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Interaction between soluble thrombomodulin and intercellular adhesion molecule-1 in predicting risk of coronary heart

Kenneth K Wu1, Nena Aleksic, Christie M Ballantyne

  • 1Vascular Biology Research Center and Department of Internal Medicine, University of Texas-Houston Health Science Center, Houston, Tex, USA. Kenneth.K.Wu@uth.tmc.edu

Circulation
|April 2, 2003
PubMed

Insights

High soluble intercellular adhesion molecule-1 (sICAM) increases coronary heart disease (CHD) risk, while high soluble thrombomodulin (sTM) decreases it. Their interaction significantly impacts CHD risk, particularly when sTM is low and sICAM is high.

Area of Science:

  • Cardiovascular Disease Epidemiology
  • Biomarker Research
  • Atherosclerosis Risk Factors

Background:

  • Previous Atherosclerosis Risk In Communities (ARIC) studies show opposing associations of soluble intercellular adhesion molecule-1 (sICAM) and soluble thrombomodulin (sTM) with coronary heart disease (CHD) risk.
  • Elevated sICAM correlates with increased CHD risk, while elevated sTM is linked to decreased CHD risk.
  • The potential interaction between sICAM and sTM in modulating CHD risk remained unexplored.

Purpose of the Study:

  • To investigate the interaction between sICAM and sTM levels in predicting the risk of incident coronary heart disease (CHD).
  • To quantify the combined effect of sICAM and sTM on CHD risk within the ARIC cohort.

Main Methods:

  • A nested case-cohort design was employed using data from the ARIC study.
  • Soluble thrombomodulin (sTM) and soluble intercellular adhesion molecule-1 (sICAM) levels were measured in 317 incident CHD cases and 726 non-cases.
  • Weighted Cox proportional hazard regression models were used to assess the interaction between sTM and sICAM and their impact on CHD risk.

Main Results:

  • Consistent with prior findings, high sICAM (upper tertile) approximately doubled CHD risk (95% CI, 1.46-2.87), while low sTM (lower tertile) approximately quadrupled CHD risk (95% CI, 2.80-5.74).
  • A statistically significant interaction (P=0.038) was observed between sTM and sICAM in predicting CHD risk.
  • Combinatorial analysis revealed a substantially elevated CHD risk ratio (RR=4.66, 95% CI, 1.89-11.46) for the group with low sTM and high sICAM compared to the group with high sTM and low sICAM.
  • Individuals with high sTM exhibited a risk ratio below 1, even with high sICAM levels, indicating a protective effect of high sTM.

Conclusions:

  • A significant interaction exists between sTM and sICAM in the prediction of CHD events.
  • Elevated sICAM confers a significantly increased risk of CHD only when sTM levels are low.
  • High sTM appears to mitigate the increased CHD risk associated with high sICAM.
Abstract

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