OBJECTIVE: To assess the relationship of lipoprotein subfractions to coronary heart disease (CHD). METHODS: Prospective 29.1-year follow-up of 1905 men measured for lipoprotein mass concentrations by analytic ultracentrifugation between 1954 and 1957. Vital status was determined for 97.2% of the cohort. Blinded physician medical record and death certificate review confirmed 179 CHD deaths. Follow-up questionnaires identified 182 nonfatal myocardial infarctions and 93 revascularization procedures from 1346 (98.3%) of the surviving cohort and from the next-of-kin of 153 men who died. RESULTS: When adjusted for age, total incident CHD was inversely related to HDL2-mass (P=0.0001) and HDL3-mass (P=0.02), and concordantly related to LDL-mass (P<10(-11)), IDL-mass (P<10(-7)), and small (P<10(-7)) and large VLDL-mass concentrations (P=0.003). The hazard reduction per mg/dl of HDL was greater for HDL2-mass than HDL3-mass (P=0.04). The lowest quartiles of both HDL2-mass (P=0.007) and HDL3-mass (P=0.001) independently predicted total incident CHD when adjusted for traditional risk factors. Risk for premature CHD (≤65 years old) was significantly greater in men within the lowest HDL2 (P=0.03) and HDL3 quartiles (P=0.04) and having higher LDL-mass concentrations (P=0.001). Serum cholesterol's relationship to incident CHD (P<10(-8)) was accounted for by adjustment for LDL-mass concentrations (adjusted P=0.90). CONCLUSIONS: Lipoprotein subfractions differ in their relationship to CHD. Published by Elsevier Ireland Ltd.
OBJECTIVE: To assess the relationship of lipoprotein subfractions to coronary heart disease (CHD). METHODS: Prospective 29.1-year follow-up of 1905 men measured for lipoprotein mass concentrations by analytic ultracentrifugation between 1954 and 1957. Vital status was determined for 97.2% of the cohort. Blinded physician medical record and death certificate review confirmed 179 CHD deaths. Follow-up questionnaires identified 182 nonfatal myocardial infarctions and 93 revascularization procedures from 1346 (98.3%) of the surviving cohort and from the next-of-kin of 153 men who died. RESULTS: When adjusted for age, total incident CHD was inversely related to HDL2-mass (P=0.0001) and HDL3-mass (P=0.02), and concordantly related to LDL-mass (P<10(-11)), IDL-mass (P<10(-7)), and small (P<10(-7)) and large VLDL-mass concentrations (P=0.003). The hazard reduction per mg/dl of HDL was greater for HDL2-mass than HDL3-mass (P=0.04). The lowest quartiles of both HDL2-mass (P=0.007) and HDL3-mass (P=0.001) independently predicted total incident CHD when adjusted for traditional risk factors. Risk for premature CHD (≤65 years old) was significantly greater in men within the lowest HDL2 (P=0.03) and HDL3 quartiles (P=0.04) and having higher LDL-mass concentrations (P=0.001). Serum cholesterol's relationship to incident CHD (P<10(-8)) was accounted for by adjustment for LDL-mass concentrations (adjusted P=0.90). CONCLUSIONS: Lipoprotein subfractions differ in their relationship to CHD. Published by Elsevier Ireland Ltd.
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