Plasma sphingomyelin level as a risk factor for coronary artery disease

Xian Cheng Jiang, Furcy Paultre, Thomas A. Pearson, Roberta G. Reed, Charles K. Francis, Min Lin, Lars Berglund, Alan R. Tall

Research output: Contribution to journalArticle

228 Citations (Scopus)

Abstract

Only a fraction of the clinical complications of atherosclerosis are explained by known risk factors. Animal studies have shown that plasma sphingomyelin (SM) levels are closely related to the development of atherosclerosis. SM carried into the arterial wall on atherogenic lipoproteins may be locally hydrolyzed by sphingomyelinase, promoting lipoprotein aggregation and macrophage foam cell formation. A novel, high-throughput, enzymatic method to measure plasma SM levels has been developed. Plasma SM levels were related to the presence of coronary artery disease (CAD) in a biethnic angiographic case-control study (279 cases and 277 controls). Plasma SM levels were higher in CAD patients than in control subjects (60±29 versus 49±21 mg/dL, respectively; P<0.0001). Moreover, the ratio of SM to SM+phosphatidylcholine (PC) was also significantly higher in cases than in controls (0.33±0.13 versus 0.29±0.10, respectively; P<0.0001). Similar relationships were observed in African Americans and whites. Plasma SM levels showed a significant correlation with remnant cholesterol levels (r=0.51, P<0.0001). By use of multivariate logistic regression analysis, plasma SM levels and the SM/(SM+PC) ratio were found to have independent predictive value for CAD after adjusting for other risk factors, including remnants. The odds ratio (OR) for CAD was significantly higher for the third and fourth quartiles of plasma SM levels (OR 2.81 [95% CI 1.66 to 4.80] and OR 2.33 [95% CI 1.38 to 3.92], respectively) as well as the SM/(SM+PC) ratio (OR 1.95 [95% CI 1.10 to 3.45] and OR 2.33 [95% CI 1.34 to 4.05], respectively). The findings indicate that human plasma SM levels are positively and independently related to CAD. Plasma SM levels could be a marker for atherogenic remnant lipoprotein accumulation and may predict lipoprotein susceptibility to arterial wall sphingomyelinase.

Original languageEnglish (US)
Pages (from-to)2614-2618
Number of pages5
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume20
Issue number12
StatePublished - 2000
Externally publishedYes

Fingerprint

Sphingomyelins
Coronary Artery Disease
Odds Ratio
Lipoproteins
Phosphatidylcholines
Sphingomyelin Phosphodiesterase
Atherosclerosis
Foam Cells
African Americans

Keywords

  • Coronary artery disease
  • Risk factors
  • Sphingomyelin

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Jiang, X. C., Paultre, F., Pearson, T. A., Reed, R. G., Francis, C. K., Lin, M., ... Tall, A. R. (2000). Plasma sphingomyelin level as a risk factor for coronary artery disease. Arteriosclerosis, Thrombosis, and Vascular Biology, 20(12), 2614-2618.

Plasma sphingomyelin level as a risk factor for coronary artery disease. / Jiang, Xian Cheng; Paultre, Furcy; Pearson, Thomas A.; Reed, Roberta G.; Francis, Charles K.; Lin, Min; Berglund, Lars; Tall, Alan R.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 20, No. 12, 2000, p. 2614-2618.

Research output: Contribution to journalArticle

Jiang, XC, Paultre, F, Pearson, TA, Reed, RG, Francis, CK, Lin, M, Berglund, L & Tall, AR 2000, 'Plasma sphingomyelin level as a risk factor for coronary artery disease', Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 20, no. 12, pp. 2614-2618.
Jiang XC, Paultre F, Pearson TA, Reed RG, Francis CK, Lin M et al. Plasma sphingomyelin level as a risk factor for coronary artery disease. Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20(12):2614-2618.
Jiang, Xian Cheng ; Paultre, Furcy ; Pearson, Thomas A. ; Reed, Roberta G. ; Francis, Charles K. ; Lin, Min ; Berglund, Lars ; Tall, Alan R. / Plasma sphingomyelin level as a risk factor for coronary artery disease. In: Arteriosclerosis, Thrombosis, and Vascular Biology. 2000 ; Vol. 20, No. 12. pp. 2614-2618.
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abstract = "Only a fraction of the clinical complications of atherosclerosis are explained by known risk factors. Animal studies have shown that plasma sphingomyelin (SM) levels are closely related to the development of atherosclerosis. SM carried into the arterial wall on atherogenic lipoproteins may be locally hydrolyzed by sphingomyelinase, promoting lipoprotein aggregation and macrophage foam cell formation. A novel, high-throughput, enzymatic method to measure plasma SM levels has been developed. Plasma SM levels were related to the presence of coronary artery disease (CAD) in a biethnic angiographic case-control study (279 cases and 277 controls). Plasma SM levels were higher in CAD patients than in control subjects (60±29 versus 49±21 mg/dL, respectively; P<0.0001). Moreover, the ratio of SM to SM+phosphatidylcholine (PC) was also significantly higher in cases than in controls (0.33±0.13 versus 0.29±0.10, respectively; P<0.0001). Similar relationships were observed in African Americans and whites. Plasma SM levels showed a significant correlation with remnant cholesterol levels (r=0.51, P<0.0001). By use of multivariate logistic regression analysis, plasma SM levels and the SM/(SM+PC) ratio were found to have independent predictive value for CAD after adjusting for other risk factors, including remnants. The odds ratio (OR) for CAD was significantly higher for the third and fourth quartiles of plasma SM levels (OR 2.81 [95{\%} CI 1.66 to 4.80] and OR 2.33 [95{\%} CI 1.38 to 3.92], respectively) as well as the SM/(SM+PC) ratio (OR 1.95 [95{\%} CI 1.10 to 3.45] and OR 2.33 [95{\%} CI 1.34 to 4.05], respectively). The findings indicate that human plasma SM levels are positively and independently related to CAD. Plasma SM levels could be a marker for atherogenic remnant lipoprotein accumulation and may predict lipoprotein susceptibility to arterial wall sphingomyelinase.",
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