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APOE alleles are not associated with calcific aortic stenosis
  1. J R Ortlepp1,
  2. M Pillich2,
  3. V Mevissen2,
  4. C Krantz2,
  5. M Kimmel2,
  6. R Autschbach3,
  7. G Langebartels3,
  8. J Erdmann4,
  9. R Hoffmann2,
  10. K Zerres5
  1. 1Interdisciplinary Intermediate Care Unit, University Hospital of Aachen, RWTH Aachen, Aachen, Germany
  2. 2Medical Clinic I, University Hospital of Aachen, RWTH Aachen, Aachen, Germany
  3. 3Clinic for Cardiac Surgery, University Hospital of Aachen, RWTH Aachen, Aachen, Germany
  4. 4Medical Clinic II, Lübeck, Germany
  5. 5Institute of Human Genetics, University Hospital of Aachen, RWTH Aachen, Aachen, Germany
  1. Correspondence to:
    Dr J R Ortlepp
    Interdisciplinary Intermediate Care, University Hospital of Aachen, Pauwelsstrasse 30, D-52057 Aachen, Germany; jrortlepp{at}ukaachen.de

Abstract

Objectives: To analyse the association of APOE alleles with aortic stenosis (AS) in a large study population.

Methods: Patients with AS (n  =  538) and a control group of the same age without heart disease (n  =  536) were recruited. Left heart catheterisation was performed and mean gradient, aortic valve area, presence of stenotic coronary artery disease (CAD) and cardiovascular risk factors (hypercholesterolaemia, hypertension, smoking, diabetes mellitus and family history of CAD) were assessed. The frequency of the APOE major alleles e2, e3 and e4 was assessed by genotyping the polymorphisms APOE334 and APOE472 with a 5′ exonuclease assay (TaqMan).

Results: Mean gradient across the aortic valve in cases was 50 (SD 20) mm Hg corresponding to a mean aortic valve area of 0.84 (SD 0.34) cm2. 270 patients with AS had stenotic CAD. Among patients with AS, the prevalence of hypercholesterolaemia (64% v 40%, p < 0.001), smoking (43% v 27%, p < 0.001), diabetes (27% v 17%, p < 0.01), family history of CAD (30% v 21%, p ⩽ 0.05), and male sex (65% v 44%, p < 0.001) was higher in those with than in those without CAD. The frequency of the major alleles was not different between cases and controls (APOE e2: 104 (19.3%) v 94 (17.5%); APOE e3: 319 (59.3%) v 332 (61.9%); APOE e4: 115 (21.3%) v 110 (20.5%); all p > 0.10).

Conclusion: APOE e4 is not associated with AS, reflecting the different genetic backgrounds of CAD and AS.

  • AS, degenerative calcific aortic stenosis
  • CAD, coronary artery disease
  • MI, myocardial infarction

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Footnotes

  • Published Online First 10 April 2006

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