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We would like to respond to the comments by Barasch et al. regarding our study “Correlation of Left Ventricular Filling Characteristics With Right Ventricular Overload and Pulmonary Artery Pressure in Chronic Thromboembolic Pulmonary Hypertension” recently published in the Journal(1). The study by Moustapha, Barasch, and colleagues (2)was published only a short time before we submitted our manuscript and so, regrettably, was not included in our references.
The objective of our study was to define a quantitative relationship between right ventricular (RV) pressure overload and left ventricular (LV) diastolic filling characteristics, measuring both as continuous variables (i.e., mean pulmonary artery pressure and E/A ratio). Furthermore, we only studied patients with chronic thromboembolic pulmonary hypertension (CTEPH) who were undergoing pulmonary thromboendarterectomy (PTE) so that we could assess the change in LV diastolic filling with resolution of an RV pressure overload state.
In the study by Moustapha et al. (2), the degree of pulmonary hypertension was defined only as a dichotomous variable (mild-moderate vs. severe). Pulmonary artery (PA) pressure was estimated by Doppler-echocardiography, not measured directly as in our study. Moustapha and colleagues reported that the group of patients with severe (systolic PA pressure >60 mm Hg) had lower E/A ratios than did the group with mild-moderate pulmonary hypertension (systolic PA pressure 40 to 60 mm Hg) (0.96 ± 0.37 vs. 1.34 ± 0.54, respectively [p < 0.05]). This relationship of low E/A ratio and severe pulmonary hypertension with associated interventricular septal distortion is, however, well recognized (3,4).
In contrast to these clearly semiquantitative results, we found a direct, logarithmic, and quantitative relationship between E/A ratio and PA pressure measured as continuous variables in patients with CTEPH. We also documented a similar direct relationship between E/A and cardiac output in the same group. The results of our study expand upon previous studies that have reported on abnormal LV diastolic function in patients with chronic pulmonary hypertension. However, it is still difficult to hypothesize that abnormal LV diastolic filling contributes significantly to dyspnea in these patients. In fact, pulmonary capillary wedge pressure increased slightly from 9.8 ± 5 to 11.5 ± 4.5 mm Hg (p = 0.04) after PTE. This suggests that dyspnea in patients with severe pulmonary hypertension is unlikely to be related to an elevated LV filling pressure.
- American College of Cardiology Foundation
- Mahmud E.,
- Raisinghani A.,
- Hassankhani A.,
- et al.
- Dittrich H.C.,
- Chow L.C.,
- Nicod P.H.