Effect of the ACE gene polymorphism on survival after myocardial infarction
Dr John Attia, Professor Rodney Scott (John Hunter Hospital), Associate Professor Catherine D'Este
Results of the Human Genome Project are giving researchers an appreciation of the sources of variation between people and populations. Part of the explanation for variations in susceptibility to disease, disease outcomes, responses to medications, etc is due to genetic polymorphisms. Polymorphisms are variants in a gene that lead to a change in level or function of that gene product. Angiotensin converting enzyme (ACE) is part of the renin-angiotensin hormone cascade, one of the major determinants of blood pressure. Drugs that interfere with ACE, termed ACE inhibitors (ACEI) are widely used now for hypertension, heart failure, and after a heart attack.
This project looks at the influence of ACE gene polymorphisms on outcomes after a heart attack and the response to ACE inhibitors. Subjects with the ââ¬ÅIââ¬ form of the gene (I for insertion of an extra 250 base pairs of DNA) have lower circulating ACE levels than those with the ââ¬ÅDââ¬ form (D for deletion), and this has been inconsistently linked to better outcomes in the setting of myocardial infarction, left ventricular hypertrophy, dilated cardiomyopathy and congestive heart failure. A four month pilot study, recruiting patients at the John Hunter Coronary Care Unit with a first heart attack, has been completed. Initial results indicate a possible role of the ACE gene in determining mortality and morbidity.