Chronic thromboembolic pulmonary hypertension has become a reversible disease with the development of PTE surgery. The dramatic and sudden decrease in PAP and PVR after PTE has provided a remarkable model to help study and elucidate RV/LV interactions and biventricular adaptations to severe RV pressure overload. Although the most obvious and striking features of this disease are right ventricular failure along with extreme elevations in PAP and PVR, recent studies have shown that LV diastolic abnormalities are common in CTEPH. Specifically, "impaired relaxation" transmitral Doppler tracings, systolic-dominant pulmonary venous flow patterns, and decreased diastolic tissue Doppler velocities have been observed in CTEPH patients . However, previous studies from our institution suggest that these findings are not indicative of intrinsic LV diastolic dysfunction, as there is a rapid improvement in the Doppler parameters immediately following PTE (including E/A ratio and mitral annular tissue Doppler velocities) .
2D speckle tracking is a novel echocardiographic technique that allows digital tracking and quantification of myocardial deformation as a function of time . The deformation can be assessed as both strain (change in length/original length) and strain rate (change in strain/time). Strain and strain rate imaging can assess both circumferential deformation (a negative value in systole, as the circumference of the LV decreases) and radial deformation (a positive value in systole, as the LV wall thickness increases).
In this study of 30 consecutive patients with CTEPH and adequate echo images undergoing PTE with pre- and postoperative RHC, we performed offline 2D speckle measurements of strain and strain rate. PTE resulted in marked improvement in mean PA pressure, PVR, and cardiac output. Additionally, patients demonstrated a statistically significant decrease in circumferential strain (i.e., more circumferential shortening) post-PTE and an increase in posterior wall radial strain (i.e., increased wall thickening). This is likely due to improved left ventricular filling and an increase in LV filling pressure after PTE  leading to an improvement in LV performance. The changes could also result from restoration of a more normal LV configuration after PTE.
Septal radial strain, however, did not change significantly post-PTE. Paradoxical
post-operative septal movement and hypokinesis is commonly observed in patients undergoing open heart surgery, and can affect tissue Doppler imaging of the septum as well [17–19]. A recent study, however, has shown normal septal strain rate after bypass graft surgery . The etiology of this regional wall motion abnormality ("post-op septum") is unknown, and may stem from RV dysfunction or a postoperative change in cardiac translation. It is unknown whether the lack of increase in radial septal strain post-PTE in this study is long-lasting, as nearly all patients who undergo PTE at our institution do not live nearby and are unavailable for long term echocardiographic follow-up.
Circumferential as well as posterior wall radial SR did change somewhat after PTE. However, these changes were small compared to the changes in absolute strain (the change in circumferential SR did not reach statistical significance [p = 0.07] and the posterior wall radial SR barely did [p = 0.04]). Like systolic strain, systolic SR is a function of myocardial contractility, preload and afterload: with an increase in LV preload following PTE and, presumably, no change in afterload or LV contractility, one might expect a similar increase in both strain and SR. Why the changes in strain were not mirrored by similar degrees of SR change is unclear. One possibility may stem from the fact that accurate SR analysis requires very precise speckle tracking. As noted in the limitations section, 2D speckle tracking measures strain directly and SR is then calculated by taking the temporal derivative of strain. Hence noise is amplified when determining SR. Although the quality of the echocardiograms was reasonable, there still may have been a degree of "scatter" and artifacts resulting in suboptimal myocardial tracking which was amplified in SR determination.
Radial septal SR did not change significantly with PTE. This is expected considering there was no observed change in radial septal strain with PTE. It is unclear whether the lack of change in septal radial SR post-PTE is long-lasting. One could also ask why LV strain improved without changes in LV dimensions or EF. First, the modified Simpson's method of discs may not apply well to left ventricles that are compressed and distorted in CTEPH, and so the EF calculations may not be completely accurate. Second, we suspect the improvement in strain could be linked to normalization of LV conformation, with a return to a more circular cross-sectional LV shape. Normalization of the LV "eccentricity index" is well documented in patients with CTEPH after PTE .
Linear regression analysis of circular strain and posterior wall radial strain vs. hemodynamic parameters revealed several findings. Despite the overall statistically significant change in circumferential and posterior wall radial strain that occurred with PTE, linear correlation of strain values with mean PA pressure, PVR, and cardiac output was poor (Table 3). However, linear regression analysis of the change in strain vs. change in RHC measurements revealed statistically significant associations. Change in circumferential strain correlated reasonably well with the changes in mean PA pressure, PVR, and cardiac output (r values of 0.69, 0.76, and 0.51 respectively; p < 0.001 for all). Change in posterior wall radial strain also demonstrated a moderate correlation with change in mean PA pressure, PVR, and cardiac output (r values of 0.7, 0.7, and 0.45; p values of < 0.001, < 0.001 and 0.02, respectively). Why did the change in strain correlate more closely with RHC parameters than strain itself? LV strain is influenced by a number of variables, including (but not limited to) longstanding hypertension, cardiac conditioning, coronary artery disease, valvular disease, chamber size, pericardial disease, and volume status [22–27]. Therefore, it is not surprising to find a range of LV strain values for any given degree of pulmonary hypertension. Examining the change in strain following PTE minimizes many of these confounding variables, and may explain the improved correlation between change in strain and RHC variables.