Benefits of tumor necrosis factor inhibitors for cardiovascular disease in ankylosing spondylitis

Jin-Xian Huang1, Yung-Heng Lee2, James Cheng-Chung Wei3

  • 1Division of Rheumatology, Department of Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.

Insights

Ankylosing spondylitis patients face higher cardiovascular disease (CVD) risk. Tumor necrosis factor inhibitors (TNFi) may benefit CVD-vulnerable patients by controlling inflammation, but results on lipids and atherosclerosis are mixed.

Area of Science:

  • Rheumatology
  • Cardiology
  • Immunology

Background:

  • Ankylosing spondylitis (AS) is linked to increased cardiovascular disease (CVD) risk.
  • Current guidelines recommend multiple CVD risk assessment strategies for AS patients.
  • Subclinical atherosclerosis screening and surrogate markers are potential CVD risk predictors.

Purpose of the Study:

  • To review the evidence on the effects of tumor necrosis factor inhibitors (TNFi) on CVD in AS patients.
  • To explore the potential of TNFi in preventing microvascular events by inhibiting inflammation.
  • To discuss the controversial findings regarding TNFi's impact on lipids and atherosclerosis.

Main Methods:

  • Narrative review of existing literature.
  • Summarization of studies investigating TNFi effects on CVD markers in AS.
  • Analysis of factors contributing to controversial results in TNFi studies.

Main Results:

  • While early reports noted CVD during TNFi treatment, recent evidence suggests successful management.
  • Studies on TNFi's effects on lipid profiles and subclinical atherosclerosis in AS yield conflicting results.
  • Potential reasons for conflicting results include genetic factors, varying TNFi efficacy, and insufficient follow-up duration.

Conclusions:

  • Long-term TNFi administration can benefit AS patients vulnerable to CVD, provided inflammation is controlled.
  • Managing traditional CVD risk factors and metabolic syndrome is crucial alongside lifestyle modifications.
  • Further assessment and treatment of metabolic syndrome-related diseases are recommended for AS patients.

Related Concept Videos

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
216
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
220
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
247
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
238
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
257
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
489