Open Access Research

Further evaluation of plasma sphingomyelin levels as a risk factor for coronary artery disease

Axel Schlitt13*, Stefan Blankenberg2, Daoguang Yan1, Hans von Gizycki1, Michael Buerke3, Karl Werdan3, Christoph Bickel2, Karl J Lackner2, Juergen Meyer2, Hans J Rupprecht2 and Xian-Cheng Jiang1

Author Affiliations

1 Department of Anatomy and Cell Biology and Scientific Computing Center, State University of New York, Downstate Medical Center, Brooklyn, USA

2 Department of Medicine II and Institute of Clinical Chemistry and Laboratory Medicine, Johannes Gutenberg-University Mainz, Germany

3 Department of Medicine III, Martin Luther-University, Halle-Wittenberg, Germany

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Nutrition & Metabolism 2006, 3:5  doi:10.1186/1743-7075-3-5

Published: 5 January 2006

Abstract

Background

Sphingomyelin (SM) is the major phospholipid in cell membranes and in lipoproteins. In human plasma, SM is mainly found in atherogenic lipoproteins; thus, high levels of SM may promote atherogenesis.

Methods

We investigated in a median follow up of 6.0 years the association of SM with the incidence of a combined endpoint (myocardial infarction and cardiovascular death) in stable and unstable patients, and its relation to other marker of atherosclerosis in 1,102 patients with angiographically documented CAD and 444 healthy controls.

Results and discussion

Logistic regression analysis showed that SM categorized by median was associated with an elevated risk for CAD (HR 3.2, 95%CI 2.5–4.0, p < 0.05). SM levels were correlated with apoB (r = 0.34) and triglyceride levels (r = 0.31). In patients with stable angina (n = 614), SM categorized by median was not related to incidence of a combined endpoint (cardiovascular death and myocardial infarction) (p = 0.844 by Log-rank test). However, in patients with acute coronary syndrome (n = 488), elevated SM was related to the combined endpoint (p < 0.05 by Log-rank test), also in a multivariate Cox regression analysis including potential confounders (HR 1.8, 95%CI 1.0–3.3, p < 0.05).

Conclusion

The results of our study reveal that 1) human plasma SM levels are a risk factor for CAD; 2) the pro-atherogenic property of plasma SM might be related to metabolism of apoB-containing or triglyceride-rich lipoproteins; and 3) plasma SM levels are a predictor for outcome of patients with acute coronary syndrome.