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Contrast enhancement imaging in coronary arteries in patients with systemic lupus erythematosus
© Puntmann et al; licensee BioMed Central Ltd. 2012
Published: 1 February 2012
Patients with SLE suffer from accelerated atherosclerosis due to systemic inflammation. We examined subclinical coronary artery involvement in patients with systemic lupus erythematous (SLE) by contrast enhanced inversion recovery (CE-IR) coronary magnetic resonance imaging.
Vessel wall inflammation plays a key role in the initiation and progression of atherosclerosis, from endothelial injury to remodeling and plaque formation. Cardiovascular (CV) magnetic resonance (CMR) provides noninvasive visualization and characterization of arterial remodeling both in the great vessels, and also the coronary arteries. Contrast-enhanced inversion-recovery (CE-IR) prepared coronary imaging allows detection of vessel wall enhancement by visualization of contrast agent uptake. We examined subclinical coronary artery involvement in patients with systemic lupus erythematous (SLE) by contrast enhanced inversion recovery (CE-IR) coronary magnetic resonance imaging.
In 19 SLE patients in stable remission (male, n=4), we performed CE-IR magnetic resonance coronary imaging 40 minutes after administration of gadolinium contrast agents. Contrast-to-noise ratio (CNR) within the coronary artery and ascending aortic vessel wall was quantified and compared to age and gender-matched apparently healthy controls (n=9).
Results. There was a significant increase in mean coronary CNR in SLE patients (SLE vs. controls: 7.7±2 vs. 3.9±0.9, p<0.01). CNR within aortic wall was significantly raised in the SLE group (11.2±2.4 vs. 6.8± 1.9, p=0.008). In SLE patients, coronary CNR correlated with history of antiphospholipid syndrome (APS) (r=0.73, p=0.003), duration of disease (r=0.63, p=0.04) and ESR (r=0.54, p=0.04). In the SLE group, multivariate linear regression identified APS as independent predictor of coronary CNR (R2=0.26, F=11.2, p<0.001), whereas systolic blood pressure showed association with aortic CNR (R2=0.23 F=5.4, p=0.01). ROC analysis to discriminate healthy controls from the SLE group by increased coronary CNR revealed an optimal cut-off of 5.2 with 100% sensitivity and specificity.
Our study for the first time demonstrates subclinical coronary artery involvement in patients with SLE and history of systemic inflammation. These findings are associated with markers of inflammation, more aggressive subtype and duration of disease, but are independent of traditional CV risk factors.
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