ANGIOTENSIN-CONVERTING ENZYME INSERTION DELETION POLYMORPHISM AND CEREBROVASCULAR-DISEASE

Citation
A. Catto et al., ANGIOTENSIN-CONVERTING ENZYME INSERTION DELETION POLYMORPHISM AND CEREBROVASCULAR-DISEASE, Stroke, 27(3), 1996, pp. 435-440
Citations number
33
Categorie Soggetti
Cardiac & Cardiovascular System","Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
27
Issue
3
Year of publication
1996
Pages
435 - 440
Database
ISI
SICI code
0039-2499(1996)27:3<435:AEIDPA>2.0.ZU;2-W
Abstract
Background and Purpose There is evidence that an allelic variation in the angiotensin-converting enzyme (ACE) gene may confer an increased r isk of vascular disease. The roles of the ACE insertion/deletion polym orphism and circulating ACE levels are unknown in cerebrovascular dise ase. Methods We studied an insertion/deletion polymorphism within intr on 16 of the ACE gene by polymerase chain reaction and plasma ACE acti vity in 467 cases of stroke, the pathological type of which was establ ished by cranial CT, and 231 control subjects. ACE genotype and activi ty were related to stroke type and mortality at 4 weeks and 3 months. Results No difference in genotype frequency was observed between all s ubjects with stroke and control subjects or between control subjects a nd subjects with cerebral infarction or cerebral hemorrhage. Plasma AC E activity was significantly lower in stroke patients at presentation (64.1 IU/L) than in control subjects (79.6 IU/L; P<.0001). Twenty-one patients (4.5%) with cerebral infarction died within 4 weeks and 56 pa tients (12%) within 3 months. These patients had significantly lower p lasma ACE activity than patients who survived. There was some evidence that risk of death within 4 weeks increased with the number of D alle les (P=.02). Among survivors, plasma ACE activity showed a mean increa se of 6.9 IU/L (95% confidence interval, 3.0 to 10.8) between levels a t presentation and at 3 months (73.6 IU/L), the latter being similar t o ACE activity in control subjects. Conclusions Low ACE activity at st roke presentation and possession of the D allele may be associated wit h increased risk of early death from acute cerebral infarction.