Angiotensin-converting enzyme insertion/deletion polymorphism has no effect on the risk of atherosclerotic stroke or hypertension.
OBJECTIVE
Stroke is a heterogeneous multifactorial disease. Hence, a large number of candidate genes are involved in stroke pathophysiology, such as blood pressure regulation and atherosclerosis. Although angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism is considered to have a role in hypertension, coronary artery disease, and myocardial infarction, its relationship with cerebrovascular disease and hypertension in stroke in different ethnic populations is still inconsistent.


METHODS
ACE I/D polymorphism, detected by polymerase chain reaction (PCR), was studied in 97 patients with large-vessel and 60 patients with small-vessel atherosclerotic stroke (44 asymptomatic, 16 symptomatic lacunes) and 85 healthy subjects with normal brain imaging. The demographic data, lipid profile and risk factors of patients and controls were obtained retrospectively.


RESULTS
ACE genotypes were in Hardy-Weinberg equilibrium in both patients and controls. Prevalences of DD, ID and II genotype were 41%, 40%, and 19%, respectively, in the stroke group. Differences in ACE I/D polymorphism distribution were statistically insignificant between the groups. This lack of association between stroke and ACE I/D polymorphism did not change in the presence of traditional risk factors (hypertension, diabetes mellitus, smoking, and dyslipidemia). Although hypertension was significantly more common in the patient groups, ACE I/D polymorphism showed no effect on hypertension risk. This lack of association also did not change according to groups or in the presence of diabetes mellitus, male gender or smoking.


CONCLUSIONS
ACE I/D polymorphism did not predict the risk of stroke or hypertension in our population living in the western Black Sea region of Turkey.
Tascilar
N
N
Department of Neurology, Zonguldak Karaelmas University Medical Faculty, Zonguldak, Turkey. doga24@yahoo.com
Dursun
A
A
Ankarali
H
H
Mungan
G
G
Ekem
S
S
Baris
S
S
D000368:Aged; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000235:genetics*; D054643:INDEL Mutation; D002537:Intracranial Arteriosclerosis / Q000453:epidemiology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D015995:Prevalence; D012189:Retrospective Studies; D012307:Risk Factors; D017422:Sequence Analysis, DNA; D020521:Stroke / Q000453:epidemiology / Q000235:genetics*; D014421:Turkey / Q000453:epidemiology
C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A