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(Stroke. 2007;38:859.)
© 2007 American Heart Association, Inc.

Letters to the Editor

Response to Letter by Muscari and Zoli

Department of Neurology (D4–5), University of Miami Miller School of Medicine, Miami, Fla

Michael D. Hill, MD, MSc

Calgary Stroke Program, Department of Clinical Neurosciences, University of Calgary, Foothills Medical Centre, Calgary, Alberta, Canada

Yuko Y. Palesch, PhD

Data Coordination Unit, Department of Biostatistics, Bioinformatics and Epidemiology, Medical University of South Carolina, Charleston, SC

Response:

We thank Drs Muscari and Zoli for calling attention to their recent study of plasma levels of the N-terminal portion of BNP precursor (NT-proBNP) in elderly subjects.¹ They reported that NT-proBNP levels showed a modest inverse correlation (Spearman =–0.24 and –0.22, respectively) with hematocrit and hemoglobin, respectively (their Table 3). Similarly, multiple linear regression of log-transformed NT-proBNP levels yielded a partial correlation coefficient r=–0.22 (P<0.0001) in their large sample (n=713 subjects).

These results prompted us to conduct a similar analysis of our ALIAS Pilot Trial data, in the 42 subjects in whom plasma BNP levels were measured.² Spearman rank-order correlation analysis revealed no significant relationship between baseline hematocrit and baseline BNP level (=–0.272, P=0.081); no relationship between 24-hour (post-ALB treatment) hematocrit and post-ALB BNP level (=–0.011, P=0.95); and no relationship between the ALB-induced decrease in hematocrit and increase in BNP level at 24 hours after ALB treatment (=–0.051, P=0.76).

We also conducted a multiple linear regression analysis incorporating both age and hematocrit level. Both initial and 24-hour BNP levels were highly correlated to the subjects’ age (P<0.001) but were not correlated to the corresponding hematocrit value (P=0.31 and 0.17, respectively). Similarly, the rise in BNP at 24 hours was highly correlated to age (P<0.001) but not to the change in hematocrit (P=0.6). A regression plot of the latter data is shown below (Figure).

View larger version (15K): [in this window] [in a new window]   Increase in plasma BNP level from baseline to 24 hours post-treatment, plotted as a function of the decrease in hematocrit from baseline to 24 hours post-treatment, in individual subjects of the ALIAS Pilot Trial who received 25% human albumin at doses ranging from 1.37 to 2.05 g/kg body weight.2

Thus, we are unable to confirm the conclusions of Drs Muscari and Zoli. It should be noted that, whereas they assessed the BNP precursor, we assayed BNP itself. This might have some bearing on the discrepancy.

Acknowledgments

Disclosures

None.

References

1. Muscari A, Berzigotti A, Bianchi G, Giannoni C, Ligabue A, Magalotti D, Sbano D, Zacchini A, Zoli. Non-cardiac determinants of NT-proBNP levels in the elderly: relevance of haematocrit and hepatic steatosis. Eur J Heart Fail. 2006; 8: 468–476.[Abstract/Free Full Text]

2. Ginsberg MD, Hill MD, Palesch YY, Ryckborst KJ, Tamariz D. The ALIAS Pilot Trial: a dose-escalation and safety study of albumin therapy for acute ischemic stroke–I: physiological responses and safety results. Stroke. 2006; 37: 2100–2106.[Abstract/Free Full Text]

This Article Extract Full Text (PDF) All Versions of this Article: 38/3/859    most recent 01.STR.0000257308.07208.1fv1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ginsberg, M. D. Articles by Palesch, Y. Y. Search for Related Content PubMed PubMed Citation Articles by Ginsberg, M. D. Articles by Palesch, Y. Y.