DISCUSSION
In this study, we show the association of both right ventricular free wall and global right atrial strain with increased systolic pulmonary artery pressure. Moreover, we demonstrate that pulmonary arterial hypertension could be associated with myocardial fibrosis of the right heart obtained with histopathological methods. These findings suggest the association of increased sPAP values with overall ventricular deformation and fibrosis. Finally, we demonstrate that strain parameters contribute to the detection of PH and assessment of pulmonary hypertension severity in patients with suspected probability of PH.
The relationship between ventricular deformation and sPAP has been previously reported (16–18). A chronic increase in afterload, manifested by an elevated pulmonary artery pressure, can cause a decrease in the elastance of myocardial fibers in patients with severe pulmonary hypertension (17,19). This will ultimately cause irreversible myocardial damage with the eventual development of ventricular fibrosis (20). As our results suggest, the progressive decrease in ventricular strain and atrial strain is modeled as a quadratic function, which suggests that these patients have an initial period of compensation by increasing contractility, possibly via the Frank-Starling mechanism, that progressively decreases as the disease advances. This may be more pronounced in the right ventricle, as the chamber directly facing the increased afterload, before impairing the right atrium. The atrial function is also altered, as observed in the evaluation of the various atrial phases. Finally, the degree of fibrosis analyzed in the pathological specimens of a subset of patients with pulmonary hypertension was associated with a prolonged decrease in ventricular function.
With the demonstration of fibrosis, usually an irreversible change, early detection and stratification of PH is critical. Our data demonstrate the clinical utility of RV-FWS and RA-GS as echocardiographic parameters that aid in this task. Strain parameters have been previously used to predict outcomes in congestive heart failure and myocardial infarction with similar results (21,22), as well as in pulmonary hypertension (23,24,25). The echocardiographic estimation of sPAP and accordingly the development of the probability of PH is usually predicated on the presence of a complete tricuspid regurgitation envelope by continuous wave Doppler. Often these envelopes are incomplete and the accuracy of the sPAP estimation is markedly reduced. One usually relies on secondary signs of PH including RV dilatation, dysfunction by TAPSE or S’, or D-shaped septum configuration in systole. Many of these findings are only present in advanced PH. RV strain measurement may permit for earlier detection of dysfunction, as it does in chemotherapy-induced LV cardiomyopathy (26) or in the RV in patients with scleroderma (27). In addition, strain measurements may assist in risk stratification in clinical contexts where conventional approaches are not sufficient. In our work, we identified strain cut-off values that demonstrate the differences in pulmonary hypertension severity categorization. Overall, RV-FWS offers to be a highly sensitive echocardiographic parameter while RA-GS offers a sufficient specific parameter to detect all categories of pulmonary hypertension. If our cut-off values are validated, they could be used in a clinical setting to aid detection and categorization of PH.