Association of serum levels of AngII, KLK1, and ACE/KLK1 polymorphisms with acute myocardial infarction induced by coronary artery stenosis
نویسندگان
چکیده
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.
منابع مشابه
Relationship between the location of the most severe myocardial perfusion defects, the most severe coronary artery stenosis and the site of subsequent myocardial infarction [Persian]
This study evaluated the relationship between the location of the most severe coronary artery stenosis and the subsequent acute myocardial infarction (AMI). Methods: Of 1590 patients who were admitted with a diagnosis of AMI, we identified 44 patients who had undergone previous myocardial perfusion SPECT. Thirty-one of these patients also had previous coronary angiography. The relationshi...
متن کاملSurvey on the Association of Seropositivity of H.pylori lgG acute myocardial infarction
Some investigatoes reported taht there is a relationship between.H.pylori chronic infection and the prevalence of acute coronary artery disease(CAD).it is suggested that H.pylori chronic infection causes some changes in serum levels of lipids an lipoproteins and produces inflamatory proteins which could give rise to thrombogenesis.in order to comfirm any correlation between positive history of...
متن کاملKLK1 A1789G gene polymorphism and the risk of coronary artery stenosis in the Chinese population.
Previous reports have shown that polymorphism of the human tissue kallikrein 1 (KLK1) A1789G gene is associated with susceptibility to hypertension. The current study aimed to confirm the association between the polymorphism in KLK1 and coronary artery stenosis (CAS). A total of 458 patients with CAS and 482 controls were used in a case-control study carried out between January 2008 and January...
متن کاملRelationship between Late Gadolinium Enhancement Extent in Cardiac Magnetic Resonance Imaging and Severity of Coronary Artery Disease in Old Myocardial Infarction
Purpose: To assess the relationship between the severity of coronary arteries involvement and the extent and pattern of myocardial scars in Cardiac Magnetic Resonance of patients with history of remote myocardial infarction. Materials and Methods: The Cardiac Magnetic Resonance images of sixty patients with history of remote ST segment or non-ST segment elevation myocardial infarction were ...
متن کاملICAM-1 Polymorphisms (G241R, K469E), in Coronary Artery Disease and Myocardial Infarction
Background: Inflammation plays a critical role in atherogenesis. The initial step in atherosclerosis is the adhesion of leukocytes to activated endothelial cells mediated by ICAM-1, an inflammatory protein. Several polymorphisms for Intracellular adhesion molecule -1(ICAM-) gene have been described. Objective: To determine the possible role of G241R and K469E polymorphisms in development of cor...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 17 شماره
صفحات -
تاریخ انتشار 2016