THU0057 Differential impact of traditional cardiac risk factors on coronary plaque prevalence in coronary artery disease (CAD)-naïve subjects with rheumatoid arthritis compared to controls:

2013 ◽  
Vol 71 (Suppl 3) ◽  
pp. 172.1-172
Author(s):  
G.A. Karpouzas ◽  
J. Malpeso ◽  
T.-Y. Choi ◽  
S. Munoz ◽  
M. Budoff
2007 ◽  
Vol 1108 (1) ◽  
pp. 466-474 ◽  
Author(s):  
T. P. GRECO ◽  
A. M. CONTI-KELLY ◽  
E. MATSUURA ◽  
T. GRECO ◽  
K. J. DIER ◽  
...  

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Youssef A Elnabawi ◽  
Amit K Dey ◽  
Agastya D Belur ◽  
Aditya Goyal ◽  
Jacob W Groenendyk ◽  
...  

Introduction: Serum uric acid (sUA), a known inflammosome-inducer, is associated with prospective risk of coronary artery disease in a dose-dependent fashion. Psoriasis (PSO), a chronic inflammatory disease associated with elevated burden of systemic inflammation and subclinical coronary artery disease, provides a reliable human model to study how sUA may relate to non-calcified coronary plaque burden (NCB) measured by computed coronary tomography angiography (CCTA). Hypothesis: We hypothesized that sUA would directly associate with NCB beyond traditional cardiovascular (CV) risk factors. Methods: 103 consecutive PSO patients and 47 healthy volunteers (HV) underwent CCTA (320 detector row, Toshiba) for coronary plaque burden quantification using QAngio (Medis). PSO severity was assessed by Psoriasis Area Severity Score (PASI) and divided into severe PSO (PASI>10) and mild-moderate PSO (PASI<10). All patients had fasting blood draws for the measurement of sUA at a certified clinical lab. Results: PSO patients were older than HV and had a higher CV risk by Framingham risk score (FRS) (Table 1). We observed a significant trend towards increase in sUA among severe PSO, mild-moderate PSO, and HV groups (mean 6.4, 5.9, 5.4 respectively, p=0.02 for trend). A positive association was observed between sUA and NCB, which was stronger in severe PSO after adjustment for traditional CV risk, alcohol, statins, and systemic/biologic PSO treatment (Severe PSO: β=0.27, p<0.001; Mild-moderate PSO: β=0.18, p=0.03), not significant in HV (β=0.18, p=0.12). Conclusions: sUA is independently associated with NCB in states of chronic inflammation such as PSO, and as such, may potentially serve as a biomarker for subclinical coronary atherosclerosis. However, larger prospective studies of CV outcomes in chronic inflammatory diseases are needed to confirm these results.


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