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Every year Center for Heart Failure Research organizes a Symposium on Heart Failure that brings together basic scientist and clinical researchers from three continents, focusing on translational cardiology that promotes and integrates high quality research from bench to bedside. Center postdoc Mathis Korseberg Stokke, MD, PhD is head of the organization commitee. He is also part of the administration of NORHEART – The Norwegian PhD School of Heart Research that offers targeted educational activities for Norwegian PhD students in cardiovascular research. One of the cornerstones of the Symposium is the poster sessions on Thursdays, giving young and established scientists a chance to show their best to colleagues from the forefront of international science and leadership in cardiology and cardiovascular research. |
Each year, the PhD fellows from the Center for Cardiological Innovation present the latest of results from their research, this year having posters in sessions for “Cardiac function during heart failure and exercise training”, “Cellular signaling: myocardial function and arrhythmias” and “Diagnostic and therapeutical strategies for cardiac disease”. The best poster in each session is awarded with a prize worth 5000 nok, given by NORHEART.
So far following center members have taken home the prize; Ida Skrinde Leren, MD, PhD, Nina Hasselberg, MD, PhD, John Aalen, MD, PhD fellow and Øyvind Lie, MD, PhD fellow. This is the second time Lie has won the prize, and earlier this year center member Ida Skrinde Leren was awarded with H.M. the King's gold medal for the best medical PhD during 2016. The medal is awarded to an outstanding, young researcher for a scientific work assessed at the University of Oslo. The work must be recognized as an effective contribution to the field of research's literature.
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Introduction: Purpose: Conclusions: |
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Introduction: Conclusions: |
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Introduction: Conclusions: |
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Background: Purpose: Conclusions: |
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Mechanical heterogeneity during ischemia is thought to contribute to arrhythmogenic alterations in cardiac electrophysiology. Several forms of mechanoelectric feedback (MEF) have been proposed to underlie these changes, and two major mechanisms are: (1) myofilament-dependent calcium surges, and (2) opening of stretch-activated channels (SAC). In this study, we tested the individual and combined contribution of these mechanisms to generating calcium waves and arrhythmogenic substrate in the ischemic border zone. In particular, we investigated how changes in calcium dynamics depend upon regional alterations in mechanics similar to those observed during an acute ischemic challenge. To assess the potential role of MEF in arrhythmias we began by constructing a coupled model of ventricular myocyte electrophysiology and sarcomere contraction dynamics. We connected fifty of these coupled sarcomere models in-series, thus creating a 1D myocyte in which contractile mechanics and electrophysiology are bidirectionally coupled in time (via calcium), and in space via calcium diffusion, strain and stress. Multiple myocytes were coupled via gap junctions to create a 1D tissue strand. These models capture the effects of mechanical feedback at the sarcomeric level, and the combined effects of mechanical and calcium heterogeneities at the multi-cellular level. When perturbed by pathologically realistic variations in stretch, we observe that both SAC and myofilament-dependent alterations in calcium sensitivity contribute to changes in action potential (AP) morphology. Additionally, in this 1D tissue strand we noticed that MEF is capable of modulating the velocity of calcium waves through accompanying regional cross-bridge attachment dependent on internal stretch heterogeneity and calcium distribution. This study investigates the impact of heterogeneous regional stretch/strain on cellular and tissue electrophysiology via myofilament calcium release and SAC opening. The combined effects of these mechanisms may be sufficient to create arrhythmogenic spatial variation in action potential during (APD) during ischemia, particularly in the border region. |
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Background: Purpose: Conclusion: |
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Background: Purpose: Conclusion: |
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Introduction: Conclusions: |
Posters by sessions
III Cardiac function during heart failure and exercise training
Vigorous exercise is associated with beneficial morphological changes in hypertrophic cardiomyopathy
Dejgaard LA, Haland TF, Lie OH, Ribe M, Leren IS, Edvardsen T, Haugaa KH
Patients with left bundle branch block are hypersensitive to afterload: Moderate elevation of systolic pressure caused marked depression of left ventricular function
Aalen J, Storsten P, Remme EW, Larsen CK, Sirnes PA, Gjesdal O, Skulstad H, Hisdal J, Smiseth OA
Regional myocardial work by magnetic resonance imaging and noninvasive left ventricular pressure: a feasibility study in in left bundle branch block
Larsen CK, Aalen J, Stokke C, Fjeld JG, Kongsgård E, Smiseth OA, Hopp E
Reduced septal function corresponds to relative downregulation of septal metabolism in TGA patients with atrial switch
Storsten P, Fjeld JG, Sherwani AG, Boe E, Remme EW, Gjesdal O, Erikssen G, Smiseth OA, Skulstad H
IV Cellular signaling: myocardial function and arrhythmias
Integrated mechanisms of mechano-electric feedback in ischemic arrhythmogenesis
Timmermann V, Wall ST, Sundnes J, Quinn TA, McCulloch AD, Edwards AG
V Diagnostic and therapeutical strategies for cardiac disease
Mechanical dispersion by strain echocardiography: a sensitive marker of left ventricular remodeling in stable coronary artery disease
Kvisvik B, Aagaard EN, Mørkrid L, Rosjø H, Smedsrud MK, Eek C, Bendz B, Haugaa KH, Edvardsen T, Gravning J
How many are too many – Frequent premature ventricular contractions and left ventricular function
Lie ØH, Saberniak J, Dejgaard LA, Anfinsen OG, Hegbom F, Edvardsen T, Haugaa KH
Increased heart rate aggravates diastolic dysfunction in left bundle branch block
Andersen OS, Krogh MR, Boe E, Storsten P, Larsen CK, Aalen J, Odland HH, Skulstad H, Smiseth OA, Remme EW