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ACE-gene polymorphism is associated with the development of allograft vascular disease in heart transplant recipients

K Pethig1, B Heublein, A Hoffmann

  • 1Department of Thoracic and Cardiovascular Surgery, Hannover Medical School, Hannover, Germany.

The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation
|December 22, 2000
PubMed

Insights

The angiotensin-converting enzyme (ACE) D genotype in heart transplant recipients is linked to increased cardiac allograft vasculopathy (CAVD) risk. This suggests genetic factors play a role in post-transplant coronary artery disease development.

Area of Science:

  • Cardiology
  • Genetics
  • Transplantation Immunology

Background:

  • Cardiac allograft vasculopathy (CAVD) is a primary cause of death after heart transplantation (HTX).
  • Previous research focused on endothelial injury, neglecting recipient genetic factors.
  • The role of recipient-related genetic factors in CAVD requires further investigation.

Purpose of the Study:

  • To investigate the impact of angiotensin-converting enzyme (ACE) polymorphism on CAVD development and progression.
  • To analyze the association between ACE genotype and CAVD in heart transplant recipients.

Main Methods:

  • Genotyped 146 heart transplant recipients for ACE insertion/deletion (I/D) polymorphism.
  • Correlated ACE genotype with the onset and progression of CAVD (luminal obstruction > 50%).
  • Followed patients for 1 to 12 years post-transplantation.

Main Results:

  • Allelic frequencies: ACE-DD (28.8%), ACE-DI (49.3%), ACE-II (21.9%).
  • Actuarial freedom from vasculopathy at 6 years: ACE-II (84.6%) vs. ACE-DD (54.4%).
  • ACE-DI genotype showed intermediate results (77.3%, p = 0.015).

Conclusions:

  • A significant association exists between the recipient ACE-D genotype and advanced CAVD.
  • Gene-environment interactions may be crucial in coronary vasculopathy after HTX.
  • Recipient genetic factors, specifically ACE polymorphism, influence CAVD progression.
Abstract

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