Rheumatoid arthritis is an independent risk factor for multi-vessel coronary artery disease: a case control study

Kenneth J Warrington1, Peter D Kent, Robert L Frye

  • 1Division of Rheumatology, Mayo Clinic, Rochester, MN, USA. kwarring@utmem.edu

Insights

Patients with rheumatoid arthritis (RA) have a higher risk of multi-vessel coronary artery disease (CAD). While overall cardiovascular event rates were similar, elevated pro-inflammatory T cells suggest a role in atherosclerosis progression.

Area of Science:

  • Cardiology
  • Rheumatology
  • Immunology

Background:

  • Rheumatoid arthritis (RA) is associated with increased cardiovascular (CV) disease risk.
  • Data on coronary atherosclerosis burden in RA patients are limited.
  • Pro-inflammatory CD4+CD28null T cells are implicated in both RA and coronary artery disease (CAD) pathogenesis.

Purpose of the Study:

  • To investigate the prevalence and extent of coronary atherosclerosis in RA patients.
  • To compare CV risk factors and outcomes between RA patients and controls with newly diagnosed CAD.
  • To explore the association of CD4+CD28null T cells with CAD in RA patients.

Main Methods:

  • Retrospective case-control study of RA patients with new-onset CAD versus matched controls with CAD.
  • Analysis of angiographic scores, CV risk factors, and CV events from chart data.
  • Flow cytometry measurement of CD4+CD28null T cells in a nested cohort.

Main Results:

  • RA patients were more likely to have multi-vessel coronary involvement at initial angiography (P = 0.002).
  • CV risk factors did not significantly differ between RA patients and controls.
  • CD4+CD28null T cell levels were significantly higher in RA patients with CAD compared to controls with stable angina (P = 0.001).

Conclusions:

  • Rheumatoid arthritis patients face an elevated risk of multi-vessel coronary artery disease.
  • While overall CV event rates were similar, increased CD4+CD28null T cells may drive atherosclerosis progression in RA.
  • Further research is needed to clarify the CV event risk and therapeutic targets in RA.

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