Angiotensin-converting enzyme gene insertion/deletion polymorphism and peripheral arterial occlusive disease.
BACKGROUND
The deletion polymorphism of the ACE gene is linked to a high risk of cardiovascular disease due to the permanent activation of the local and systemic renin-angiotensin systems (RAS). The aim of this prospective study was 1. to compare the ACE insertion/deletion polymorphism in individuals with a healthy vasculature with that of patients suffering from peripheral arterial occlusive disease (PAOD), and 2. to determine whether associations existed between specific clinical parameters and the ACE genotype which the PAOD patients expressed.


METHODS
Determinations of ACE I/D gene polymorphism were made using a polymerase chain reaction (PCR) technique on 98 patients with clinical stage II PAOD according to Fontaine and 240 healthy individuals who served as controls. All patients and controls came from central Germany. Clinical variables which included duration of clinical symptoms, a familial history of the disease, arteriosclerosis score (ASF, providing an estimate of the extent of atheromatosis at femoral artery bifurcation) and plasma ACE activity were correlated with the genotypes taking the cardiovascular disease risk factors which were present into consideration.


RESULTS
Differences in ACE genotypes between patients with PAOD (D/I: 0.57/0.43) and control group individuals (D/I: 0.59/0.41) were not observed. In comparison with the II genotype, the DD genotype was associated with a shorter duration of disease (p = 0.01), a positive family medical history (p = 0.022) and a higher plasma ACE activity (p = 0.026). The ASF did not correlate with the ACE I/D gene polymorphism.


CONCLUSIONS
Evidence that the deletion allele is linked to the manifestation of PAOD could not be found in the patients studied. One can assume, however, that the deletion allele has a progression promoting effect on the disease.
Taute
B M
BM
Department of Internal Medicine/Angiology, Martin-Luther-University of Halle-Wittenberg, Germany.
Handschug
K
K
Taute
R
R
Seifert
H
H
Gläser
C
C
Podhaisky
H
H
D000368:Aged; D001161:Arteriosclerosis / Q000235:genetics; D002869:Chromosome Aberrations / Q000235:genetics*; D005260:Female; D017353:Gene Deletion; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000235:genetics*; D011446:Prospective Studies; D012084:Renin-Angiotensin System / Q000235:genetics
D007703:Peptidyl-Dipeptidase A