Atherosclerosis
Volume 148, Issue 1 , Pages 95-100, January 2000

Is lipoprotein(a)-cholesterol a better predictor of vascular disease events than total lipoprotein(a) mass? A nested case control study from the West of Scotland Coronary Prevention Study

  • Allan Gaw

      Affiliations

    • Department of Pathological Biochemistry, 4th Floor Queen Elizabeth Building, Royal Infirmary University/NHS Trust, Glasgow G31 2ER, UK
    • Corresponding Author InformationCorresponding author. Tel.: +44-141-2114599; fax: +44-141-5532558
  • ,
  • E.Ann Brown

      Affiliations

    • Department of Pathological Biochemistry, 4th Floor Queen Elizabeth Building, Royal Infirmary University/NHS Trust, Glasgow G31 2ER, UK
  • ,
  • Gillian Docherty

      Affiliations

    • Robertson Centre for Biostatistics, University of Glasgow, Glasgow, UK
  • ,
  • Ian Ford

      Affiliations

    • Robertson Centre for Biostatistics, University of Glasgow, Glasgow, UK
  • ,
  • for the West of Scotland Coronary Prevention Study Group

      Affiliations

Received 2 March 1999; received in revised form 12 April 1999; accepted 21 June 1999. published online 16 August 2004.

Abstract 

The clinical utility of a new assay for plasma lipoprotein(a)-cholesterol (Lp(a)-C) was assessed in parallel with our routine Lp(a) mass measurements in a nested-case control study of subjects within the placebo arm of the West of Scotland Coronary Prevention Study (WOSCOPS). A total of 238 control patients and 108 patients who had suffered a serious vascular event during the course of the WOSCOPS were examined. Lp(a) mass was assessed within 2 years of sampling by an ELISA method on baseline EDTA plasma samples which had been stored at −70°C. Subsequently, the Lp(a) mass was re-measured by an immunoturbidimetric assay ∼8 years after sampling. On the same stored aliquot the Lp(a)-C was measured. These analyses allowed us to assess whether the Lp(a)-C assay could provide any additional information over and above that which would be obtained from our Lp(a) mass assays. In addition the apo(a) isoform sizes of these subjects were measured using a high resolution immunoblotting system. The Lp(a)-C and Lp(a) mass measurements provided exactly the same information in the study, as they were equally non-discriminatory between cases and controls. The only difference between the two patient groups was the percentage of ‘null’ apo(a) alleles (control: 25.6% versus cases: 19.4%). We conclude that these results reinforce the concordance of the two assay systems and confirm that the Lp(a)-C assay provides no added information over and above that gained from traditional Lp(a) mass assays, which may be faster and less expensive.

Keywords:  Lipoprotein(a), Cholesterol, WOSCOPS

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  • 1 Executive Committee: James Shepherd (chairman), Stuart M. Cobbe, A. Ross Lorimer, James H. McKillop, Ian Ford, Christopher J. Packard, Peter W. Macfarlane, Christopher Isles; Data and Safety Monitoring Committee: Michael F. Oliver (chairman), Anthony F. Lever, Byron W. Brown, John G.G. Ledingham, Stuart J. Pocock, Basil M. Rifkind; Cardiovascular End-points Committee: Stuart M. Cobbe (chairman), Barry D. Vallance, Peter W. Macfarlane; Adverse Events Review Board: A. Ross Lorimer, James H. McKillop, David Ballantyne; Data centre staff: Liz Anderson, David Duncan, Sharon Kean, Audrey Lawrence, June McGrath, Vivette Montgomery, John Norrie; Population screening: Melvyn Percy; Clinical coordination, monitoring, and administration: Elspeth Pomphrey, Andrew Whitehouse, Patricia Cameron, Pamela Parker, Fiona Porteous, Leslie Fletcher, Christine Kilday; Computerised ECG analysis: David Shoat (deceased), Shahid Latif, Julie Kennedy; Laboratory operations: M. Anne Bell, Robert Birrell; Company liaison and general support: Margot Mellies, Joseph Meyer, Wendy Campbell.

PII: S0021-9150(99)00259-2

Atherosclerosis
Volume 148, Issue 1 , Pages 95-100, January 2000