Response to Letter Regarding Article, “Endogenous Erythropoietin and Outcome in Heart Failure”
We thank Dr Incalzi and coauthors for their thorough reading of our article.1 They raise an important issue on chronic obstructive pulmonary disease (COPD)–related arterial hypoxemia and its influence on erythropoietin production. We agree that besides the presence of heart failure (and its known comorbidities), other factors can influence the level of erythropoietin.
However, in several clinical studies, no increase in erythropoietin was found in nonanemic patients with COPD compared with healthy control subjects.2,3 In our heart failure study population, 28% (167 of 605) were diagnosed with COPD, which is consistent with data from other heart failure studies.4 The presence of COPD did not influence erythropoietin levels in our study as assessed by univariable linear regression analysis (β=0.026; P=0.53). To evaluate whether COPD influenced mortality of all causes in this heart failure cohort, we adjusted our multivariable Cox regression model for the presence of COPD. The addition of COPD did not strengthen our model, and more important, COPD was not an independent predictor of prognosis (hazard ratio, 1.18; 95% confidence interval, 0.90 to 1.56; P=0.24). Finally, the presence of COPD in patients with higher-than-expected erythropoietin levels based on their hemoglobin value was not significantly higher compared with patients with low or normal levels of erythropoietin. From these results, we conclude that the presence of COPD had no significant influence on the data that we presented.
Dr Voors has received unrestricted research grants from Amgen and Ortho Biotech. Dr van Veldhuisen has received lecture fees from Amgen and is a member of the Executive Committee of the Darbepoetin Morbidity/Mortality Heart Failure Trial (RED-HF). The other authors report no conflicts.