Left ventricular diastolic dysfunction in pulmonary hypertension predicts functional capacity and clinical worsening: a tissue phase mapping study

Background: The function of the right and left ventricles is intimately related through a shared septum and pericardium. Therefore, right ventricular (RV) disease in pulmonary hypertension (PH) can result in abnormal left ventricular (LV) myocardial mechanics. To assess this, we implemented novel cardiovascular magnetic resonance (CMR) tissue phase mapping (TPM) to assess radial, longitudinal and tangential LV myocardial velocities in patients with PH. Methods: Respiratory self-gated TPM was performed using a rotating golden-angle spiral acquisition with retrospective cardiac gating. TPM of a mid ventricular slice was acquired in 40 PH patients and 20 age-and sex-matched healthy controls. Endocardial and epicardial LV borders were manually defined, and myocardial velocities calculated using in-house software. Patients without proximal CTEPH (chronic thromboembolic PH) and not receiving intravenous prostacyclin therapy (n = 34) were followed up until the primary outcome of disease progression (death, transplantation, or progression to intravenous therapy) or the end of the study. Physicians who determined disease progression were blinded to CMR data. Conventional ventricular volumetric indices and novel TPM metrics were analyzed for prediction of 6-min walk distance (6MWD) and disease progression. Results: Peak longitudinal (p < 0.0001) and radial (p = 0.001) early diastolic (E) wave velocities were significantly lower in PH patients compared with healthy volunteers. Reversal of tangential E waves was observed in all patients and was highly discriminative for the presence of PH (p < 0.0001). The global radial E wave (beta = 0.41, p = 0.017) and lateral wall radial systolic (S) wave velocities (beta = 0.33, p = 0.028) were the only independent predictors of 6MWD in a model including RV ejection fraction (RVEF) and LV stroke volume. Over a median follow-up period of 20 months (IQR 7.9 months), 8 patients commenced intravenous therapy and 1 died. Global longitudinal E wave was the only independent predictor of clinical worsening (6.3x increased risk, p = 0.009) in a model including RVEF and septal curvature. Conclusions: TPM metrics of LV diastolic function are significantly abnormal in PH. More importantly, abnormal LV E wave velocities are the only independent predictors of functional capacity and clinical worsening in a model that includes conventional metrics of biventricular function.