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 (16ā18). 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 Sā, 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.