Objectives: This study was designed to observe left ventricular filling by Doppler echocardiography before and after single lung transplantation in patients with severe pulmonary hypertension.
Background: Right ventricular pressure overload causes the deformation of the left ventricle by septal flattening toward its cavity, which may result in impaired left ventricular early filling. Recent studies have demonstrated the ability of single lung transplantation to restore right ventricular function in patients with severe pulmonary hypertension. However, changes in left ventricular filling after single lung transplantation have not been well studied.
Methods: We performed Doppler echocardiography in nine patients with severe pulmonary hypertension before, early (<3 months), and late (>1 year) after single lung transplantation. The study group consisted of eight female patients and one male patient with mean age of 32 years (range, 15 to 48 years). Six patients were diagnosed as having primary pulmonary hypertension and three as having secondary pulmonary hypertension. Nine age-matched normal subjects served as a control group. Doppler measurements included the following: transmitral flow early (E) and atrial (A) velocities, integrals (Ei and Ai), and left ventricular isovolumic relaxation time. The ratio of E/A and atrial filling fraction (Ai/Ei+Ai, AFF) were also determined. Left ventricular geometry was assessed from mid-short axis view with a circular shape factor (CSF).
Results: Early after lung transplantation, the left ventricular geometry became more circular with CSF (mean±SD) increasing from 0.63±0.09 to 0.88±0.05 (p<0.05). However, impaired early filling persisted in the patient group (E/A 0.7±0.1 vs preoperative 0.6±0.1, AFF 0.61±0.1 vs 0.64±0.1; both p=not significant). One year later, the left ventricular filling had returned to normal range with E/A 1.4±0.6 and AFF 0.35±0.1.
Conclusions: This study observed that the impaired left ventricular early filling persisted shortly after single lung transplantation in patients with severe pulmonary hypertension, despite findings that left ventricular geometry was restored earlier after reversal of pulmonary hypertension. The abnormal filling pattern appeared to be resolved 1 year later. The findings suggest the impaired early filling may be caused by intrinsic left ventricular abnormalities other than ventricular interaction in these patients.