Anti-endothelial cell antibodies in rheumatic heart disease

V Scalzi1, H Abu Hadi, C Alessandri

  • 1Dipartimento di Clinica e Terapia Medica, Sapienza Università di Roma, Roma, Italy.

Insights

Yemeni rheumatic heart disease (RHD) patients show higher anti-endothelial cell antibodies (AECA) and lower mannose-binding lectin (MBL) levels. AECA correlate with disease severity, suggesting a role in RHD pathogenesis.

Area of Science:

  • Immunology
  • Cardiology
  • Rheumatology

Background:

  • Rheumatic heart disease (RHD) is a significant cause of valvular damage worldwide.
  • The immunological underpinnings of RHD pathogenesis require further elucidation.
  • Autoantibodies and complement factors may play a role in the progression of RHD.

Purpose of the Study:

  • To investigate the prevalence of anti-endothelial cell antibodies (AECA), anti-cardiolipin antibodies (aCL), and serum mannose-binding lectin (MBL) in Yemeni RHD patients.
  • To correlate these immunological markers with clinical and echocardiographic features of RHD.
  • To explore the potential pathogenic role of AECA in RHD.

Main Methods:

  • A cohort of 140 Yemeni RHD patients and 140 healthy controls were recruited.
  • Serum levels of AECA, aCL, and MBL were quantified using solid-phase enzyme-linked immunosorbent assays (ELISAs).
  • Echocardiography was performed to assess RHD severity, including aortic stenosis.

Main Results:

  • Forty percent of RHD patients were positive for AECA, while only 7.8% were positive for aCL.
  • Serum MBL levels were significantly lower in RHD patients compared to healthy controls (median 4221 ng/ml vs. 5166 ng/ml).
  • AECA titres showed a positive correlation with patient age, RHD duration, and aortic stenosis severity.

Conclusions:

  • AECA may be involved in the pathogenesis of RHD, potentially linking endothelial activation to valvular damage.
  • Lower MBL levels in RHD patients suggest a possible role for complement dysregulation.
  • These findings highlight the potential of AECA as biomarkers and therapeutic targets in RHD.

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