Authors Reply:
We read with great interest the letter to the editor written by Balta et al. It provides extremely relevant comments to our article, which showed that red blood cell distribution width (RDW) is a predictor of readmission in cardiac patients.1 This independent relationship as well as the ready availability of RDW at no additional cost may encourage its wider use in clinical practice. We used RDW on admission and the 95th percentile cutoff for our measurements to harmonize our methods with previous studies such as NHANES III (National Health and Nutrition Examination Survey III).2 Our study's retrospective design had the inherent limitations of such an approach. It did not provide a proven biological mechanism for the action of RDW. As Balta et al mention in their letter, multiple pathways are hypothesized, including the role of the cholesterol content of erythrocyte membranes that is reflected in the RDW as well as with clinical instability in coronary artery disease.3
We are clearly in agreement with the mounting evidence for the various associations of RDW and adverse outcomes.4, 5, 6 Its availability and low cost make it an attractive factor to consider in the risk stratification of patients. Even though our article makes a strong case for the robustness of RDW as a predictor of adverse outcome (in this case readmission), its better use would be as an additional factor for the risk stratification of patients as described previously in the literature.7, 8 Indeed, a previous report has shown no correlation between RDW and C‐reactive protein, a well‐known inflammatory marker.9 Therefore, the information that RDW provides is likely to be independent of inflammatory markers, and the practice of combining the assessment of RDW and inflammatory markers is becoming more substantiated.
RDW is showing a lot of potential in its associations with adverse outcomes, far beyond its established role in the differential diagnosis of anemia. Further studies are needed to evaluate the concomitant impact of RDW together with other serum inflammatory markers and to define the nature of the mechanism behind its various associations.
Georges Ephrem, MD, MS Department of Cardiovascular Disease Hofstra–North Shore–LIJ Health System Manhasset, New York
References
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