Background: The enzyme ‘Angiotensin-Converting Enzyme (ACE)’ modulates the fibrinolytic balance by converting angiotensin I into
angiotensin II, which increase the activity of plasminogen activator inhibitor-1 (PAI-1). Besides, it degrades bradykinin, which an
important mediator of the tissue-type plasminogen activator (t-PA). Thus, decreases fibrinolysis and may result in increased
thrombotic risk. An insertion/deletion (I/D) polymorphism in the ACE gene has been identified and correlated with the enzyme
serum levels. Studies concerning the association of this polymorphism and the risk of cardiovascular diseases in different
populations showed inconsistent results. Objective: This study aimed to investigate the association between ACE I/D polymorphism
and the risk of myocardial infarction among the Sudanese population. Materials and methods: This is a case-control study, in which
blood samples were collected from a total of 100 Sudanese subjects, 50 patients with myocardial infarction and 50 age- and sexmatched
healthy volunteers as a control group. Genomic DNA was extracted by guanidine chloride method and ACE I/D
polymorphism was analysed by Allele-Specific Polymerase Chain Reaction (AS-PCR). Data of this study was collected using a
structured interview questionnaire and analysed by statistical package for social sciences (SPSS). Results: The frequency D/D
Genotype was higher in the control group than patients (72% vs 60%), while of the I/D genotype was higher in the patients than
controls (40% vs 28%); the II genotype was absent in both study groups. The frequency of D allele was 0.80 in patients with MI and
0.86 in the control group, while the frequency of I Allele was 0.20 in the patients with MI and 0.14 in the control group. No
statistically significant association was reported between ACE I/D polymorphic genotypes and MI (P.value= 0.29). Conclusion: ACE
I/D polymorphism is not associated with the risk of MI among the Sudanese population.
Keywords: Myocardial infarction; Angiotensin converting enzyme; Insertion/deletion polymorphism