Relation between severity of coronary artery disease, left ventricular function and myocardial infarction, and influence of the ACE I/D gene polymorphism.
Left ventricular (LV) systolic function is partly determined by severity of coronary artery disease and is improved by angiotensin-converting enzyme (ACE) inhibition, at least in post-infarct patients. Because the ACE insertion/deletion (I/D) gene polymorphism is associated with circulating and tissue ACE activity, we sought to evaluate the role of this genetic variant on LV function in patients studied with coronary angiography, taking into account coronary vessel anatomy and history of infarction. Coronary artery disease extent scores, coronary artery patency, and LV ejection fraction were assessed in 400 consecutive Caucasian patients referred for established or suspected ischemic heart disease. A previous infarction had occurred in 141 patients an average of 3.7 years before the study. The ACE DD genotype, compared with the ACE ID/II genotype, was associated with a 2.7% higher ejection fraction in noninfarct patients (p = 0.047) but a 5.0% lower ejection fraction in post-infarct patients (p = 0.047). An interaction effect between the ACE I/D gene polymorphism, the infarction status, and LV ejection fraction was observed in the whole population (p = 0.003), in patients with no disease and 1-, 2-, and 3-vessel diseases (p = 0.03 and p = 0.06, respectively), and in those with chronically occluded coronary vessels (p = 0.02). The influence of the ACE I/D gene polymorphism on LV function is modulated by infarction status and coronary anatomy.
Cardiology Department, Unité INSERM U-258, Hôpital Broussais, Assistance Publique-Hôpitaux de Paris, France.
F
F
Ledru
D
D
Blanchard
S
S
Battaglia
X
X
Jeunemaitre
D
D
Courbon
L
L
Guize
J L
JL
Guermonprez
P
P
Ducimetière
B
B
Diébold
D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D015986:Confounding Factors, Epidemiologic; D017023:Coronary Angiography; D003327:Coronary Disease / Q000150:complications / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D011110:Polymorphism, Genetic; D012720:Severity of Illness Index; D013318:Stroke Volume; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000235:genetics*
D000806:Angiotensin-Converting Enzyme Inhibitors