Cardiovascular and cerebrovascular diseases in ankylosing spondylitis: current insights

Michael T Nurmohamed1, Irene van der Horst-Bruinsma, Walter P Maksymowych

  • 1Department of Internal Medicine, VU University Medical Centre, PO Box 7057, Amsterdam, The Netherlands. mt.nurmohamed@vumc.nl

Insights

Ankylosing spondylitis patients face higher cardiovascular risk due to inflammation and traditional factors. Managing this risk requires addressing both inflammation and traditional risk factors for better patient outcomes.

Area of Science:

  • Rheumatology
  • Cardiology
  • Immunology

Background:

  • Ankylosing spondylitis (AS) is associated with elevated cardiovascular (CV) risk.
  • Evidence strongly suggests increased atherosclerotic disease in AS patients.
  • The exact role of AS-specific cardiac issues in this heightened CV risk requires further investigation.

Purpose of the Study:

  • To explore the contributing factors to increased cardiovascular risk in ankylosing spondylitis.
  • To investigate the interplay between chronic inflammation, traditional CV risk factors, and AS-related cardiac manifestations.
  • To inform clinical practice regarding CV risk management strategies for AS patients.

Main Methods:

  • Review of current evidence on cardiovascular risk in ankylosing spondylitis.
  • Analysis of the contribution of traditional cardiovascular risk factors.
  • Evaluation of the role of chronic inflammation and AS-specific cardiac manifestations.

Main Results:

  • Both traditional CV risk factors and the chronic inflammatory process significantly contribute to atherosclerotic risk in AS.
  • Emerging evidence points to inflammation as a key etiological factor in AS-related cardiac issues.
  • The precise impact of AS-specific cardiac manifestations on overall CV risk needs further elucidation.

Conclusions:

  • Cardiovascular risk management is crucial for patients with ankylosing spondylitis.
  • Management should encompass assessment and treatment of traditional CV risk factors.
  • Effective suppression of the underlying inflammatory process is a key therapeutic goal.

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