Key result
In a mouse model of persistent truncus arteriosus, passive tissue stiffness increased 4.5-fold in the right ventricle and 2.2-fold in the left ventricle compared to controls.
Population
Fgf8;Isl1Cre conditional mutant embryonic mouse hearts and littermate controls at embryonic day 12.5, n=10
Comparison
Genetic mutation causing persistent truncus… vs Littermate controls with normal cardiac…
Design
Preclinical
Authors
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Ventricular stiffness increases may contribute to dysfunction in congenital models; hypothesis-generating and requires human validation before clinical consideration.
Effect estimate: 4.5-fold increase
Absolute Event Rate: 0.163% vs 0.037%
p-value: p=0.002
In a mouse model of persistent truncus arteriosus, the left and right ventricles exhibit marked early increases in passive tissue stiffness despite the outflow tract being the most severely affected structure morphologically.
Buffinton et al. (2017) studied Persistent truncus arteriosus (PTA) (n=10). Fgf8;Isl1Cre mutation vs. Littermate controls was evaluated on Strain energy density (SED) of the right ventricle at normalized aspirated length 0-0.2 (kJ/m3) (4.5-fold increase, p=0.002). In a mouse model of persistent truncus arteriosus, passive tissue stiffness increased 4.5-fold in the right ventricle and 2.2-fold in the left ventricle compared to controls.
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