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Fatemeh Hajibabaie1,1, Mohammad Hossein Modarressi3, Masoumeh Sadeghi4* and Laleh Shariati5,6*
1Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
2Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
3Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
4Cardiac Rehabilitation Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
5Isfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
6Department of Biomaterials, Nanotechnology and Tissue Engineering, School of Advanced Technologies in Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
*Corresponding Author: Masoumeh Sadeghi, Cardiac Rehabilitation Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran and Laleh Shariati, Isfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences and Cardiac Rehabilitation Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran.
Received: July 07, 2020; Published: July 30, 2020
Introduction: Premature myocardial infarction (MI) is characterized by high re-infarction rates, the occurrence of severe heart failure and therefore significant cardiovascular long-term mortality at a young age. Previous studies demonstrated that one of the most important risk factors in younger patients is family history and genetic factors. This research was launched to assess the association of ACTA2 genetic variations with premature MI.
Materials and Methods: Out of eighty unrelated patients with premature MI referred to health center, patients with autosomal dominant premature MI were included in the study. Exclusion criteria included hypercholesterolemia, hyperlipidemia, diabetes and smoking. Genomic DNA was extracted from the whole peripheral blood. Eight exons and intron/exon boundaries of the ACTA2 gene were amplified, and all the amplicons were subject to Sanger sequencing.
Results: According to the criteria, 16 patients were included in our research. No mutations were found in ACTA2 gene in our pro-bands.
Keywords: Premature Myocardial Infarction; ACTA2; Pathogenesis
Citation: Masoumeh Sadeghi, Laleh Shariati., et al. “ACTA2 Mutations and Risk of Premature Myocardial Infarction". Acta Scientific Nutritional Health 4.8 (2020): 60-66.
Copyright: © 2020 Masoumeh Sadeghi, Laleh Shariati., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.