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(Circulation. 2008;117:185-191.)
© 2008 American Heart Association, Inc.

Genetics

Lack of Association Between the MEF2A Gene and Myocardial Infarction

Wolfgang Lieb, MD; Björn Mayer, MD; Inke R. König, PhD; Iris Borwitzky, MD; Anika Götz, PhD; Silke Kain, MD; Christian Hengstenberg, MD; Patrick Linsel-Nitschke, MD; Marcus Fischer, MD; Angela Döring, MD; H. -Erich Wichmann, MD; Thomas Meitinger, MD; Reinhold Kreutz, MD; Andreas Ziegler, PhD; Heribert Schunkert, MD; Jeanette Erdmann, PhD

From Medizinische Klinik II (W.L., B.M., I.B., A.G., P.L.-N., H.S., J.E.), Institut für Humangenetik (W.L.), and Institut für Medizinische Biometrie und Statistik (I.R.K., A.G., A.Z.), Universität zu Lübeck, Lübeck; Institut für klinische Pharmakologie und Toxikologie, Charité, Berlin (S.K., R.K.); Klinik und Poliklinik für Innere Medizin II, Universität Regensburg, Regensburg (C.H., M.F.); Institut für Epidemiologie (A.D., H.-E.W.) and Institut für Humangenetik (T.M.), GSF-Forschungszentrum für Umwelt und Gesundheit, Neuherberg; Institut für Medizinische Informationsverarbeitung, Biometrie und Epidemiologie, Ludwig-Maximilians-Universität München, München (H.-E.W.); and Insitut für Humangenetik, Technische Universität München, Klinikum rechts der Isar, München (T.M.), Germany.

Correspondence PD Dr rer nat Jeanette Erdmann, Medizinische Klinik II, Universität zu Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany. E-mail j.erdmann{at}cardiogenics.eu

Received July 17, 2007; accepted October 26, 2007.

Background— Coronary artery disease (CAD) and myocardial infarction (MI) are caused in part by genetic factors. Recently, the MEF2A gene was linked to MI/CAD in a single pedigree with autosomal-dominant pattern of inheritance. In addition, genetic variants within the gene have been associated with MI in case-control settings, producing inconsistent results.

Methods and Results— The MEF2A gene was sequenced in MI patients from 23 MI families (5 affected members per family), but no mutation was identified in any of these extended families. Moreover, the Pro279Leu variant in exon 7 was analyzed in 1181 unrelated MI patients with a positive family history for MI/CAD, in 533 patients with sporadic MI, and in 2 control populations (n=1021 and n=1055), showing no evidence for association with MI/CAD. In addition, a (CAG)n repeat in exon 11 was genotyped in 543 sporadic MI patients and in 1190 controls without evidence for association with MI. Finally, analyzing 11 single-nucleotide polymorphisms from the GeneChip Mapping 500K Array, genotyped in 1644 controls and 753 cases, failed to provide evidence for association (region-wide P=0.23).

Conclusions— Studying independent samples of >1700 MI patients, 2 large control populations, and multiple families with apparently mendelian inheritance of the disease, we found no evidence for any linkage or association signal in the MEF2A gene.

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