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Hyperhomocysteinemia and transplant coronary artery disease

Angel Caldera1, G William Dec

  • 1Department of Medicine, Albert Einstein Medical Center, Philadelphia, PA, USA.

Transplantation
|November 27, 2002
PubMed

Insights

Hyperhomocysteinemia is common in heart transplant recipients and linked to transplant coronary artery disease (TCAD). Lowering homocysteine may be beneficial, but further research is needed.

Area of Science:

  • Cardiology
  • Transplantation Immunology
  • Vascular Biology

Background:

  • Transplant coronary artery disease (TCAD) significantly impacts heart transplant recipient outcomes.
  • Both immunologic and non-immunologic factors contribute to TCAD pathogenesis.
  • Hyperhomocysteinemia is a known risk factor for atherosclerotic vascular disease.

Purpose of the Study:

  • To determine the prevalence of hyperhomocysteinemia in heart transplant recipients.
  • To review the literature on the association between hyperhomocysteinemia and TCAD.
  • To explore potential therapeutic interventions for hyperhomocysteinemia in this population.

Main Methods:

  • A comprehensive literature search was conducted using MEDLINE.
  • Keywords included "hyperhomocysteinemia," "transplant coronary artery disease," and "heart transplant."
  • The review focused on studies investigating the prevalence and clinical significance of hyperhomocysteinemia.

Main Results:

  • Hyperhomocysteinemia affects 51% to 76% of heart transplant recipients.
  • Worsening renal function and impaired vitamin metabolism are key contributors.
  • Higher homocysteine levels correlate with increased prevalence and severity of TCAD.
  • Vitamin supplementation effectively reduces homocysteine levels and is safe.

Conclusions:

  • Hyperhomocysteinemia is highly prevalent in heart transplant recipients.
  • A strong association exists between hyperhomocysteinemia and TCAD.
  • Further large-scale, placebo-controlled trials are necessary to confirm the clinical benefits of homocysteine-lowering therapies on TCAD progression.
Abstract

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