Association of Hyperapobetalipoproteinemia with Endogenous Hypertriglyceridemia and Atherosclerosis

  1. ALLAN D. SNIDERMAN, M.D.;
  2. CHRISTINA WOLFSON, M.Sc.;
  3. BABIE TENG, M.Sc.;
  4. FRANK A. FRANKLIN, M.D., Ph.D.;
  5. PAUL S. BACHORIK, Ph.D.; and
  6. PETER O. KWITEROVICH, Jr., M.D.
  1. Montreal
    , Canada; and
    Baltimore, Maryland

    Abstract

    Researchers disagree on whether plasma triglyceride levels are an independent risk factor for atherosclerotic coronary artery disease. We hypothesized that patients with endogenous hypertriglyceridemia would differ: Some would have normal values of plasma low-density lipoprotein (LDL) B protein; others, despite their normal level of LDL cholesterol, would have increased levels of LDL B protein. We believed the latter patients—those with hyperapobetalipoproteinemia—would be the ones at risk for atherosclerosis. We studied two populations. Group 1, consisting of 162 patients with type IV lipoprotein patterns, was divided into two groups. One subgroup (A), which included 38 patients with elevated plasma LDL B protein levels, had a significantly higher prevalence of atherosclerotic disease than the other subgroup (B) of 36 patients with normal levels of plasma LDL B protein (10 patients versus two, p < 0.02). Group 2 consisted of 100 patients who had had myocardial infarction. Eighty-one percent of the 47 hypertriglyceridemic and 70% of the 53 normotriglyceridemic patients had elevated plasma LDL B protein levels (129 mg/dL or greater)—a proportion significantly higher than that in Group 1 (p < 0.001). Thus, an elevated plasma level of LDL B protein not only identifies subgroups of patients with type IV lipoprotein patterns, but also may be an important marker for atherosclerotic disease.

    Article and Author Information

    • ▸From the Cardiovascular Research Unit, Royal Victoria Hospital, McGill University; Montreal, Quebec, Canada; and the Lipid Research-Atherosclerosis Unit, Departments of Pediatrics and Medicine, The Johns Hopkins University School of Medicine; Baltimore, Maryland.

    • Grant support: in part by grant MA 5480, Medical Research Council of Canada; Clinical Research Grant 6-315, March of Dimes Defect Foundation; contract NO1-Hv1-21582, National Heart, Lung, and Blood Institute; and grant GRC-RR-52, General Clinical Research Centre, Program of the Division of Research Resources, National Institutes of Health. Dr. Sniderman is the Edwards Professor of Cardiology at McGill University.

    • ▸Requests for reprints should be addressed to Allan Sniderman, M.D.; Cardiovascular Research Unit, Room M4.14, Royal Victoria Hospital, 687 Pine Avenue West; Montreal, Quebec, Canada H3A 1A1.

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