Literature DB >> 16611667

Plasma sphingomyelin and subclinical atherosclerosis: findings from the multi-ethnic study of atherosclerosis.

Jennifer Clark Nelson1, Xian-Cheng Jiang, Ira Tabas, Alan Tall, Steven Shea.   

Abstract

Plasma sphingomyelin has been shown to be an independent risk factor for coronary heart disease, but the relation of plasma sphingomyelin to earlier, subclinical atherosclerotic disease has not been reported. The authors examined the association between plasma sphingomyelin and three measures of subclinical cardiovascular disease (carotid intimal-medial wall thickness, ankle-arm blood pressure index, and Agatston coronary artery calcium score) among 6,814 middle-aged, asymptomatic adults in the Multi-Ethnic Study of Atherosclerosis, which was initiated in 2000. The sphingomyelin level was positively correlated with lipids and the Framingham risk score (p < 0.01 for both), and the mean level was higher in women than men (50 (standard deviation (SD), 16) vs. 45 (SD, 15) mg/dl) (p < 0.01) and higher in never versus current smokers (49 (SD, 16) vs. 45 (SD, 17) mg/dl) (p < 0.01). Women with sphingomyelin levels of 60 or more mg/dl had more severe subclinical disease by all three measures than did the referent group with sphingomyelin levels of 39 or less mg/dl, although associations were not significant after multivariate adjustment for standard cardiovascular disease risk factors. Men with sphingomyelin levels of 60 or more mg/dl versus those with sphingomyelin levels of 39 or less mg/dl had higher calcium scores (135 vs. 99 Agatston units) (p = 0.01). These observations are consistent with the hypothesis that plasma sphingomyelin is in the biologic pathway that mediates the risk for subclinical disease attributable to standard cardiovascular disease risk factors.

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Year:  2006        PMID: 16611667     DOI: 10.1093/aje/kwj140

Source DB:  PubMed          Journal:  Am J Epidemiol        ISSN: 0002-9262            Impact factor:   4.897


  62 in total

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Review 9.  Sphingolipids, insulin resistance, and metabolic disease: new insights from in vivo manipulation of sphingolipid metabolism.

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