Background Traditional cardiac risk factors (CRFs) are associated with cardiovascular outcomes in both Rheumatoid arthritis (RA) and the general population. Their distribution in RA approximates that in controls. However, their relative impact on cardiovascular outcomes in this disease may be different in view of the high inflammatory burden present. Subclinical atherogenesis has been associated with accelerated risk of future clinical events. However, the role of individual CRFs on coronary plaque characteristics in CAD-naïve subjects with RA is unknown.
Objectives To evaluate the impact of classic CRFs and their interactions on coronary plaque prevalence and burden in CAD-naïve subjects with RA compared to controls.
Methods One hundred and fifty RA subjects and an equal number of age and sex-matched controls underwent non-invasive coronary plaque evaluation with computed tomography angiography (CTA); this imaging modality reliably evaluates plaque presence, burden, and defines its composition as non-calcified, mixed, or densely calcified. A 15-segment American Heart Association model was used for plaque evaluation; 2250 segments were assessed respectively in RA and controls. Proportions of affected segments, segment involvement scores (SIS, number of affected segments out of 15 evaluated/patient) and plaque burden scores (PBS, sum of the plaque amount per each segment averaged over all 15 segments/patient) were evaluated. CRFs were defined by National Cholesterol Education Program (NCEP-ATPIII) criteria. Differences between groups were evaluated by non parametric and Fisher’s exact tests.
Results CRFs were evenly distributed (p>0.5), except for hyperlipidemia and family history (FHx) of CAD that was higher in controls (p<0.0001 for both). Female gender was not protective in RA as in controls (OR=1.17, p=0.8 vs. 0.33, p=0.04). Current smoking did not render a higher coronary plaque risk in RA vs. controls (OR=1.5, p=0.26 vs. 2.3, p=0.2). The impact of other individual CRFs and their interactions on plaque prevalence appears in table 1. Hypertension (HTN) or diabetes (DM) alone, and their interaction, had a higher impact on plaque presence in RA vs. controls (p<0.0001, 0.0025, and <0.0001 respectively). The interaction of HTN with hyperlipidemia also associated with higher plaque in RA (p=0.01). Additionally, HTN, and its interaction with DM or hyperlipidemia associated with higher SIS and PBS in RA compared to controls (p=0.0002, 0.0004, and 0.007 for SIS and p<0.0001, 0.0002, and 0.003 for PBS respectively- not shown).
Conclusions HTN, diabetes, hyperlipidemia and their interactions associate with a higher proportion of affected coronary segments and plaque burden in RA compared to controls, while smoking alone is not. Female gender is not protective against such plaque in RA.
Disclosure of Interest None Declared