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Reply: Tidal Carbon Dioxide as a Prognostic Feature in Inoperable Chronic Thromboembolic Pulmonary Hypertension.

included in the current analysis. Operability was assessed via ventilation-perfusion scan, pulmonary angiography, and thoracic computed tomography. The follow-up period was extended to January 2015 for the current analysis. Baseline ETCO2 levels obtained at rest were available for all patients and have not been reported or analyzed previously. The ethics committee of the Faculty of Medicine of the University of Giessen approved the study (approval no. 71/12). The mean follow-up period was 64.86 40.2 months, during which 41 (27.2%) of the patients died. Median ETCO2 at baseline was substantially decreased (27 mm Hg [interquartile range: 24–34] mm Hg), and was almost similar to the results fromWelch and coworkers in PAH. Univariate Cox regression analysis significantly related ETCO2 as a continuous variable to overall survival (hazard ratio, 0.91; 95% confidence interval [CI], 0.86–0.96; P = 0.002). Welch and coworkers demonstrated the prognostic value of ETCO2 in their PAH cohort, using a cutoff of 29 mm Hg (1). We assessed the clinical value of their ETCO2 cutoff in our cohort. Patients with inoperable CTEPH who had ETCO2, 29 mm Hg showed significantly impaired pulmonary hemodynamics and a more advanced functional class compared with patients who had ETCO2> 29 mm Hg (Table 1). In addition, ETCO2 dichotomized at 29 mm Hg was found to be significantly associated with overall survival (hazard ratio, 0.37; 95% confidence interval, 0.17–0.81; P = 0.012). This was supported by Kaplan-Meier analysis, which showed that patients with inoperable CTEPH and ETCO2> 29 mm Hg had significantly better 5-year overall survival than those with ETCO2, 29 mm Hg (89.3% vs. 73.2%, respectively; log-rank P, 0.009), and by backward stepwise multivariate Cox regression analysis (based on likelihood ratio, using ETCO2 dichotomized at 29 mmHg and adjusting for age, sex, and cardiac index; multivariate hazard ratio, 0.24; 95% confidence interval, 0.06–0.94; P = 0.04). Limitations of our study include its retrospective design and the fact that perfusion defects were not directly quantified at the time of diagnosis. Therefore, the degree of perfusion defect could not be assessed retrospectively in our study and merits further investigation. In conclusion, our analysis revealed two important findings: the ETCO2 cutoff defined by Welch and coworkers demonstrated clinical relevance in patients with inoperable CTEPH, and ETCO2 emerged as a clinically relevant prognostic factor not only in PAH but also in inoperable CTEPH, mirroring the presence of ventilation/perfusion mismatch as a pathophysiological hallmark in both disease entities.