Exercise right ventricular global longitudinal strain as a marker for exercise tolerance in patients with chronic thromboembolic pulmonary disease

Abstract Background Patients with chronic thromboembolic pulmonary disease (CTEPD) may have residual dyspnea on exertion, even after improvement of pulmonary hypertension (PH). Therefore, evaluation of dynamic right ventricular (RV) function using exercise cardiac magnetic resonance (exCMR) in CTEPD may offer insights into its hemodynamic pathophysiology and help explain exercise intolerance. While RV ejection fraction (RVEF) is recognized as a prognosticator in PH, global longitudinal strain (RVGLS) has an advantage in its load insensitiveness. However, the dynamic changes of RVGLS and its relationship to exercise tolerance in CTEPD have not yet been investigated. Objective To assess the dynamic RV function and the association between RVGLS and exercise tolerance in CTEPD. Methods ExCMR was conducted in CTEPD with PH (CTEPH, n=9), CTEPD without PH (CWoPH, n=10), and healthy subjects (Control, n=18). A cardiopulmonary exercise test (CPX) was performed to measure maximal workload (MWL). CMR was scanned at rest and during exercise at 40% MWL with pedaling in the supine position. Images of short axis views were analyzed by Aquarius to acquire left ventricular end-diastolic volume index (LVEDVI), end-systolic volume index (LVESVI), right ventricular end-diastolic volume index (RVEDVI), and end-systolic volume index (RVESVI). RV stroke volume (RVSV) index (RVSVI) was calculated as the difference of RVEDVI and RVESVI. RVEF was calculated by RVSV divided by RVEDV. RVGLS was analyzed from 4 chamber views using cvi42. Data are presented as mean ± SD. Two-way repeated measures analysis of variance post-hoc Bonferroni’s multiple comparisons test or Pearson correlation analysis was performed. Results Heart rate increased similary in each group during exercise (Figure1A). LVEDVI was smaller in CTEPH and decreased further during exercise (Figure 1B). Compared to Control, RVEDVI and RVESVI were higher in CTEPH, with no significant difference in CWoPH at rest (Figures 1C,1D). Exercise decreased RVESVI and increased RVSVI in Control, whereas it increased both RVEDVI and RVESVI, and did not increase RVSVI in CWoPH (Figures 1C, 1D, 1E). Exercise increased RVEF in Control, but decreased in CWoPH (Figure 1F). RVGLS was analyzed in CWoPH (n=6) and CTEPH (n=7). Exercise did not change RVGLS in CWoPH but worsened in CTEPH (Figure 2A). RVGLS during exercise (exRVGLS) correlated with %peak VO2 (R²=0.47, p0.01, Figure 2B), VE vs. VCO2 slope (R²=0.37, p=0.03, Figure 2C), the ratio of the change in mean pulmonary artery pressure to cardiac output (ΔP/Q, R²=0.45, p=0.02, Figure 2D), but did not correlate with RVGLS at rest. Conclusions Exercise-induced RV dilatation and impaired RVSV augmentation were found in CWoPH. RVGLS at rest was impaired in both CTEPH and CWoPH, while exRVGLS did not change during exercise. exRVGLS in CTEPD correlated with exercise tolerance and severity of exercise-induced PH. exRVGLS may be a valuable marker for evaluating exercise tolerability.