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      Associations of lipoprotein cholesterols, apolipoproteins A-I and B, and triglycerides with carotid atherosclerosis and coronary heart disease. The Atherosclerosis Risk in Communities (ARIC) Study.

      Arteriosclerosis and thrombosis : a journal of vascular biology / American Heart Association
      Apolipoprotein A-I, analysis, Apolipoproteins B, Arteriosclerosis, blood, etiology, Carotid Artery Diseases, Cholesterol, Coronary Artery Disease, Female, Humans, Linear Models, Male, Middle Aged, Prospective Studies, Risk Factors, Triglycerides

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          Abstract

          Previous research shows generally greater proportional elevation in apolipoprotein B (apoB) levels than in low-density lipoprotein cholesterol (LDL-C) in coronary heart disease (CHD) case subjects compared with control subjects. The Atherosclerosis Risk in Communities study provided general populations of 7261 men and women free of cardiovascular symptoms for evaluating the associations between intima-media thickening in extracranial carotid arteries measured using ultrasound imaging and fasting plasma LDL-C, high-density lipoprotein cholesterol (HDL-C), apoB, apolipoprotein A-I (apoA-I), triglycerides, and HDL density subfractions. A CHD group was selected for comparison. Lipid factors show approximately linear associations with carotid thickness: positive for LDL-C and plasma apoB and negative for HDL-C and apoA-I levels. Apolipoproteins and HDL density subfractions did not contribute to the association after accounting for LDL-C and HDL-C. Compared with control subjects, persons whose carotid thickness exceeded 0.9 mm had greater proportional elevations in LDL-C than in apoB, whereas HDL-C reductions were small. CHD case subjects showed greater proportional elevations of apoB than LDL-C. Although the lipid profiles associated with asymptomatic carotid wall thickening and stenotic coronary disease are similar, the differences found suggest that LDL-C is the most important lipid factor in earlier stages of atherogenesis, whereas the metabolism of triglyceride-rich lipoproteins and its effects on LDL and HDL may be more relevant to later atherothrombotic processes.

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