A5052756241- Cardiac electrophysiology and arrhythmias
- Cardiovascular Effects of Exercise
- Cardiomyopathy and Myosin Studies
- Ion channel regulation and function
- Cardiac Ischemia and Reperfusion
- Cardiac Imaging and Diagnostics
- Neuroscience and Neural Engineering
- Cardiac Arrest and Resuscitation
- Cardiac Arrhythmias and Treatments
- Electron Spin Resonance Studies
- Cardiovascular and exercise physiology
- Cardiovascular Function and Risk Factors
- Muscle Physiology and Disorders
- Childhood Cancer Survivors' Quality of Life
- Neonatal Respiratory Health Research
- Signaling Pathways in Disease
- Respiratory Support and Mechanisms
University of Oslo
2016-2023
Institutt for Eksperimentell Medisinsk Forskning
2012-2023
Oslo University Hospital
2013-2023
Aims Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) predisposes to tachyarrhythmias (VTs) during high heart rates due physical or psychological stress. The essential role of catecholaminergic effects on cardiomyocytes in this situation is well documented, but the importance rate per se for arrhythmia initiation CPVT1 largely unexplored. Methods and results Sixteen patients performed a bicycle stress-test. Occurrence VT triggers, i.e. premature complexes (PVC), depended...
Background: Circulating SN (secretoneurin) concentrations are increased in patients with myocardial dysfunction and predict poor outcome. Because inhibits CaMKIIδ (Ca 2+ /calmodulin-dependent protein kinase IIδ) activity, we hypothesized that upregulation of protects against cardiomyocyte mechanisms arrhythmia. Methods: levels other biomarkers were assessed catecholaminergic polymorphic ventricular tachycardia (CPVT; n=8) resuscitated after arrhythmia–induced cardiac arrest (n=155). In vivo...
Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) is caused by mutations in the cardiac ryanodine receptor (RyR2) that lead to disrupted Ca(2+) handling cardiomyocytes and tachycardia. The aim of this study was test whether exercise training could reduce propensity for arrhythmias mice with CPVT1-causative missense mutation Ryr2-R2474S restoring normal handling.Ryr2-R2474S (RyR-RS) performed a 2 week interval treadmill protocol. Each session comprised five 8 min intervals...
In conditions with abnormally increased activity of the cardiac ryanodine receptor (RyR2), Ca2+/calmodulin-dependent protein kinase II (CaMKII) can contribute to a further destabilization RyR2 that results in triggered arrhythmias. Therefore, inhibition CaMKII such has been suggested as strategy suppress and However, suppression lead development arrhythmogenic Ca2+ alternans. The aim this study was test whether caused by increases propensity for We studied spontaneous release events...
Abnormal cellular Ca2+ handling contributes to both contractile dysfunction and arrhythmias in heart failure. Reduced transient amplitude due decreased sarcoplasmic reticulum content is a common finding failure models. However, models also show increased propensity for diastolic release events which occur when exceeds certain threshold level. Such can initiate arrhythmias. In this study we aimed investigate if of these aspects altered homeostasis could be found left ventricular...
Available evidence suggest that Ca2+/calmodulin-dependent protein kinase type IIδ (CaMKIIδ) and reactive oxygen species (ROS) are important in early ischemia-reperfusion arrhythmias (IRA). Since ROS can activate CaMKIIδ by oxidation of two methionines at positions 281/282, oxidized-CaMKIIδ (Ox-CaMKIIδ) has been proposed to be for IRA. However, direct this is missing.We exposed Langendorff-perfused hearts ventricular cardiomyocytes from C57BL/6 mice global simulated ischemia, respectively,...
Arrhythmias in the early phase of reperfusion after myocardial infarction (MI) are common, and can lead to hemodynamic instability or even cardiac arrest. Reactive oxygen species (ROS) thought play a key role underlying mechanisms, but evidence from large animal models is scarce, effects systemic antioxidative treatment remain contentious.MI was induced 7 male female pigs (Norwegian landrace, 35-40 kg) by clamping left anterior descending artery (LAD) during open thorax surgery. Ischemia...
Aim: Dysfunction of the cardiac ryanodine receptor (RyR2) is an almost ubiquitous finding in animal models heart failure (HF) and results abnormal Ca 2+ release cardiomyocytes that contributes to contractile impairment arrhythmias. We tested whether exercise training (ET), as recommended by current guidelines, had potential stabilize RyR2-dependent rats with post-myocardial infarction HF. Materials Methods: subjected male Wistar left coronary artery ligation or sham operations. After 1 week,...
Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) is an inherited arrhythmogenic disorder caused by missense mutations in the cardiac ryanodine receptors (RyR2), that result increased β-adrenoceptor stimulation-induced diastolic Ca2+ leak. We have previously shown exercise training prevents arrhythmias CPVT1, potentially reducing oxidation of Ca2+/calmodulin-dependent protein kinase II (CaMKII). Therefore, we tested whether oxidation-resistant form CaMKII protects mice...
Genotype-positive hypertrophic cardiomyopathy (HCM) mice had beneficial effects of exercise initiated before phenotype development. Exercised HCM increased capacity, smaller left atria, no increase in hypertrophy, or reduction function, and a similar degree fibrosis despite central extracellular matrix (ECM) genes, including collagens, compared with sedentary mice.
Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main source(s): South-Eastern Norway Regional Health Authority Introduction Ventricular arrhythmias are common during the early phase reperfusion after an ischemic event. Spontaneous diastolic release Ca2+ from sarcoplasmic reticulum (SR) contribute to in this stage, and reactive oxygen species (ROS) have been implicated process, through destabilization key handling proteins. Specifically, ROS has shown...