Background: The presence of low attenuation noncalcified plaque (LANCP) and positive remodeling index (RI) are characteristic vessel changes in unstable coronary plaques. LANCP ( Click to show full abstract
Background: The presence of low attenuation noncalcified plaque (LANCP) and positive remodeling index (RI) are characteristic vessel changes in unstable coronary plaques. LANCP (<30 Hounsfield Units) contain necrotic cores that are characterized by endothelial dysfunction, oxidative stress, and inflammation. They have been shown to be a better predictor of future cardiovascular events compared to traditional cardiovascular risk factors in the general population. Coronary arterial remodeling describes changes of vessel size at the site of atherosclerotic lesions. Positive remodeling (expansion) of early lesions maintains lumen size despite plaque accumulation. This explains why these lesions might pass undetected by conventional angiography. Plaque rupture is often apparent at sites with only modest luminal stenoses but marked positive remodeling. Accelerated atherosclerosis leading to premature coronary artery disease remains the major cause of late death in SLE. Objectives: We sought to characterize LANCP and positive RI in patients with systemic lupus erythematosus. Methods: A total of 72 patients who met the ACR or SLICC classification criteria for SLE had CT angiogram studies, 30 of which had follow up CT angiograms. A total of 100 healthy controls who had two CT angiograms were included in the study. Each noncalcified plaque (NCP) detected within the vessel wall was evaluated for minimum CT density and vascular remodeling index. A LANCP was defined as an NCP with a density <30 Hounsfield units. Lesions with remodeling ⩾0% were considered to have positive RI. T-test was used to evaluate baseline characteristics between lupus patients and controls. Paired t-test or Wilcoxon signed ranks test was used to compare LANCP volume and RI between baseline and follow-up. Fisher’s exact test was used to evaluate the association between change in LANCP, RI, demographic and clinical variables. Results: Lupus patients had a significantly higher burden of LANCP at baseline compared to healthy controls in all age subgroups except in those >60 years of age. LANCP volume was associated with age (p<0.01) and body mass index (p<0.01). No significant differences were observed between RI in lupus and controls at baseline. Despite a significant progression of the total noncalcified plaque burden in lupus compared to controls (p<0.0001), the LANCP in lupus patients regressed (p<0.001). No demographic or clinical differences were observed between lupus patients whose LANCP progressed and those whose LANCP regressed. Lupus patients who were not treated with statins had a more significant regression of their LANCP burden (p<0.01) compared to controls who were on statins, while lupus patients who were taking statins had a significant progression (p<0.01). There were only 5 cardiovascular events in the studied group and there were no differences in remodeling index or low density noncalcified plaque observed but the number of events was small. Conclusion: Lupus patients have a significantly higher burden of LANCP at baseline compared to healthy controls in all age subgroups except in those >60 years of age. The LANCP burden regresses more rapidly over time in lupus compared to controls. Surprisingly, the most significant LANCP plaque volume regression was seen in lupus patients who were never treated with statins, while the most significant progression was observed in those taking statins. Positive RI was ubiquitous, with no evidence of progression or differences compared to controls. These characteristic vessel changes may identify SLE patients at need for more frequent noninvasive cardiac monitoring. Acknowledgement: The Hopkins Lupus Cohort is funded by NIH AR RO-1 43727 and RO-1 69572 Disclosure of Interests: George Stojan: None declared, Jessica Li: None declared, Laurence Magder: None declared, Matthew Budoff: None declared, Michelle A Petri Shareholder of: Pfizer, Merck, Grant/research support from: AstraZeneca, Exagen, Consultant for: Eli Lilly, GSK, Merck EMD Serono, Janssen, Amgen, Novartis, Quintiles, Exagen, Inova Diagnostics, AstraZeneca, Blackrock, Glenmark, UCB, and the Annenberg Center for Health Sciences
               
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