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Beyond Framingham risk factors and coronary calcification: does aortic valve calcification improve risk prediction? The Heinz Nixdorf Recall Study
  1. Hagen Kälsch1,
  2. Nils Lehmann2,
  3. Amir A Mahabadi1,
  4. Marcus Bauer1,
  5. Kaffer Kara1,
  6. Patricia Hüppe1,
  7. Susanne Moebus2,
  8. Stefan Möhlenkamp3,
  9. Nico Dragano4,
  10. Axel Schmermund5,
  11. Andreas Stang6,
  12. Karl-Heinz Jöckel2,
  13. Raimund Erbel1,
  14. on behalf of the Investigator Group of the Heinz Nixdorf Recall Study
  1. 1Department of Cardiology, West-German Heart Center Essen, University Duisburg-Essen, Essen, Germany
  2. 2Biometry, and Epidemiology, Institute of Medical Informatics, University Duisburg-Essen, Essen, Germany
  3. 3Department of Cardiology, Krankenhaus Bethanien, Moers, Germany
  4. 4Medical Faculty, Centre for Health and Society, Institute of Medical Sociology, University Clinic Düsseldorf, Düsseldorf, Germany
  5. 5Cardioangiological Center Bethanien, Frankfurt/Main, Germany
  6. 6Medical Faculty, Institute of Clinical Epidemiology, University Halle-Wittenberg, Halle, Germany
  1. Correspondence to Dr Hagen Kälsch, Department of Cardiology, West-German Heart Center Essen, University Clinic Duisburg-Essen, Hufelandstrasse 55, Essen 45122, Germany; Hagen.Kaelsch{at}uk-essen.de

Abstract

Background Aortic valve calcification (AVC) is considered a manifestation of atherosclerosis. In this study, we investigated whether AVC adds to cardiovascular risk prediction beyond Framingham risk factors and coronary artery calcification (CAC).

Methods A total of 3944 subjects from the population based Heinz Nixdorf Recall Study (59.3±7.7 years; 53% females) were evaluated for coronary events, stroke, and cardiovascular disease (CVD) events (including all plus CV death) over 9.1±1.9 years. CT scans were performed to quantify AVC. Cox proportional hazards regressions and Harrell’s C were used to examine AVC as event predictor in addition to risk factors and CAC.

Results During follow-up, 138 (3.5%) subjects experienced coronary events, 101 (2.6%) had a stroke, and 257 (6.5%) experienced CVD events. In subjects with AVC>0 versus AVC=0 the incidence of coronary events was 8.0% versus 3.0% (p<0.001) and the incidence of CVD events was 13.0% versus 5.7% (p<0.001). The frequency of events increased significantly with increasing AVC scores (p<0.001). After adjustment for Framingham risk factors, high AVC scores (3rd tertile) remained independently associated with coronary events (HR 2.21, 95% CI 1.28 to 3.81) and CVD events (HR 1.67, 95% CI 1.08 to 2.58). After further adjustment for CAC score, HRs were attenuated (coronary events 1.55, 95% CI 0.89 to 2.69; CVD events 1.29, 95% CI 0.83 to 2.00). When adding AVC to the model containing traditional risk factors and CAC, Harrell's C indices did not increase for coronary events (from 0.744 to 0.744) or CVD events (from 0.759 to 0.759).

Conclusions AVC is associated with incident coronary and CVD events independent of Framingham risk factors. However, AVC fails to improve cardiovascular event prediction over Framingham risk factors and CAC.

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