Abstract
A parental history of premature coronary heart disease (CHD) is an established risk factor for CHD events in descendants. The study aim was to investigate whether subclinical coronary artery calcification (CAC) differs between asymptomatic individuals (a) without a parental CHD history, (b) with a parental history and (c) without knowledge of parental CHD history. The inclusion of individuals without knowledge of parental CHD history is a new approach. We also differentiated between CHD of mother and father to gain insight into their individual contributions. Data was obtained for 4,301 subjects aged 45–75 years free of overt CHD from the baseline screening of the population-based Heinz Nixdorf Recall study. CAC, measured by electron-beam computed tomography, was modeled conducting logistic regressions. Model 1 included family history, Model 2 was adjusted for age (and gender) and Model 3 added common CHD risk factors. The CAC score was dichotomized using the age and sex-specific 75th percentile. The odds ratio (OR) for CAC ≥ age and sex-specific 75th percentile was 1.33 among individuals with parental premature CHD history (95 % confidence interval [95 %CI]: 1.08, 1.63), which did not change after full adjustment (OR 1.40, 95 %CI: 1.13, 1.74). Individuals with an unknown biological father or mother had a high chance of elevated CAC scores (fully adjusted; father: OR 1.38, 95 %CI: 1.01, 1.90, mother: OR 1.86, 95 %CI: 0.90, 3.84) compared to the reference group. The current study showed an association between parental CHD history and CAC independent of common CHD risk factors. This association affirms the use of parental CHD history in cardiovascular risk assessment among asymptomatic adults in routine practice. The observation that individuals who did not know their mother or father are prone to increased CAC scores needs further confirmation in large scale studies.
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Abbreviations
- CAC:
-
Coronary artery calcification
- CHD:
-
Coronary heart disease
- CI:
-
Confidence interval
- CVD:
-
Cardiovascular disease
- Gen3:
-
Third generation cohorts
- HDL:
-
High-density lipoprotein
- HNR:
-
Heinz Nixdorf Recall study
- LDL:
-
Low-density lipoprotein
- PROCAM:
-
Prospective cardiovascular Münster
- OR(s):
-
Odds ratio(s)
- sig.:
-
Significance
- SES:
-
Socioeconomic status
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Acknowledgments
We would like to thank the Heinz Nixdorf Foundation (Chairman Martin Nixdorf, former Chairman: †Dr. jur. Schmidt), Germany, for their generous support of this study. The study is also supported by the German Ministry of Education and Science (BMBF), and the German Aerospace Center (Deutsches Zentrum für Luft- und Raumfahrt, DLR), Bonn, Germany. Assessment of psychosocial factors is funded by the German Research Foundation (DFG; Project SI 236/8-1 and SI 236/9-1). We kindly acknowledge the support of Sarstedt AG & Co. (Nümbrecht, Germany) with regard to the laboratory equipment. We are indebted to all study participants and to the dedicated personnel of both the study centre of the Heinz Nixdorf Recall Study and the EBT-scanner facilities as well as to the investigative group, in particular D. Grönemeyer, R Seidel, U Roggenbuck and S Slomiany.
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None of the authors has declared any conflict of interests or has any financial disclosure to report.
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This study was conducted on behalf of the Heinz Nixdorf Recall Investigative Group.
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Appendix: Advisory Board
Appendix: Advisory Board
Meinertz T, Hamburg, Germany (Chair); Bode C, Freiburg, Germany; de Feyter PJ, Rotterdam, Netherlands; Güntert B, Hall i. T., (Austria); Gutzwiller F, Bern, Switzerland; Heinen H, Bonn, Germany; Hess O, Bern, Switzerland; Klein B, Essen, Germany; Löwel H, Neuherberg, Germany; Reiser M, Munich, Germany; Schmidt G, Essen, Germany; Schwaiger M, Munich, Germany; Steinmüller C, Bonn, Germany; Theorell T, Stockholm, Sweden; Willich SN, Berlin, Germany.
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Wahl, S., Möhlenkamp, S., Erbel, R. et al. Screening results for subclinical coronary artery calcification in asymptomatic individuals in relation to a detailed parental history of premature coronary heart disease. Eur J Epidemiol 28, 301–310 (2013). https://doi.org/10.1007/s10654-012-9743-1
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DOI: https://doi.org/10.1007/s10654-012-9743-1