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Genetic Susceptibility of Myocardial Infarction

Published online by Cambridge University Press:  21 February 2012

Slobodan Zdravkovic
Affiliation:
Division of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. slobodan.zdravkovic@ki.se
Andreas Wienke
Affiliation:
Martin Luther University Halle-Wittenberg, Institute of Medical Epidemiology, Biostatistics and Informatics, Halle (Saale), Germany.
Nancy L. Pedersen
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Ulf de Faire
Affiliation:
Division of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Cardiovascular Laboratory, Department of Cardiology, Karolinska Hospital, Stockholm, Sweden.
Corresponding
E-mail address:

Abstract

The aim of this study was to determine the influence of genetic factors on the first episode of acute myocardial infarction. Probandwise concordances, tetrachoric correlations and quantitative genetic analyses of liability were applied to data drawn from the Swedish Twin Registry and the Swedish Acute Myocardial Infarction Register. All same-sexed twin pairs born between 1886 and 1958 who were alive in 1987 were included in the analyses. Our results show that concordance rates for acute myocardial infarction in monozygotic (MZ) twins were similar across sexes (among males .26 and females .27). For dizygotic (DZ) twins the concordances were .20 for males and .16 for females, yielding a greater MZ–DZ concordance differential for females than males. Tetrachoric correlations were greater for MZ than DZ twins for both sexes (.49 for male MZ and .34 for male DZ-twins and .56 and .35 for female MZ and DZ twins respectively). Quantitative genetic analyses of liability resulted in equal variance components for males and females (.36) but significantly different thresholds (prevalences). In conclusion, liability to first occurrence of acute myocardial infarction is moderately influenced by genetic variants in both sexes. The familial influence on phenotypic variance is exclusively explained by additive genetic factors.

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