachycardia is more common in men than in women. Focal atrial tachycardias do not reveal a clear dominance between the sexes. Knowledge about sex-related differences in heart rhythm disorders are relevant for its diagnostics. Therefore, important aspects will be discussed in this article.
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http://dx.doi.org/10.1024/1661-8157/a003657DOI Listing
March 2021

The Link Between Sex Hormones and Susceptibility to Cardiac Arrhythmias: From Molecular Basis to Clinical Implications.

Front Cardiovasc Med 2021 17;8:644279. Epub 2021 Feb 17.

Arrhythmia and Electrophysiology, Department of Cardiology, University Heart Center, Zurich, Switzerland.

It is well-known that gender is an independent risk factor for some types of cardiac arrhythmias. For example, males have a greater prevalence of atrial fibrillation and the Brugada Syndrome. In contrast, females are at increased risk for the Long QT Syndrome. However, the underlying mechanisms of these gender differences have not been fully identified. Recently, there has been accumulating evidence indicating that sex hormones may have a significant impact on the cardiac rhythm. In this review, we describe in-depth the molecular interactions between sex hormones and the cardiac ion channels, as well as the clinical implications of these interactions on the cardiac conduction system, in order to understand the link between these hormones and the susceptibility to arrhythmias.
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http://dx.doi.org/10.3389/fcvm.2021.644279DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7925388PMC
February 2021

[CME ECG 68: Gender Specificities in Heart Rhythm Disorders].

Praxis (Bern 1994) 2021 ;110(3):131-139

Klinik für Kardiologie, Universitäres Herzzentrum, Universitätsspital Zürich.

CME ECG 68: Gender Specificities in Heart Rhythm Disorders Sex differences in heart rhythm disorders have been described, especially due to differences of hormone status in women and men. In general, women do have a higher baseline heart rate than men and shorter refractory periods of most structures in the conduction system, except the ventricles. This is particularly apparent in paroxysmal supraventricular tachycardias. The incidence of a dual AV nodal physiology is the same in both sexes. However, an AV-nodal reentry tachycardia is much more frequent in women than in men. The embryonal disposition for an accessory pathway, as well as the resultant AV reentry tachycardia is more common in men than in women. Focal atrial tachycardias do not reveal a clear dominance between the sexes. Knowledge about sex-related differences in heart rhythm disorders are relevant for its diagnostics. Therefore, important aspects will be discussed in this article.
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http://dx.doi.org/10.1024/1661-8157/a003656DOI Listing
March 2021

[CME ECG 67/Answers: Arrhythmia on Exertion].

Praxis (Bern 1994) 2021 Jan;110(1):19-21

Klinik für Kardiologie, Universitäres Herzzentrum, Universitätsspital Zürich.

CME ECG 67/Answers: Arrhythmia on Exertion Ventricular tachycardias are potentially life-threatening cardiac arrhythmias with a heart rate >100 beats/min, originating from the specific conduction system below the His or the ventricular myocardium. The morphology of the surface ECG can provide valid information about the underlying mechanism and the associated cardiac disorder. The according pathomechanism is of paramount importance for further management. This article is intended to provide an insight into the various causes and treatment options as well as the differential diagnosis of ventricular tachycardias.
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http://dx.doi.org/10.1024/1661-8157/a003608DOI Listing
January 2021

[CME ECC 67: Arrhythmia on Exertion].

Praxis (Bern 1994) 2020 ;109(16):1231-1237

Klinik für Kardiologie, Universitäres Herzzentrum, Universitätsspital Zürich.

CME ECC 67: Arrhythmia on Exertion Ventricular tachycardias are potentially life-threatening cardiac arrhythmias with a heart rate >100 beats/min, originating from the specific conduction system below the His or the ventricular myocardium. The morphology of the surface ECG can provide valid information about the underlying mechanism and the associated cardiac disorder. The according pathomechanism is of paramount importance for further management. This article is intended to provide an insight into the various causes and treatment options as well as the differential diagnosis of ventricular tachycardias.
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http://dx.doi.org/10.1024/1661-8157/a003607DOI Listing
December 2020

Familial Arrhythmogenic Cardiomyopathy: Clinical Determinants of Phenotype Discordance and the Impact of Endurance Sports.

J Clin Med 2020 Nov 23;9(11). Epub 2020 Nov 23.

University Heart Center Zurich, Division of Cardiology, 8091 Zurich, Switzerland.

Arrhythmogenic cardiomyopathy (ACM) is primarily a familial disease with autosomal dominant inheritance. Incomplete penetrance and variable expression are common, resulting in diverse clinical manifestations. Although recent studies on genotype-phenotype relationships have improved our understanding of the molecular mechanisms leading to the expression of the full-blown disease, the underlying genetic substrate and the clinical course of asymptomatic or oligo-symptomatic mutation carriers are still poorly understood. We aimed to analyze different phenotypic expression profiles of ACM in the context of the same familial genetic mutation by studying nine adult cases from four different families with four different familial variants (two plakophilin-2 and two desmoglein-2) from the Swiss Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) Registry. The affected individuals with the same genetic variants presented with highly variable phenotypes ranging from no disease or a classical, right-sided disease, to ACM with biventricular presentation. Moreover, some patients developed early-onset, electrically unstable disease whereas others with the same genetic variants presented with late-onset electrically stable disease. Despite differences in age, gender, underlying genotype, and other clinical characteristics, physical exercise has been observed as the common denominator in provoking an arrhythmic phenotype in these families.
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http://dx.doi.org/10.3390/jcm9113781DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7700696PMC
November 2020

Impact of Genetic Variant Reassessment on the Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy Based on the 2010 Task Force Criteria.

Circ Genom Precis Med 2021 Feb 24;14(1):e003047. Epub 2020 Nov 24.

Department of Cardiology, University Heart Center Zurich, University Hospital Zurich, Switzerland (S.C., A.G., D.A., F.R., C.B.B., F.D., A.M.S.).

Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy, which is associated with life-threatening ventricular arrhythmias. Approximately 60% of patients carry a putative disease-causing genetic variant, but interpretation of genetic test results can be challenging. The aims of this study were to systematically reclassify genetic variants in patients with ARVC and to assess the impact on ARVC diagnosis.

Methods: This study included patients from the Multicenter Zurich ARVC Registry who hosted a genetic variant deemed to be associated with the disease. Reclassification of pathogenicity was performed according to the modified 2015 American College of Medical Genetics criteria. ARVC diagnosis (categories: definite, borderline, possible) based on the 2010 Task Force Criteria was reclassified after genetic readjudication.

Results: In 79 patients bearing 80 unique genetic variants, n=47 (58.8%) genetic variants were reclassified, and reclassification was judged to be clinically relevant in n=33 (41.3%). Variants in plakophilin-2 () were shown to reclassify less frequently as compared with other genes (, n=1, 8.3%; desmosomal non-, n=20, 66.7%; nondesmosomal, n=26, 68.4%; =0.001for overall comparison; versus desmosomal non-=0.001; versus nondesmosomal, <0.001). Genetic reclassification impacted ARVC diagnosis. Eight patients (10.1%) were downgraded from definite to borderline/possible disease at the time of initial genetic testing as well as last follow-up, respectively. Separate genetic reclassification in family members led to downgrading of n=5 (38.5%) variants.

Conclusions: Given that approximately half of genetic variants were reclassified, with 10.1% of patients losing their definite disease status, accurate determination of variant pathogenicity is of utmost importance in the diagnosis of ARVC.
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http://dx.doi.org/10.1161/CIRCGEN.120.003047DOI Listing
February 2021

[CME ECG 66/Answers: Torsade de Pointes: The Danger of a Rotating Heart Axis].

Praxis (Bern 1994) 2020 ;109(13):1035-1038

Universitätsspital Zürich, Klinik für Kardiologie.

CME ECG 66/Answers: Torsade de Pointes: The Danger of a Rotating Heart Axis Torsade de pointes tachycardia is a potentially life-threatening heart rhythm disorder, caused by prolongation of the QT interval resulting in triggered activity. This QT prolongation can be congenital or acquired. If acquired, it is mainly caused by pharmacological therapy. The hallmark of torsade de pointes is an undulating QRS axis with a twist of the QRS complex around the ECG's baseline. Often, this polymorphic ventricular tachycardia is self-limiting, but degeneration into ventricular fibrillation is possible, which makes torsade de pointes tachycardia dangerous. This article aims to provide insights into etiology, diagnostics, prevention and management of this heart rhythm disorder.
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http://dx.doi.org/10.1024/1661-8157/a003584DOI Listing
October 2020

Differentiating hereditary arrhythmogenic right ventricular cardiomyopathy from cardiac sarcoidosis fulfilling 2010 ARVC Task Force Criteria.

Heart Rhythm 2021 Feb 22;18(2):231-238. Epub 2020 Sep 22.

University Heart Center, University Hospital Zurich, Switzerland. Electronic address:

Background: The clinical presentation of cardiac sarcoidosis (CS) may resemble that of arrhythmogenic right ventricular cardiomyopathy (ARVC).

Objective: The purpose of this study was to identify clinical variables to better discriminate between patients with genetically determined ARVC and those with CS fulfilling definite 2010 ARVC Task Force Criteria (TFC).

Methods: In this multicenter study, 10 patients with CS fulfilling definite 2010 ARVC TFC were age and gender matched with 10 genetically proven ARVC patients. A cardiac F-fluorodeoxyglucose positron emission tomographic (F-FDG PET) scan was required for patients to be included in the study.

Results: The 2010 ARVC TFC did not reliably differentiate between the 2 diseases. CS patients presented with longer PR intervals, advanced atrioventricular block (AVB), and longer QRS duration (P <.001 and P = .009, respectively), whereas T-wave inversions (TWIs) in the peripheral leads were more common in ARVC patients (P = .009). CS patients presented with more extensive left ventricular involvement and lower left ventricular ejection fraction (LVEF), whereas ARVC patients had a larger right ventricular outflow tract (RVOT) (P = .044). PET scan positivity was only present in CS patients (90% vs 0%).

Conclusion: The 2010 ARVC TFC do not reliably differentiate between CS patients fulfilling 2010 ARVC TFC and those with hereditary ARVC. Prolonged PR interval, advanced AVB, longer QRS duration, right ventricular apical involvement, reduced LVEF, and positive F-FDG PET scan should raise the suspicion of CS, whereas larger RVOT dimensions, subtricuspid involvement and peripheral TWI favor a diagnosis of hereditary ARVC.
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http://dx.doi.org/10.1016/j.hrthm.2020.09.015DOI Listing
February 2021

[CME ECC 66: Torsade de Pointes: The Danger of a Rotating Heart Axis].

Praxis (Bern 1994) 2020 Sep;109(12):944-951

Universitätsspital Zürich, Klinik für Kardiologie.

CME ECC 66: Torsade de Pointes: The Danger of a Rotating Heart Axis Torsade de pointes tachycardia is a potentially life-threatening heart rhythm disorder, caused by prolongation of the QT-interval resulting in triggered activity. This QT-prolongation can be congenital or acquired. If acquired, it is mainly caused by pharmacological therapy. The hallmark of torsade de pointes is an undulating QRS axis with a twist of the QRS complex around the ECG's baseline. Often, this polymorphic ventricular tachycardia is self-limiting, but degeneration into ventricular fibrillation is possible, which makes torsade de pointes tachycardia dangerous. This article aims to provide insights into etiology, diagnostics, prevention and management of this heart rhythm disorder.
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http://dx.doi.org/10.1024/1661-8157/a003583DOI Listing
September 2020

Arrhythmogenic cardiomyopathy: An in-depth look at molecular mechanisms and clinical correlates.

Trends Cardiovasc Med 2020 Jul 29. Epub 2020 Jul 29.

Division of Cardiology, University Heart Center Zurich, Rämistrasse 100, CH-8091, Zurich, Switzerland; Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland. Electronic address:

Arrhythmogenic cardiomyopathy (ACM) is a familial disease, with approximately 60% of patients displaying a pathogenic variant. The majority of genes linked to ACM code for components of the desmosome: plakophilin-2 (PKP2), desmoglein-2 (DSG2) and desmocollin-2 (DSC2), plakoglobin (JUP) and desmoplakin (DSP). Genetic variants involving the desmosomes are known to cause dysfunction of cell-to-cell adhesions and intercellular gap junctions. In turn, this may result in failure to mechanically hold together the cardiomyocytes, fibrofatty myocardial replacement, cardiac conduction delay and ventricular arrhythmias. It is becoming clearer that pathogenic variants in desmosomal genes such as PKP2 are not only responsible for a mechanical dysfunction of the intercalated disc (ID), but are also the cause of various pro-arrhythmic mechanisms. In this review, we discuss in detail the different molecular interactions associated with desmosomal pathogenic variants, and their contribution to various ACM phenotypes.
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http://dx.doi.org/10.1016/j.tcm.2020.07.006DOI Listing
July 2020

Zurich International Symposium on Arrhythmogenic Cardiomyopathies.

Eur Heart J 2020 04;41(16):1535-1537

Director, Zurich ARVC Program, University Heart Center Zurich, Switzerland.

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http://dx.doi.org/10.1093/eurheartj/ehaa145DOI Listing
April 2020

[CME ECG 65/Answers: The Athlete's ECG].

Praxis (Bern 1994) 2020;109(5):385-387

Universitätsspital Zürich, Klinik für Kardiologie.

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http://dx.doi.org/10.1024/1661-8157/a003454DOI Listing
January 2020

[CME ECC 65: The Athlete's ECG].

Praxis (Bern 1994) 2020 ;109(4):253-258

Universitätsspital Zürich, Klinik für Kardiologie.

CME ECC 65: The Athlete's ECG Regular, intensive training in athletes causes a modulation of the heart due to higher vagal tone and emerging hypertrophy. To assess these changes, which can be seen in an athlete's ECG as well, an international group of experts constituted contemporary standards for ECG interpretation in athletes, the "Seattle Criteria" which are discussed in this article: Athletes often have a physiologic sinus bradycardia with a heart rate between 30 and 60 bpm and a pronounced respiratory arrhythmia. A junctional rhythm with retrograde depolarisation of the atria frequently occurs as well, especially at rest. Early repolarisation is also an occasional phenomenon in athletes. Depending on its morphology and the history of the athlete it may be regarded as physiologic. This article shall help to evaluate an athlete's ECG in a physician's routine.
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http://dx.doi.org/10.1024/1661-8157/a003453DOI Listing
July 2020

Clinical predictors of left ventricular involvement in arrhythmogenic right ventricular cardiomyopathy.

Am Heart J 2020 05 7;223:34-43. Epub 2020 Feb 7.

Department of Cardiology, University Heart Center Zurich, Switzerland; Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland. Electronic address:

Aim: The impact of clinical characteristics for predicting patterns of ventricular involvement in arrhythmogenic right ventricular cardiomyopathy (ARVC) are not well defined. The aims of this study were to characterize different patterns of ventricular involvement in patients with ARVC and to stratify them based on clinical characteristics exercise and underlying genetic mutations.

Methods: Sixty-four patients with definite ARVC from the Swiss ARVC Registry were enrolled. Right and left ventricular functions were assessed at baseline and most recent follow-up. All patients received genetic testing. Serum high-sensitivity cardiac Troponin T (hs-cTNT) and N-terminal of pro-brain natriuretic peptide (NT-proBNP) were determined at baseline.

Results: Thirty-five patients (55%) had isolated right ventricular (RV) involvement, 12 patients (19%) had biventricular (BiV) involvement at baseline and 17 patients (26%) had no left ventricular (LV) involvement at baseline, but revealed new onset LV involvement at mean follow-up of 7.5 years. Patients with BiV involvement at baseline harbored significantly more desmoplakin and multiple mutations and patients with new-onset LV involvement at follow-up frequently showed non-desmosomal mutations. Patients engaging in competitive sports more often showed LV involvement during follow-up. Baseline hs-cTNT and NT-proBNP levels were higher in patients developing BiV involvement.

Conclusion: Multiple mutations are more common in ARVC patients with BiV involvement. Competitive exercise is associated with disease progression resulting in BiV involvement. Hs-cTNT and NT-proBNP are elevated in patients with BiV involvement and may help to identify ARVC patients at risk for developing BiV disease.
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http://dx.doi.org/10.1016/j.ahj.2020.01.019DOI Listing
May 2020

First magnetic resonance imaging-guided cardiac radioablation of sustained ventricular tachycardia.

Radiother Oncol 2020 11 14;152:203-207. Epub 2020 Feb 14.

Department of Radiation Oncology, University Hospital Zurich, University of Zurich, Switzerland.

Purpose: To report the feasibility of magnetic resonance imaging-guided cardiac single fraction radioablation (MRgRA) in a patient with dilated cardiomyopathy and recurrent sustained ventricular tachycardia (VT) leading to electrical storms (ES).

Materials/methods: A workflow to perform Stereotactic Arrhythmia Radioablation (STAR) on a hybrid MR-Linac with real-time tracking and beam-gating was established. Challenges of the MRgRA approach included: (a) the safety of a non-MR compatible cardiac implantable electronic device (CIED) in the MR-Linac field, (b) artefacts caused by the CIED and (c) respiratory motion management with cine-tracking of the moving heart. The specific absorption rate and slew rate of the MR-Linac were within the specifications of a MR-conditional CIED. Phantom measurements showed CIED distortion artefacts of less than 1.5 mm. During MR simulation, tracking could be established on the upper liver to avoid interference with the moving heart and CIED extinction artefacts. Areas of anatomical scarring and critical substrate were identified using invasive three-dimensional electroanatomical mapping of the clinical VT during electrophysiological studies and cardiac MR imaging/computed tomography to build a volumetric target.

Results: A 71-year-old male patient with non-ischemic dilated cardiomyopathy and recurrent therapy-refractory sustained VT with repetitive implantable cardioverter-defibrillator (ICD) shocks was treated with a single fraction of 25 Gy @85% isodose, cine-tracking time was 46 min, beam-on time 24 min. 24 h post intervention the patient developed an aggravation of the clinical VT and prolonged ES. VT ceased following high-dose dexamethasone administration after 48 h. After this point, the patient remained without any episodes of sustained ventricular tachyarrhythmia requiring ICD interventions until the last follow-up at three months.

Conclusion: Real-time tracking and beam-gating were successfully applied in this first MRgRA to treat sustained VT.
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http://dx.doi.org/10.1016/j.radonc.2020.01.008DOI Listing
November 2020

[CME ECG 64: Exercise Intolerance and Dyspnea on Exertion].

Praxis (Bern 1994) 2019 Sep;108(13):843-844

Klinik für Kardiologie, Universitäres Herzzentrum, Universitätsspital Zürich.

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http://dx.doi.org/10.1024/1661-8157/a003323DOI Listing
September 2019

[CME ECG 63/Answers: Stress-Induced Ventricular Arrhythmias].

Praxis (Bern 1994) 2019 Jun;108(8):567-572

1 Klinik für Kardiologie, Universitäres Herzzentrum, Universitätsspital Zürich.

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http://dx.doi.org/10.1024/1661-8157/a003244DOI Listing
June 2019

Clinical Characteristics of Patients with a Right Ventricular Thrombus in Arrhythmogenic Right Ventricular Cardiomyopathy.

Thromb Haemost 2019 Aug 10;119(8):1373-1378. Epub 2019 Jun 10.

University Heart Center Zurich, University Hospital of Zurich, University of Zurich, Zurich, Switzerland.

Background:  Thrombus formation within the left ventricle (LV) is a well-known clinical entity and is often associated with underlying myocardial disease, whereas right ventricular (RV) thrombi are rarely observed. This study aimed to investigate the clinical characteristics of patients with arrhythmogenic RV cardiomyopathy (ARVC) who developed an RV thrombus.

Methods And Results:  This study included patients with an RV thrombus from the ARVC databases of the University Heart Center in Zurich, Switzerland, and the Fuwai Hospital in Beijing, China. In total, there were 13 ARVC patients who had an RV thrombus detected. The mean age was 33 ± 15 (range: 11-51) years. Eight patients (62%) were male. The mean Task Force score was 6 ± 1. Nine of these patients (69%) had an RV thrombus only whereas four patients had biventricular thrombi. All 13 ARVC patients had a severely impaired RV function (RV fractional area change 16 ± 9% and RV ejection fraction 15 ± 4%); LV ejection fraction (LVEF) was 40 ± 15%. ARVC patients with an additional LV thrombus had a lower LVEF than the others (24 ± 11 vs. 47 ± 11,  = 0.02). Under therapeutic anticoagulation, complete thrombus resolution was observed in 9/13 patients (69%).

Conclusion:  RV thrombus formation is a potential complication of ARVC with impaired RV function. In patients with biventricular involvement, thrombi may also occur within the LV. Anticoagulation is generally effective to dissolve RV thrombi. This study highlights the need for awareness during cardiac imaging to detect this rare complication of ARVC.
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http://dx.doi.org/10.1055/s-0039-1688829DOI Listing
August 2019

[CME ECG 62/Answer: An Atypical Right Bundle Branch Block?]

Praxis (Bern 1994) 2019 Jan;108(2):157-160

1 Klinik für Kardiologie, Universitäres Herzzentrum, Universitätsspital Zürich.

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http://dx.doi.org/10.1024/1661-8157/a003152DOI Listing
January 2019

Hemodynamic Changes in the Right Ventricle Induced by Variations of Cardiac Output: A Possible Mechanism for Arrhythmia Occurrence in the Outflow Tract.

Sci Rep 2019 01 14;9(1):100. Epub 2019 Jan 14.

University Heart Center, Department of Cardiology, Zurich, 8091, Switzerland.

The rationale of this paper is to investigate right ventricular (RV) hemodynamics in relation to changes in cardiac output, and in particular to study exercise-induced stresses at the RV outflow tract (RVOT), which is a common site of ventricular arrhythmias in the athlete's heart. We hypothesize that the thin-walled RVOT is exposed to high wall shear stresses (WSS) during physiological states associated with high cardiac output such as exercise, and therefore, may be particularly prone to substrate formation leading to ventricular tachyarrhythmias. 3D Particle Tracking Velocimetry (3D-PTV), an optical imaging method, has been performed in a novel anatomically accurate compliant silicone right heart model derived from a high resolution MRI heart scan of a healthy male proband. RV and RVOT flow patterns at resting conditions were obtained from two healthy athletic male proband's hearts and two patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) via phase contrast magnetic resonance imaging (PC-MRI). The healthy case was used as a reference for validating the in vitro flow patterns of the silicone model, while the diseased cases were used to generalize our findings and investigate possible changes in hemodynamic stresses with RV morphological remodelling. Our results showed that both healthy and diseased geometries consistently displayed an increased WSS in the RVOT relative to the rest of the RV. We found that increases in cardiac output may lead to increases of mean kinetic energy (MKE), laminar viscous dissipation and WSS at the RVOT. Furthermore, higher peak WSS magnitudes were found for the diseased cases. The identified high WSS regions may correlate with the common site of RVOT ventricular tachycardia in athletes and patients with ARVC/D. Our results imply that exercise, as well as anatomical and functional remodeling might alter RV wall shear stress both in magnitude and spatial distribution, leading to increased hemodynamic stresses in the RVOT.
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http://dx.doi.org/10.1038/s41598-018-36614-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6331649PMC
January 2019

[CME ECG 62: An Atypical Right Bundle Branch Block?]

Praxis (Bern 1994) 2019 Jan;108(1):17-18

1 Klinik für Kardiologie, Universitäres Herzzentrum, Universitätsspital Zürich.

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http://dx.doi.org/10.1024/1661-8157/a003151DOI Listing
January 2019

An autoantibody identifies arrhythmogenic right ventricular cardiomyopathy and participates in its pathogenesis.

Eur Heart J 2018 11;39(44):3932-3944

The Labatt Family Heart Centre (Department of Pediatrics) and Translational Medicine, The Hospital for Sick Children & Research Institute and the University of Toronto, Room 1725D, 555 University Avenue, Toronto, Ontario, Canada.

Aims: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterized by right ventricular myocardial replacement and life-threatening ventricular arrhythmias. Desmosomal gene mutations are sometimes identified, but clinical and genetic diagnosis remains challenging. Desmosomal skin disorders can be caused by desmosomal gene mutations or autoantibodies. We sought to determine if anti-desmosome antibodies are present in subjects with ARVC.

Methods And Results: We evaluated ARVC subjects and controls for antibodies to cardiac desmosomal cadherin proteins. Desmoglein-2 (DSG2), desmocollin-2, and N-cadherin proteins on western blots were exposed to sera, in primary and validation cohorts of subjects and controls, as well as the naturally occurring Boxer dog model of ARVC. We identified anti-DSG2 antibodies in 12/12 and 25/25 definite ARVC cohorts and 7/8 borderline subjects. Antibody was absent in 11/12, faint in 1/12, and absent in 20/20 of two control cohorts. Anti-DSG2 antibodies were present in 10/10 Boxer dogs with ARVC, and absent in 18/18 without. In humans, the level of anti-DSG2 antibodies correlated with the burden of premature ventricular contractions (r = 0.70), and antibodies caused gap junction dysfunction, a common feature of ARVC, in vitro. Anti-DSG2 antibodies were present in ARVC subjects regardless of whether an underlying mutation was identified, or which mutation was present. A disease-specific DSG2 epitope was identified.

Conclusion: Anti-DSG2 antibodies are a sensitive and specific biomarker for ARVC. The development of autoimmunity as a result of target-related mutations is unique. Anti-DSG2 antibodies likely explain the cardiac inflammation that is frequently identified in ARVC and may represent a new therapeutic target.
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http://dx.doi.org/10.1093/eurheartj/ehy567DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6247665PMC
November 2018

[CME ECG 61/Answer: Management of Premature Ventricular Contractions].

Praxis (Bern 1994) 2018 Jul;107(15):854-862

1 Klinik für Kardiolgie, Unversitäres Herzzentrum, Universitätsspital Zürich.

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http://dx.doi.org/10.1024/1661-8157/a003019DOI Listing
July 2018

[CME ECG 61: Management of Premature Ventricular Contractions].

Praxis (Bern 1994) 2018 Jul;107(14):755-757

1 Klinik für Kardiolgie, Unversitäres Herzzentrum, Universitätsspital Zürich.

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http://dx.doi.org/10.1024/1661-8157/a003018DOI Listing
July 2018

Feasibility of zero or near zero fluoroscopy during catheter ablation procedures.

Cardiol J 2019 3;26(3):226-232. Epub 2018 Apr 3.

Arrhythmia and Electrophysiology, Department of Cardiology, University Heart Center, University Hospital Zurich, Switzerland.

Background: Awareness of risks associated with radiation exposure to patients and medical staff has significantly increased. It has been reported before that the use of advanced three-dimensional electroanatomical mapping (EAM) system significantly reduces fluoroscopy time, however this study aimed for zero or near zero fluoroscopy ablation to assess its feasibility and safety in ablation of atrial fibrillation (AF) and other tachyarrhythmias in a "real world" experience of a single tertiary care center.

Methods: This was a single-center study where ablation procedures were attempted without fluoroscopy in 34 consecutive patients with different tachyarrhythmias under the support of EAM system. When transseptal puncture (TSP) was needed, it was attempted under the guidance of intracardiac echocardiography (ICE).

Results: Among 34 patients consecutively enrolled in this study, 28 (82.4%) patients were referred for radiofrequency ablation (RFA) of AF, 3 (8.8%) patients for ablation of right ventricular outflow tract (RVOT) ventricular extrasystole (VES), 1 (2.9%) patient for ablation of atrioventricular nodal reentry tachycardia (AVNRT), 2 (5.9%) patients for typical atrial flutter ablation. In 21 (62%) patients the en- tire procedure was carried out without the use of fluoroscopy. Among 28 AF patients, 15 (54%) patients underwent ablation without the use of fluoroscopy and among these 15 patients, 10 (67%) patients required TSP under ICE guidance while 5 (33%) patients the catheters were introduced to left atrium through a patent foramen ovale. In 13 AF patients, fluoroscopy was only required for double TSP. The total procedure time of AF ablation was 130 ± 50 min. All patients referred for atrial flutter, AVNRT, and VES of the RVOT ablation did not require any fluoroscopy.

Conclusions: This study demonstrates the feasibility of zero or near zero fluoroscopy procedure including TSP with the support of EAM and ICE guidance in a "real world" experience of a single tertiary care center. When fluoroscopy was required, it was limited to TSP hence keeping the radiation dose very low.
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http://dx.doi.org/10.5603/CJ.a2018.0029DOI Listing
April 2020

CME-EKG 60/Auflösung.

Praxis (Bern 1994) 2018 Feb;107(5):289-291

1 Klinik für Kardiologie, Universitäres Herzzentrum, Universitätsspital Zürich.

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http://dx.doi.org/10.1024/1661-8157/a002907DOI Listing
February 2018