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Reducing inflammation in rheumatoid arthritis (RA) did not improve myocardial flow reserve (MFR), a measure of cardiovascular risk. However, reduced interleukin-1b correlated with less subclinical myocardial injury.

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Area of Science:

  • Cardiology
  • Rheumatology
  • Immunology

Background:

  • Coronary microvascular dysfunction (CMD), measured by myocardial flow reserve (MFR), is linked to higher cardiovascular risk in rheumatoid arthritis (RA).
  • Tumor necrosis factor inhibitors are used to treat active RA, but their effect on cardiovascular risk markers is not fully understood.

Purpose of the Study:

  • To assess if reducing inflammation with tumor necrosis factor inhibitors improves MFR in RA patients.
  • To determine the association between anti-inflammatory treatment and other cardiovascular risk indicators.

Main Methods:

  • 66 RA patients initiating tumor necrosis factor inhibitors underwent cardiac perfusion positron emission tomography scans to measure MFR at baseline and 24 weeks.
  • Inflammatory markers, including hsCRP, IL-1b, and hs-cTnT, were measured at baseline and 24 weeks.
  • Coronary microvascular dysfunction was defined as MFR <2.5 without obstructive coronary artery disease.

Main Results:

  • Nearly 50% of RA patients had coronary microvascular dysfunction at baseline.
  • No significant change in mean MFR or hs-cTnT was observed after 24 weeks of tumor necrosis factor inhibitor treatment.
  • A reduction in hsCRP and IL-1b correlated with a decrease in hs-cTnT, indicating reduced subclinical myocardial injury.

Conclusions:

  • In this RA cohort, anti-inflammatory treatment did not improve MFR, despite a high prevalence of coronary microvascular dysfunction.
  • Reduced IL-1b levels, but not other inflammatory markers, were associated with decreased subclinical myocardial injury.