Key result
In experimental right ventricular pressure loading, end-diastolic wall stress correlated moderately with fibrosis (r=0.47, P=0.0011) and strongly with RV function indexes like TAPSE (r=0.85, P=0.0038).
Why the study?
Right ventricle pressure loading causes fibrosis and dysfunction, but the relation of RV wall stress to biventricular fibrosis and dysfunction is incompletely defined.
Wall stress may drive RV fibrosis and dysfunction; hypothesis-generating for clinical translation in pressure overload.
Right ventricle (RV) pressure loading can lead to RV fibrosis and dysfunction. We previously found increased RV, septal hinge-point and left ventricle (LV) fibrosis in experimental RV pressure loading. However, the relation of RV wall stress to biventricular fibrosis and dysfunction is incompletely defined. Rabbits underwent progressive pulmonary artery banding (PAB) over 3 wk with hemodynamics, echocardiography, and myocardial samples obtained at a terminal experiment at 6 wk. An additional group received PAB and treatment with an endothelin receptor antagonist. The endocardial and epicardial borders of short-axis echo images were traced and analyzed with invasive pressures to yield regional end-diastolic (ED) and end-systolic (ES) wall stress. To increase clinical translation, computer model-derived wall stress was compared with Laplace wall stress. The relation of wall stress with fibrosis (picrosirius red staining) and ventricular function was analyzed. ED wall stress in all regions and RV and LV free-wall ES wall stress were increased in PAB rabbits versus sham animals. Laplace wall stress correlated well with computational models. In PAB, fibrosis was highest in the RV free wall, then septal hinge regions, and lowest in the septum and LV free wall. Fibrosis was moderately related to ED ( r = 0.47, P = 0.0011), but not ES wall stress. RV ED wall stress was strongly related to echo indexes of function (strain rate: r = 0.71, P = 0.048; E′, r = −0.75, P = 0.0077; tricuspid annular plane systolic excursion: r = 0.85, P = 0.0038) and RV fractional area change ( r = 0.77, P = 0.027). ED, more than ES, wall stress is related moderately to fibrosis and strongly to function in experimental RV pressure loading, especially at the septal hinge-point regions, where fibrosis is prominent. This suggests that wall stress partially links RV pressure loading, fibrosis, and dysfunction and may be useful to follow clinically. NEW & NOTEWORTHY Biventricular fibrosis and dysfunction impact outcomes in RV pressure loading, but their relation to wall stress is poorly defined. Using a pulmonary artery band rabbit model, we entered echocardiography and catheter data into a computer model to yield regional end-diastolic (EDWS) and end-systolic (ESWS) wall stress. EDWS, more than ESWS, correlated with fibrosis and dysfunction, especially at the fibrosis-intense septal hinge-point regions. Thus, wall stress may be clinically useful in linking RV pressure loading to regional fibrosis and dysfunction.
No takes yet. Share an insight, caveat, or question.
Gold et al. (2019) studied Right ventricular pressure loading. Pulmonary artery banding (PAB) vs. Sham was evaluated on Correlation between end-diastolic wall stress and fibrosis (r = 0.47, p=0.0011). In experimental right ventricular pressure loading, end-diastolic wall stress correlated moderately with fibrosis (r=0.47, P=0.0011) and strongly with RV function indexes like TAPSE (r=0.85, P=0.0038).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: