Angiotensin-converting enzyme gene polymorphism is not associated with coronary atherosclerosis and myocardial infarction in a sample of Italian patients.
BACKGROUND
The deletion (D) allele of the angiotensin-converting enzyme (ACE) gene has been proposed as a genetic marker of the risk of ischaemic heart disease. However, the relationships between ACE genotypes, the development of coronary atherosclerosis and the occurrence of major coronary events are still controversial.


METHODS
To investigate whether the ACE I/D (insertion/deletion) polymorphism predicts the risk of coronary stenosis and myocardial infarction (MI), ACE genotypes were determined in 394 consecutive patients who underwent coronary angiography. The presence determined in 394 consecutive patients who underwent coronary angiography. The presence of coronary artery disease (CAD) (defined by > 50% stenosis) was detected in 236 patients (CAD+); 85 of these individuals had a history of MI. Patients with coronary stenosis < 10% (n = 158) served as controls (CAD-). ACE genotypes were determined by agarose gel sizing after polymerase chain reaction (PCR) amplification.


RESULTS
The distribution of ACE genotypes in CAD+ patients was not significantly different from that in CAD-patients (chi 2 = 2.63, P < 0.27). After controlling for other coronary risk factors, no significant increase in risk of CAD or MI was found to be associated with the D allele, regardless of whether the D allele was assumed to have a dominant, a codominant or a recessive effect. Similar results were observed in CAD+ patients at lower risk because of low body mass index and apolipoprotein B concentrations. Smoking, apolipoprotein B and history of hypertension were found to be independent predictors of CAD and MI.


CONCLUSIONS
Our study did not provide evidence of a significant association between ACE genotypes and the development of coronary atherosclerosis. It also failed to support a role of ACE I/D polymorphism in favouring the conversion of coronary stenosis to MI.
Arca
M
M
Istituto di Terapia Medica Sistematica, Università di Roma La Sapienza, Italy. itmsricci@caspur.it
Pannitteri
G
G
Campagna
F
F
Candeloro
A
A
Montali
A
A
Cantini
R
R
Seccareccia
F
F
Campa
P P
PP
Marino
B
B
Ricci
G
G
D000368:Aged; D000704:Analysis of Variance; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000201:enzymology* / Q000235:genetics; D005838:Genotype; D006801:Humans; D007558:Italy; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000201:enzymology* / Q000235:genetics; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012307:Risk Factors
D007703:Peptidyl-Dipeptidase A