Written by Joyce Smith, BS. This study reveals several novel findings regarding the progression of plaque and coronary atherosclerosis (CA) in people with rheumatoid arthritis (RA) that could have substantial clinical and research implications.
Rheumatoid arthritis is a chronic progressive autoimmune disease causing inflammation in the joints and resulting in painful deformity and immobility, especially in the fingers, wrists, feet, and ankles. Individuals with rheumatoid arthritis have a higher rate of cardiovascular events than the general population 1. In a 2014 study by Karpouzas et al, coronary plaque in RA participants was found to be more prevalent and severe, and imposed a greater societal burden than in the control group of age and gender matched individuals who had no autoimmune disease 2. There is evidence in autoimmune disease-free men and women that atherosclerosis, as seen on coronary computed tomography angiography (ACTA), is an independent predictor of acute coronary syndrome 3,4, yet when plaque size is stabilized, the risk of future cardiovascular events (CVEs) is decreased 5. However, changes in coronary plaque load and composition have yet to be determined in individuals with RA.
The objective of this study 6 was to examine the incidence and progression of CA in patients with rheumatoid arthritis and to evaluate the impact and interactions on their coronary plaque progression with respect to inflammation, cardiac risk factors and length of medication use. Researchers hypothesized that higher cumulative inflammation might be associated with greater coronary plaque formation and that longer exposure to RA-specific medications such as glucocorticoids and disease-modifying antirheumatic drugs (DMARDs) might inhibit plaque growth or composition.
One hundred and one participants who had undergone baseline coronary computed tomography angiography had follow up assessments approximately seven months later. The accumulation of plaque and changes in plaque composition were assessed. Plaque composition was defined as non-calcified (NCP), mixed (MP), or calcified plaque (CP).
Seventy patients (69%) had coronary plaque at baseline. After a seven-month follow up, researchers found that plaque had increased in 48% of all patients, and that plaque progression was related to older age, greater obesity, higher cumulative inflammation, and hypertension (P<0.05). They found that inflammation was independent of plaque progression in people with RA. Overall, total plaque burden and coronary calcification scores increased (P<0.012). Nine patients had NCP progression, 21 had MP progression and 35 had CP increase.
Longer exposure to biologics such as DMARDs was associated with a decreased probability of NCP progression. These drugs helped prevent the maturation and remodeling of NCPs and lowered their risk of progressing to CAC in patients without baseline calcification and the effect was achieved independent of inflammation, and prednisone or statin use (P< 0.05 for all). Longer statin treatment further restricted NCP progression and reduced the effect of inflammation on total plaque and CAC increase (P<0.05). Maintaining strict systolic blood pressure control further reduced the effect of inflammation on total plaque progression.
Overall, findings point to inflammation as a consistent and independent predictor of coronary atherosclerotic disease progression in RA and should, therefore, be specifically targeted as a means of reducing cardiovascular risk. The use of BDMARDs and statins and the maintenance of blood pressure control in RA individuals may also directly or indirectly inhibit plaque formation.
Source: Karpouzas, George A., Sarah R. Ormseth, Elizabeth Hernandez, and Matthew J. Budoff. “Impact of cumulative inflammation, cardiac risk factors and medication exposure on coronary atherosclerosis progression in rheumatoid arthritis.” Arthritis & Rheumatology (2019).
Posted April 29, 2020.
Joyce Smith, BS, is a degreed laboratory technologist. She received her bachelor of arts with a major in Chemistry and a minor in Biology from the University of Saskatchewan and her internship through the University of Saskatchewan College of Medicine and the Royal University Hospital in Saskatoon, Saskatchewan. She currently resides in Bloomingdale, IL.
References:
- Naranjo A, Sokka T, Descalzo MA, et al. Cardiovascular disease in patients with rheumatoid arthritis: results from the QUEST-RA study. Arthritis Res Ther. 2008;10(2):R30.
- Karpouzas GA, Malpeso J, Choi TY, Li D, Munoz S, Budoff MJ. Prevalence, extent and composition of coronary plaque in patients with rheumatoid arthritis without symptoms or prior diagnosis of coronary artery disease. Ann Rheum Dis. 2014;73(10):1797-1804.
- Motoyama S, Ito H, Sarai M, et al. Plaque Characterization by Coronary Computed Tomography Angiography and the Likelihood of Acute Coronary Events in Mid-Term Follow-Up. J Am Coll Cardiol. 2015;66(4):337-346.
- Gu H, Gao Y, Wang H, et al. Sex differences in coronary atherosclerosis progression and major adverse cardiac events in patients with suspected coronary artery disease. Journal of cardiovascular computed tomography. 2017;11(5):367-372.
- Inoue K, Motoyama S, Sarai M, et al. Serial coronary CT angiography-verified changes in plaque characteristics as an end point: evaluation of effect of statin intervention. JACC Cardiovascular imaging. 2010;3(7):691-698.
- Karpouzas GA, Ormseth SR, Hernandez E, Budoff MJ. Impact of Cumulative Inflammation, Cardiac Risk Factors, and Medication Exposure on Coronary Atherosclerosis Progression in Rheumatoid Arthritis. Arthritis & rheumatology (Hoboken, NJ). 2020;72(3):400-408.
