Homocysteine and post-angioplasty restenosis

P Ambrosi1

  • 1Service de Cardiologie B, Hôpital de la Timone, Marseille, France. pambrosi@ap-hm.fr

Insights

Moderate hyperhomocysteinemia may be a weak risk factor for restenosis after coronary angioplasty. Folic acid may lower this risk, but further studies are needed before routine recommendation.

Area of Science:

  • Cardiovascular Research
  • Metabolic Disorders

Background:

  • Hyperhomocysteinemia is linked to arterial neointimal proliferation in various conditions.
  • Animal models show homocysteine exacerbates neointimal proliferation after injury.

Purpose of the Study:

  • To review the effect of moderate hyperhomocysteinemia on restenosis after coronary angioplasty.
  • To evaluate the role of homocysteine in restenosis and the potential benefit of folic acid.

Main Methods:

  • Review of existing literature on hyperhomocysteinemia and restenosis.
  • Analysis of findings from animal models and human clinical trials.

Main Results:

  • Restenosis after coronary angioplasty is inconsistently associated with hyperhomocysteinemia in humans.
  • A clinical trial indicated folic acid reduces homocysteinemia and restenosis risk.

Conclusions:

  • Hyperhomocysteinemia is likely a weak risk factor for coronary restenosis post-angioplasty.
  • The causative role of homocysteine in restenosis remains unclear.
  • More research on restenosis prevention after coronary stenting is required before recommending routine folic acid administration.
Abstract

Related Concept Videos

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers

Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Peripheral Artery Disease III: Interprofessional Care01:27

Peripheral Artery Disease III: Interprofessional Care

Peripheral Artery Disease (PAD) is characterized by narrowed arteries that diminish blood flow to the extremities. Effective management of PAD requires an interprofessional approach involving various healthcare professionals. The critical aspects of interprofessional care for PAD patients focus on risk factor modification, drug therapy, exercise therapy, nutrition therapy, critical limb ischemia care, and interventional radiology and surgical procedures.The primary treatment goal for PAD...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...