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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

Published on: November 1, 2015

Novel cardiovascular risk prediction models in patients with systemic lupus erythematosus

V K Kawai1, J F Solus, A Oeser

  • 1Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, USA.

Lupus
|October 7, 2011
PubMed

Insights

New risk scores incorporating coronary artery calcium (CAC) show promise for identifying coronary heart disease (CHD) risk in women with systemic lupus erythematosus (SLE). These scores may better predict risk than traditional methods, especially when subclinical atherosclerosis is present.

Area of Science:

  • Cardiology
  • Rheumatology
  • Preventive Medicine

Background:

  • Women with systemic lupus erythematosus (SLE) face a higher risk of coronary heart disease (CHD) than the general population.
  • Traditional risk scores like the Framingham risk score (FRS) often underestimate CHD risk in SLE patients.
  • Subclinical coronary atherosclerosis, detectable via coronary artery calcium (CAC) scoring, is prevalent in SLE.

Purpose of the Study:

  • To evaluate if novel risk scores, incorporating inflammation or vascular age (derived from CAC), improve CHD risk prediction in women with SLE.
  • To compare the performance of conventional risk scores (FRS, Reynolds risk score - RRS) with coronary age-modified scores (camFRS, camRRS) in SLE patients.
  • To assess risk score differences between SLE patients and controls, and within SLE patients based on the presence or absence of CAC.

Main Methods:

  • Calculated FRS and RRS for 121 women with SLE and 65 age-matched female controls.
  • Derived coronary age from CAC scores to compute coronary age-modified FRS (camFRS) and RRS (camRRS).
  • Compared risk scores between SLE and control groups, and between SLE patients with and without CAC.

Main Results:

  • CAC was found in 17% of SLE patients versus 6% of controls (p=0.033).
  • FRS, camFRS, RRS, and camRRS did not differ significantly between SLE and control groups (p>0.05).
  • All calculated risk scores were significantly higher in SLE patients with CAC compared to those without (p<0.001).
  • camFRS identified significantly more SLE patients (8%) as having ≥10% risk compared to FRS (1%) and RRS (2%) (p=0.016).
  • RRS showed limited utility, but coronary age modification improved CHD risk prediction in SLE.

Conclusions:

  • Conventional risk scores underestimate CHD risk in women with SLE, particularly those with subclinical atherosclerosis.
  • Coronary age-modified risk scores, especially camFRS, demonstrate potential for improved CHD risk stratification in SLE patients.
  • Further research into incorporating vascular age and inflammatory markers may enhance cardiovascular risk assessment in SLE.

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