Relation between right ventricular wall stress, fibrosis, and function in right ventricular pressure loading

Area of Science:

• Cardiology
• Cardiovascular Physiology
• Biomedical Engineering

Background:

• Right ventricle (RV) pressure overload is a significant clinical issue leading to fibrosis and impaired function.
• The precise relationship between RV wall stress and biventricular fibrosis/dysfunction remains incompletely understood.
• Previous studies identified fibrosis in RV pressure loading, but linking it directly to regional wall stress is crucial.

Purpose of the Study:

• To investigate the relationship between regional right ventricle (RV) wall stress and biventricular fibrosis and dysfunction in a rabbit model of RV pressure loading.
• To compare computer model-derived wall stress with traditional Laplace wall stress for clinical relevance.
• To determine whether end-diastolic or end-systolic wall stress is more closely associated with fibrosis and functional impairment.

Main Methods:

• Progressive pulmonary artery banding (PAB) was used in rabbits to induce RV pressure overload over 3 weeks.
• Hemodynamics, echocardiography, and myocardial tissue samples were collected at 6 weeks.
• Regional end-diastolic (ED) and end-systolic (ES) wall stress were calculated using echocardiography and invasive pressures, validated by computational models.
• Picrosirius red staining quantified fibrosis, and echocardiographic parameters assessed ventricular function.

Main Results:

• Pulmonary artery banding significantly increased ED wall stress in all regions and ES wall stress in RV and LV free walls.
• Fibrosis was most pronounced in the RV free wall, followed by septal hinge regions, and least in the septum and LV free wall.
• RV ED wall stress showed moderate correlation with fibrosis (r=0.47) and strong correlations with multiple echocardiographic measures of RV function (e.g., strain rate r=0.71, E' r=-0.75).
• ED wall stress, particularly in septal hinge regions, was more strongly related to fibrosis and dysfunction than ES wall stress.

Conclusions:

• End-diastolic wall stress is a key determinant linking RV pressure loading to regional fibrosis and biventricular dysfunction.
• The septal hinge-point region is particularly vulnerable to fibrosis and dysfunction under pressure overload.
• Regional wall stress, especially ED wall stress, may serve as a valuable clinical marker for assessing RV remodeling and function.