Published online before print May 27, 2004, doi: 10.1161/01.STR.0000131655.45227.f7
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(Stroke. 2004;35:1594.)
© 2004 American Heart Association, Inc.
Original Contributions |
II Genotype of the Angiotensin-Converting Enzyme Gene Increases the Risk for Subarachnoid Hemorrhage From Ruptured Aneurysm
From the Departments of Neurology (A.Slowik, A.B., J.P., T.D., A.Szczudlik) and Neurosurgery (M.B., T.K., R.C.), Jagiellonian University, Medical College, Krakow, Poland; and the Department of Neurology (D.A.F.), University of Michigan, Ann Arbor, Mich.
Correspondence to Agnieszka Slowik, MD, Department of Neurology, Jagiellonian University, 31-503 Krakow, Botaniczna 3, Poland. E-mail slowik{at}neuro.cm-uj.krakow.pl
Background and Purpose— Evidence exists in support of a role of genetic factors in susceptibility to aneurysmal subarachnoid hemorrhage (SAH) in humans. Meta-analysis of 2 previous studies showed that the I allele of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism was a weak, but significant, risk factor for aneurysmal SAH. Moreover, a recent study has shown that the local renin-angiotensin system (RAS) is involved in the development of intracranial aneurysm. The aim of this study was to investigate the association between ACE I/D polymorphism and a risk for aneurysmal SAH in a Polish population.
Methods— Ninety patients with aneurysmal SAH (mean age: 48.9±14.0 years) and 128 healthy controls matched for age and sex were genotyped for the ACE I/D polymorphism. Aneurysmal SAH was diagnosed by cranial computed tomography and/or lumbar puncture and digital subtraction angiography. ACE gene polymorphism was detected by polymerase chain reaction amplification of the intron 16-specific I/D fragments, 490-bp and 190-bp, respectively.
Results— The ACE genotype distribution in patients with aneurysmal SAH (II, 52.2%; ID, 15.6%; DD, 32.2%) differed significantly from controls (II, 23.4%; ID, 50.8%; DD, 25.8%) (P<0.001). A logistic regression model showed that the II genotype of ACE gene was independent from female sex and smoking as a risk factor for aneurysmal SAH (OR, 4.57; 95% CI, 2.35 to 8.90).
Conclusion— Here we report that II genotype of ACE gene is a risk factor for aneurysmal SAH.
Key Words: aneurysm • genetics • subarachnoid hemorrhage • angiotensin-converting enzyme
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