Association of serum levels of AngII, KLK1, and ACE/KLK1 polymorphisms with acute myocardial infarction induced by coronary artery stenosis

Abstract

Introduction:The study aims to confirm the association of acute myocardial infarction (AMI) with serum angiotensin II (AngII), kallikrein1 (KLK1), and ACE/KLK1 polymorphisms.Materials and methods:Serum AngII/KLK1 levels and ACE and KLK1 genotypes were determined in 208 patients with AMI and 216 normal controls. Binary logistic regression was used for data analysis.Results:The differences in serum AngII levels were statistically significant between the groups. After adjusting for potential confounding factors, high serum levels of AngII and KLK1 significantly increased the risk of AMI. The individuals with ACE DD and KLK1 GG genotypes significantly increased the risk of AMI compared with those harboring the ACE II and KLK1 AA genotypes (OR = 8.77, 95% CI = 1.74–44.16).Conclusions:(1) Increasing the serum levels of AngII increased the risk of AMI. (2) The risk of AMI increased significantly when the serum levels of AngII and KLK1 simultaneously increased. (3) Individuals with the combined genotypes of ACE DD and KLK1 GG showed significantly increased risk of AMI compared with those with the combined genotypes of ACE II and KLK1 AA.

Associations of ACE I/D polymorphism with the levels of ACE, kallikrein, angiotensin II and interleukin-6 in STEMI patients

“…The diagnosis of hypertension and diabetes mellitus was performed according to World Health Organization criteria A smoking habit was defined as a daily intake of >10 cigarettes continuing for more than 1 year. The other criteria are consistent with a previous study 4 . The fasting blood samples tested for routine blood, lipid profiles and coagulation tests were routinely performed in the hospital laboratory.…”

“…A human angiotensin I-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism, due to I/D of a 287-base pair element in intron 16 of this gene, is associated with the development of AMI by modifying ACE activity and contributing to enhanced plaque vulnerability, ulceration and thrombosis 2,3 . Our recent case-control study has also demonstrated that the ACE DD genotype is an independent risk factor for STEMI 4 .…”

“…Human ACE, AngII, KLK1 and IL-6 levels in plasma were measured in strict accordance with the manufacturer’s instructions, as described previously 4 . Briefly, polyclonal antibodies specific for these three proteins were precoated onto 96-well plates and incubated for 24 hours at 4 °C.…”

Influence of ACE Gene I/D Polymorphism on Cardiometabolic Risk, Maximal Fat Oxidation, Cardiorespiratory Fitness, Diet and Physical Activity in Young Adults

“…In this line, a human angiotensin I-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism, located on chromosome 17q23, is associated with CVD [5,6]. The ACE I/D polymorphism consists in the presence (insertion, I) or absence (deletion, D) of a 287 base pair fragment in intron 16 of ACE gene [7].…”

“…The ACE gene produces the protein ACE, which converts angiotensin (AngI) into angiotensin II (AngII), a potent vasoactive peptide that leads to effects mainly hypertensive, highlighting its role in the physiology of blood vessels and inflammation [5,8]. Indeed, higher plasma levels of ACE have been reported when the D allele was present [5], accordingly, the ACE DD genotype has been established as an independent risk factor of CVD and hypertension [6,9]. Similarly, a recent meta-analysis [10] has shown a higher risk of hypertrophic cardiomyopathy in the DD genotype than in the II genotype; therefore, a protective effect against CVD risk can be attributed to the II genotype.…”