Chest
Clinical Investigations: Cardiology/Cardiac SurgeryAssessment of Left Ventricular Diastolic Function After Single Lung Transplantation in Patients With Severe Pulmonary Hypertension
Section snippets
Study Patients
Between 1991 and 1996, 47 single lung transplantation procedures were performed in 45 consecutive patients at the University of Kentucky Hospital. Clinical diagnoses were severe pulmonary hypertension in 14 patients and end-stage of COPD in the remaining 31. Of the 14 pulmonary hypertension patients, 9 who had complete Doppler echocardiographic examinations preoperatively and postoperatively were selected for this study. Nine age-matched normal subjects served as a control group.
Doppler Echocardiography
Two-dimensional
Clinical and Doppler Echocardiographic Features
In the patient group, there were 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 the other three were diagnosed as having secondary pulmonary hypertension due to ventricular septal defect, atrial septal defect, and pulmonary vasculitis from systemic lupus erythematosus, respectively. Five patients received a left lung transplant and four received a right lung transplant.
Doppler
Discussion
It is important to restore right ventricular function after single lung transplantation in pulmonary hypertension patients. A number of studies have shown that the right ventricular function improves dramatically immediately after transplantation,2, 3, 4, 5, 6, 7, 8 and the improvement is maintained for at least 2 years.5 Interestingly, our study indicated that the impaired left ventricular early filling persisted early after transplantation, despite the fact that pulmonary hypertension was
Conclusions
This study observed left ventricular filling dynamics by Doppler echocardiography before and after single lung transplantation in patients with severe pulmonary hypertension. The impaired early filling persisted shortly after transplantation, despite restoration of left ventricular geometry after reversal of pulmonary hypertension. The abnormal filling was not resolved until 1 year later. The findings suggest the impaired early filling may be caused by intrinsic left ventricular abnormalities
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Cited by (28)
Impact of lung transplantation on diastolic dysfunction in recipients with pretransplant pulmonary hypertension
2023, Journal of Thoracic and Cardiovascular SurgerySurvival and left ventricular dysfunction post lung transplantation for pulmonary arterial hypertension
2022, Journal of Critical CareCitation Excerpt :We hypothesize that both chronic adverse remodelling of the left ventricle and withdrawal of mechanical ventilation are contributing etiological factors. Although diastolic dysfunction has predominantly been described in the literature [30,31], we observed systolic dysfunction in 19 patients diagnosed with LVD by echocardiography. In our cohort, diastolic function was not routinely assessed in the postoperative period.
Impact of Left Ventricular Diastolic Dysfunction on Lung Transplantation Outcome in Patients With Pulmonary Arterial Hypertension
2017, American Journal of TransplantationLeft Ventricular Dysfunction after Lung Transplantation for Pulmonary Arterial Hypertension
2015, Transplantation ProceedingsRisk of death and need for transplantation in chronic pulmonary hypertension
2014, American Journal of the Medical SciencesRight ventricular assist device in end-stage pulmonary arterial hypertension: Insights from a computational model of the cardiovascular system
2012, Progress in Cardiovascular DiseasesCitation Excerpt :Such abrupt redistribution of volume can result in pulmonary edema, even in the setting of normal LV systolic and diastolic function.26 In addition, recent studies in animals27,28 and humans29,30 with PAH have provided evidence of LV diastolic dysfunction, manifest as reduced chamber size (i.e., leftward shifted end-diastolic pressure-volume relationship). Indeed, our patient hemodynamic parameter fitting algorithm indicated that with increasing disease severity and progressively lower cardiac outputs, LV diastolic stiffness increased substantially (i.e., higher LV diastolic stiffness coefficient, α, Table 2).
Presented in part at the 46th Annual Scientific Session of the American College of Cardiology, Anaheim, Calif, March 1997.