Diana Zaliaduonyte-Peksiene1, Sandrita Simonyte2, Vaiva Lesauskaite2, Jolanta Vaskelyte3, Olivija Gustiene4, Vaida Mizariene4, Renaldas Jurkevicius4, Giedre Jariene2, Abdonas Tamosiunas2, Remigijus Zaliunas4. 1. Department of Cardiology, Medical Academy, Lithuanian University of Health Sciences, Lithuania diana.peksiene@gmail.com. 2. Institute of Cardiology, Medical Academy, Lithuanian University of Health Sciences, Lithuania. 3. Department of Cardiology, Medical Academy, Lithuanian University of Health Sciences, Lithuania Institute of Cardiology, Medical Academy, Lithuanian University of Health Sciences, Lithuania. 4. Department of Cardiology, Medical Academy, Lithuanian University of Health Sciences, Lithuania.
Abstract
INTRODUCTION: The development of left ventricular remodelling after acute myocardial infarction is a predictor of heart failure and mortality. The purpose of the present study was to assess whether the polymorphism of angiotensinogen (AGT) gene with threonine (T) instead of methionine (M) at amino acid 235 in exon 2 (M235T) had effects on cardiac remodelling after acute myocardial infarction. METHODS: One hundred and forty-one patients (mean age 56.4±11.1 years) with a first acute myocardial infarction were enrolled. Within 24-72 hours of the onset of the symptoms and at a four month period two-dimensional echocardiography was performed. Remodelling was defined as a 20% increase from the baseline in left ventricular end-diastolic volume. The genotypes of the study group were compared with the reference group (n=1010) genotypes. AGT M235T polymorphism was determined using polymerase chain reaction amplification. RESULTS: At follow-up, 49 patients (34.7%) were classified as having left ventricular remodelling. Anterior localization of the infarct (p=0.008), leucocyte count at admission (p=0.040), global left ventricular longitudinal strain (p=0.021) and MM genotype of AGT (p=0.024) were independent predictors of ventricular remodelling after myocardial infarction. CONCLUSIONS: Anterior wall infarction, increased leucocyte count, decreased longitudinal strain of left ventricular and polymorphism of AGT M235T may predict remodelling after myocardial infarction.
INTRODUCTION: The development of left ventricular remodelling after acute myocardial infarction is a predictor of heart failure and mortality. The purpose of the present study was to assess whether the polymorphism of angiotensinogen (AGT) gene with threonine (T) instead of methionine (M) at amino acid 235 in exon 2 (M235T) had effects on cardiac remodelling after acute myocardial infarction. METHODS: One hundred and forty-one patients (mean age 56.4±11.1 years) with a first acute myocardial infarction were enrolled. Within 24-72 hours of the onset of the symptoms and at a four month period two-dimensional echocardiography was performed. Remodelling was defined as a 20% increase from the baseline in left ventricular end-diastolic volume. The genotypes of the study group were compared with the reference group (n=1010) genotypes. AGTM235T polymorphism was determined using polymerase chain reaction amplification. RESULTS: At follow-up, 49 patients (34.7%) were classified as having left ventricular remodelling. Anterior localization of the infarct (p=0.008), leucocyte count at admission (p=0.040), global left ventricular longitudinal strain (p=0.021) and MM genotype of AGT (p=0.024) were independent predictors of ventricular remodelling after myocardial infarction. CONCLUSIONS: Anterior wall infarction, increased leucocyte count, decreased longitudinal strain of left ventricular and polymorphism of AGTM235T may predict remodelling after myocardial infarction.
Authors: Kory J Lavine; Alexander R Pinto; Slava Epelman; Benjamin J Kopecky; Xavier Clemente-Casares; James Godwin; Nadia Rosenthal; Jason C Kovacic Journal: J Am Coll Cardiol Date: 2018-10-30 Impact factor: 24.094
Authors: Ildikó Rácz; László Fülöp; Rudolf Kolozsvári; Gábor T Szabó; Annamária Bódi; Andrea Péter; Attila Kertész; Ida Hegedüs; István Édes; László Balkay; Zsolt Köszegi Journal: Anatol J Cardiol Date: 2014-07-11 Impact factor: 1.596