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Transcript
Right ventricular strain in rats with heart failure: a phase contrast MRI study
Espe EKS1, Aronsen JM1,2, Zhang L1, Sjaastad I1
1Institute
for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo,
Norway;
2Bjørknes
College, Oslo, Norway;
Purpose
The role of the right ventricle (RV) in experimental heart failure is largely unexplored, particularly due
to difficulties in measuring RV function in vivo. We sought to measure RV strain in a rat model of heart
failure using phase-contrast magnetic resonance imaging (PC-MRI).
Methods
Six weeks after induction of left ventricular myocardial infarction (MI), 23 male Wistar rats were
examined with PC-MRI, in addition to 8 sham-operated animals. PC-MRI was used to measure
longitudinal and circumferential strain in the RV free-wall (SLFW and SCFW) and in the intraventricular
septum (SLS and SCS). RV ejection fraction was also measured. After MRI, left ventricular end
diastolic pressure (LVEDP) was recorded as an index of RV afterload. The rats were divided into two
groups; one with low RV afterload (LVEDP<15 mmHg) and one with high RV afterload (LVEDP >=15
mmHg). In N=23/4 (MI/sham) of the animals, the hearts were excised and the RV myocardial tissue
was investigated using qPCR analysis to measure expression of collagen I and III, BNP, Acta1 and
Myh7.
Results
Peak SLFW and RV ejection fraction was significantly lower in the high-afterload group than in the lowafterload group and sham. Peak SLS, SCFW and SCS were not different between the groups. Peak
SLFW exhibited strong correlations to BNP (ρ=0.51, p=0.007), Acta1 (ρ=0.65, p<0.001), Myh7 (ρ=0.39,
p<0.05), RV ejection fraction (ρ=-0.69, p<0.001) and EDP (ρ=0.55, p=0.001). Peak SCFW correlated
with Acta1 (ρ=0.40, p=0.04) and RV ejection fraction (ρ=-0.50, p=0.004). Peak SLS was only
correlated with RVEF (ρ =-0.44, p=0.01).
Conclusion
We have demonstrated that PC-MRI can measure RV strain in rats, and confirmed that strain in the
RV free-wall is closely related to RV ejection fraction and afterload. We also demonstrate a relation
between RV strain and molecular markers of RV remodeling in a rat model of myocardial infarction.