PURPOSE:In the thorax at the level of the aortic valve, the anteroposterior space is occupied by the left atrium, aortic root, and right ventricular outflow tract (RVOT). In this limited space, changes in pressure/volume within these structures may affect the movement of the others during the cardiac cycle. Past studies have found associations between aortic root excursion (AoE) and several parameters, including LV systolic function, LA volume, and LV filling pressure. There has been little work, however, evaluating the relationship between right heart parameters and AoE. We hypothesized that RV overload and pulmonary hypertension would affect AoE independent of LV systolic function.
METHODS:We studied 20 consecutive patients with chronic thromboembolic pulmonary hypertension (CTEPH) and normal LVEF and PCWP. Each patient underwent transthoracic echocardiography and right heart catheterization. LVEF was 68±7%, with mean pulmonary artery pressure (mPAP) 49±9 mmHg and PCWP 10±3 mmHg. Anteroposterior AoE was measured as the difference between systolic and end-diastolic position of the aorta on M-mode imaging at the level of the aortic valve. Results were compared to findings from 10 controls with normal LVEF (65±3%) and PAP.
RESULTS:Mean AoE for CTEPH patients was approximately half that of controls (6.6±2.5 vs 12.9±2.7 mm, p <0.0001). There was a significant inverse linear correlation between mPAP and AoE in the CTEPH group (r = 0.66, p = 0.0015). However, AoE in this group showed no correlation with LVEF (r = 0.06, p = 0.80).
CONCLUSION:AoE is significantly attenuated in CTEPH despite normal LVEF. Furthermore, there is a significant inverse relationship between AoE and mPAP, independent of LVEF.
CLINICAL IMPLICATIONS:Since space is limited in the AP dimension at the aortic valve, increasing RVOT pressure with resultant decreased AoE likely alters LA expansion. This may limit end-systolic LA volume therefore decreasing early diastolic LV filling drive and creating a decreased E/A LV filling ratio. If so, perhaps this contributes to the observed poor outcomes in patients with pulmonary HTN who develop atrial fibrillation. Further investigation is needed.
DISCLOSURE:Charles Parise, No Financial Disclosure Information; No Product/Research Disclosure Information