Plasma sphingomyelin in subclinical atherosclerosis: findings from the multi-ethic study of atherosclerosis

Abstract

Conclusion: Plasma sphingomyelin is a component of the biologic pathway mediating risk for subclinical atherosclerosis that is normally attributable to standard cardiovascular risk factors. Summary: Plasma sphingomyelin is an independent risk factor for coronary heart disease. In this study, the authors sought to determine the relation of plasma sphingomyelin to subclinical atherosclerotic disease. The relationship between plasma sphingomyelin and three different measurements of subclinical cardiovascular disease (ankle and arm blood pressure index, carotid intimal-medial thickness, and Agatston coronary artery and calcium score) were assessed. Study subjects included 6814 asymptomatic middle-aged adults from a multiethnic study of atherosclerosis first initiated in 2000. Plasma sphingomyelin levels correlated positively with lipid levels and the Framingham risk score (P < .01 for both). The mean level of plasma sphingomyelin was higher in women than men (50 ± 16 mg/dL vs 45 ± 15 mg/dL, P < .01). Plasma sphingomyelin levels were higher in never (49±16 mg/dL) vs current smokers (45±17 mg/dL, P < .01). Levels of subclinical vascular disease as assessed by all three measures were higher in women with sphingomyelin levels of ≥60 mg/dL than in women with sphingomyelin levels of <39 mg/dL. This association did not remain significant after multivariant adjustment for standard cardiovascular risk factors. Men with sphingomyelin levels of >60 mg/dL had higher calcium scores (135 vs 99 Agatston units, P = .01) than men with sphingomyelin levels <39 mg/dL. Comment: Sphingomyelin accumulates in atheromas in animal models and in human atheroma. Much sphingomyelin found in arteries arises from synthesis within the arterial tissue (Circulation 1961;23:370-5). However, synthesis of sphingomyelin within arterial tissue appears slow compared with the total amount accumulated, suggesting plasma levels of sphingomyelin may also contribute to accumulation of sphingomyelin within arterial tissue. The unadjusted data from this study provide some support that plasma sphingomyelin is a component of a pathway that mediates risk for subclinical disease attributable to traditional cardiovascular risk factors.