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.
Hypertrophic cardiomyopathy is a genetic cardiac disease with variable penetrance. Long-term vigorous exercise is associated with physiological left ventricular (LV) hypertrophy and dilation in healthy subjects, but effects in patients with hypertrophic cardiomyopathy is unknown.
To evaluate the impact of vigorous exercise ion LV dimensions in hypertrophic cardiomyopathy phenotype positive patients (HCM+) and in hypertrophic cardiomyopathy genotype positive, phenotype negative relatives (HCM-).
Lifetime vigorous exercise correlated with larger LV volumes in HCM+ (hypertrophic cardiomyopathy phenotype positive) and HCM- (hypertrophic cardiomyopathy genotype positive, phenotype negative) patients. HCM- athletes had greater LV mass than non-athletes, while this difference was not observed in HCM+ patients. This indicates that long term vigorous exercise does not aggravate disease progression in hypertrophic cardiomyopathy.
Left bundle branch block (LBBB) in otherwise healthy individuals carries a good prognosis, whereas LBBB in patients with arterial hypertension is associated with increased morbidity and mortality. We hypothesized that elevated blood pressure has a direct depressive effect on left ventricular (LV) function in individuals with LBBB.
Moderate elevation of afterload in patients with LBBB caused marked depression of LV systolic function. This was attributed to aggravation of septal function.
Myocardial work during myocardial shortening is positive and during lengthening negative. The purpose of this study was to determine if regional myocardial work can be calculated from strain by feature tracking magnetic resonance imaging (FTMRI) and noninvasive left ventricular (LV) pressure.
FTMRI in combination with noninvasive LV pressure demonstrated markedly different workloads on the septum and LV lateral wall in patients with LBBB. Work distribution corresponded well with regional glucose metabolism. These results suggest that FTMRI in combination with noninvasive LV pressure is feasible as a clinical tool to measure regional myocardial work.
In patients with transposition of the great arteries (TGA) and atrial switch, the right ventricle (RV) becomes the systemic ventricle. These patients have increased risk of heart failure. We have previously demonstrated reduced septal function by regional strain and work analyses.
To determine whether reduced septal function in TGA-patients is reflected in reduced metabolism.
In TGA patients with systemic RV, a reduced septal function was accompanied by reduction in septal metabolism. Global function of the systemic RV was maintained due to preserved function of the RV free wall. The change in septal function and metabolism may be initial markers of decompensation of the systemic ventricle.
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.
Both cardiac biomarkers and traditional echocardiographic measurements ate important in the early identification of subclinical left ventricular (LV) remodeling. However, it is largely unknown whether LV mechanical dispersion is relevant in this context.
We wanted to elucidate the role of LV mechanical dispersion in the identification of subclinical LV remodeling, as assessed by sensitive cardiac biomarkers, in patients with stable coronary artery disease (CAD).
LV mechanical dispersion may give additional information of LV remodeling to traditional echocardiographic measurements in patients with stable CAD.
Frequent premature ventricular contractions (PVCs) may induce cardiomyopathy. A PVC burden of 24% (approx. 24000 PVCs/24 hours) has previously been related to reduced left ventricular (LV) ejection fraction (EF).
We wanted to explore the threshold number of PVCs including LV systolic dysfunction. We hypothesized that strain echocardiography can reveal systolic dysfunction at a lower PVC threshold than previously reported.
% PVC correlated significantly with systolic function by GLS but not by LVEF. Systolic dysfunction was recognized by abnormal GLS at >8% PVCs, a lower threshold than previously reported. This may suggest an earlier indication for PVC burden reducing therapy.
In left bundle branch block (LBBB) left ventricular (LV) pressure decay is slowed due to dyssynchronous relaxation. We hypothesized that the slowed pressure decay would aggravate diastolic function at increased heart rate when duration of filling is limited.
Increasing HR increased LV diastolic stiffness and diastolic pressure in LBBB.