Key result
In a male rat model of PAH, compensated systolic function was explained by RV hypertrophy, while altered RV end-diastolic mechanics were driven by passive myocardial stiffening.
No takes yet. Share an insight, caveat, or question.
RV stiffening without fibrosis may drive late diastolic changes in PAH; leaves open human translation and targeted therapies.
Kwan et al. (2021) studied Pulmonary arterial hypertension. Pulmonary arterial hypertension model was evaluated on Right ventricular mechanics. In a male rat model of PAH, compensated systolic function was explained by RV hypertrophy, while altered RV end-diastolic mechanics were driven by passive myocardial stiffening.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: