Angiotensin-converting enzyme insertion/deletion polymorphism and cerebrovascular disease
A Catto1, A M Carter, J H Barrett
1Diabetes and Thrombosis Research Group, Division of Medicine, University of Leeds, Leeds, UK.
Stroke
|March 1, 1996
Summary
Low angiotensin-converting enzyme (ACE) activity and the ACE D allele may increase early death risk in stroke patients. ACE levels normalize in survivors over time.
Area of Science:
- Genetics and Molecular Biology
- Neurology and Cerebrovascular Disease Research
- Cardiovascular and Metabolic Science
Background:
- Allelic variations in the angiotensin-converting enzyme (ACE) gene are linked to vascular disease risk.
- The specific roles of the ACE insertion/deletion polymorphism and circulating ACE levels in cerebrovascular disease remain unclear.
Purpose of the Study:
- To investigate the association between the ACE insertion/deletion polymorphism and plasma ACE activity with stroke.
- To determine the relationship between ACE genotype/activity and stroke type, and mortality outcomes.
Main Methods:
- Polymerase chain reaction was used to analyze the ACE insertion/deletion polymorphism in intron 16.
- Plasma ACE activity was measured in 467 stroke patients and 231 control subjects.
- Genotype and activity were correlated with stroke type and mortality at 4 weeks and 3 months.
Main Results:
- No significant differences in ACE genotype frequencies were found between stroke patients and controls, or among different stroke subtypes.
- Stroke patients exhibited significantly lower plasma ACE activity at presentation (64.1 IU/L) compared to controls (79.6 IU/L).
- Lower plasma ACE activity was associated with increased risk of early death within 4 weeks (P=.02 for D allele) and 3 months. Survivors showed a normalization of ACE activity by 3 months.
Conclusions:
- Low plasma ACE activity at stroke presentation and carriage of the ACE D allele may indicate an elevated risk of early mortality.
- These findings suggest potential biomarkers for risk stratification in acute cerebral infarction.
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