Abstract
As functional properties of the coronaries may differ between coronary heart disease (CHD) patients with or without angina pectoris (AP), it is possible that different genetic mechanisms could be involved in the various CHD phenotypes. The primary aim of this study was, therefore, to determine the relative importance of genetic factors for AP as well as the impact of AP on CHD death in general. All same-sexed twins born between 1886 and 1958 included in the Swedish Twin Registry served as a base for this study. Information from the Swedish Cause of Death Register was used for diagnosing CHD death. Standard methods applied in twin research such as survival and quantitative genetic models were used. The impact of AP on CHD death was significant among both sexes, with larger estimates for males (hazard ratio and 95% CI 2.0 (1.8–2.3)) than females (1.6 (1.4–1.8)). Probandwise concordances and intraclass correlations for AP and CHD death were in general greater in monozygotic than dizygotic twins among both sexes. Heritability analyses resulted in moderate heritability estimates for AP in both sexes (0.39 (0.29–0.49) for males and 0.43 (0.08–0.51) for females). The correlation between AP and CHD was exclusively explained by the influence of familial factors in both sexes. In conclusion, our data imply genetic influences for AP and CHD death among both sexes and that AP is important as a risk factor for CHD death in both males and females, due in part to shared genetic pathways.
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Acknowledgements
The present study was supported by the Swedish Research Council (09533), the Swedish Council for the Planning and Coordination of Research, King Gustaf the V and Queen Victoria's Foundation, the Swedish Heart and Lung Foundation, and by the NIA/NIH Grant 7P01 AG08761. The Swedish Twin Registry is supported by grants from the Swedish Department of Higher Education, the Swedish Research Council and AstraZeneca.
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Zdravkovic, S., Wienke, A., Pedersen, N. et al. Genetic influences on angina pectoris and its impact on coronary heart disease. Eur J Hum Genet 15, 872–877 (2007). https://doi.org/10.1038/sj.ejhg.5201846
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DOI: https://doi.org/10.1038/sj.ejhg.5201846
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