(Circulation. 2007;115:e314.)
© 2007 American Heart Association, Inc.
Correspondence |
Division of Research, Kaiser Permanente of Northern California, Oakland, Calif
Departments of Epidemiology and Biostatistics and Medicine, University of California at San Francisco, San Francisco, Calif
Amgen, Inc, Thousand Oaks, Calif
Department of Medicine, University of California at San Francisco, San Francisco, Calif
We appreciate the comments by Andreotti et al regarding additional possible reasons that may explain the excessive risk of adverse clinical events associated with reduced hemoglobin levels in the setting of chronic heart failure.1 Our study shows that lower glomerular filtration rate and either low or very high levels of hemoglobin were each independent predictors of death and hospitalization for heart failure.1 Suppressed erythropoietin levels secondary to associated chronic kidney disease are common in heart failure, and we agree that erythropoietin seems to have multiple effects on both the erythroid lineage and nonerythroid progenitor cells in the bone marrow,2 as well as potential direct myocardial effects. Recent data suggest that progenitor cells may play an important role in myocyte repair and clinical outcomes in patients with coronary heart disease and heart failure.3,4 The exact mechanisms underlying the development of anemia complicating heart failure are multifactorial, however, and they involve renal and nonrenal pathways (eg, chronic inflammation, use of selected therapies, bone marrow suppression, etc). Therefore, we suggest that both erythropoietin-dependent and multiple erythropoietin-independent factors likely contribute to the high rates of death and other adverse outcomes linked to anemia in the setting of heart failure.
| Acknowledgments |
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Dr Ackerson received research support for this study from Amgen, Inc. S. Robbins is an employee of and has ownership interest in Amgen, Inc. Dr Massie has received research support and honoraria from Amgen, Inc, and serves on its advisory board. Dr Go, J. Yang, and K. Lepper received research support for this study from Amgen, Inc. Dr Shlipak reports no conflicts of interest.
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