Shortening of Doppler-Derived Deceleration Time of Early Diastolic Transmitral Flow in the Presence of Pulmonary Hypertension Through Ventricular Interaction

Deceleration time (DT) of the early transmitral flow velocity has recently been highlighted as a simple, noninvasive indicator of pulmonary arterial wedge pressure. In patients with pulmonary hypertension without left-sided heart disease, however, increased right ventricular pressure may result in an abnormal ventricular septal motion, which may impact on left ventricular (LV) early diastolic filling. We sought to determine if DT may be influenced by the severity of pulmonary hypertension in patients without left-sided heart disease. Doppler-derived transmitral flow and hemodynamic parameters were simultaneously assessed in 26 patients with pulmonary hypertension (primary pulmonary hypertension = 11; chronic thromboembolism = 15). Transmitral Doppler variables including DT were correlated with hemodynamics and LV deformity index measured in early diastole with 2-dimensional echocardiography. DT significantly correlated with the total pulmonary resistance (r = −0.70, p <0.001). Multivariate analysis revealed that DT was independently determined by total pulmonary resistance, but not by pulmonary arterial wedge pressure, heart rate, or patientʹs age in our study population. DT showed a correlation with LV deformity index (r = −0.74, p <0.001). These results indicate that DT may shorten in association with the severity of pulmonary hypertension and that the shortened DT in pulmonary hypertension may be attributable to right ventricular pressure overload which causes geometric changes. ermine if deceleration time (DT) of the early transmitral flow velocity may be influenced by the severity of pulmonary hypertension in patients without left-sided heart disease, Doppler-derived transmitral flow and hemodynamic parameters were simultaneously assessed in 26 patients with pulmonary hypertension. DT showed significant inverse correlations with the total pulmonary resistance and left ventricular deformity index, suggesting that DT shortens in association with the severity of pulmonary hypertension, and that the shortened DT in pulmonary hypertension may be attributable to right ventricular pressure overload which causes geometric changes.