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(Stroke. 2005;36:1824.)
© 2005 American Heart Association, Inc.

Letters to the Editor

Comment on the Phosphodiesterase 4D Replication Study by Bevan et al

Solveig Gretarsdottir, PhD; Jeffrey Gulcher, MD, PhD; Gudmar Thorleifsson, PhD; Augustine Kong, PhD Kari Stefansson, MD, DrMed

DeCODE Genetics, Reykjavik, Iceland

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We observe with interest the results of the study by Bevan et al,¹ where they attempted to replicate our findings associating the PDE4D gene with stroke. We appreciate the effort by the authors and their presentation of their data in some detail. The latter allowed us to compare their results with ours, including some unpublished results. In our original publication,² the main findings are summarized in Figure 4, where haplotypes are grouped into 3 categories: the at-risk haplotypes, the "wild-type," and the protective haplotype. Although the definition of the at-risk haplotypes involved multiple markers, the protective haplotype, in our data, is characterized by one single-nucleotide polymorphism, specifically allele A of SNP45. This makes it particularly suitable for a replication in a different population. In Table I of Bevan et al, allele A has frequency of 15.4% in 621 stroke patients and 18.7% in 848 controls. We calculated that this corresponds to 191 copies of allele A and 1051 Gs in stroke patients, and 317 As and 1379 Gs in controls. Applying Fisher exact test gives a 2-sided probability value of 0.02 and a 1-sided probability value of 0.01. For the same allele counts, estimated risk of A relative to G is 0.79, or equivalently risk of G relative to A is 1.26. This agrees well with our estimated relative risk of 1.33 for allele G for all stroke patients (in Table 1 of Gretarsdottir et al²). Hence, even though Bevan et al did not consider this . . . [Full Text of this Article]