![]() Tachyarrhythmias remain a major cause of cardiac death, with an incident rate of 1.4% occurring within the first month post-AMI. This includes adverse electrophysiological remodeling, such as atrial and ventricular arrhythmias, which may be prevented by mineralocorticoid receptor antagonist (MRA) treatment. A study on animal models performed in 2017 showed that the activation of MRs increases cardiomyocyte oxidative stress and inflammation, which leads to adverse cardiac tissue remodeling. Evidence has shown that the MRs in cardiac tissue are crucial for the process of cardiac remodeling and arrhythmias. Conversely, MRs in other structures such as the brain, heart, blood vessels or adipose tissue have multiple and less clearly characterized roles. MRs are located in the kidney, colon and salivary glands, and facilitate sodium reabsorption upon activation of the renin–angiotensin–aldosterone system. Ĭortisol is the final product of the hypothalamic–pituitary–adrenal axis (HPA) and is a primary stress hormone that acts via glucocorticoid receptors (GRs) and mineralocorticoid receptors (MRs), both of which are present in cardiomyocyte nuclei. ![]() However, these neurohormonal changes may have deleterious effects if their activity is long enough to cause an increase in sensitivity to catecholamines and an increase in the mineralocorticoid receptors present in the myocardium. A cascade of events during the early phase of an AMI activates the neurohormonal system in an effort to preserve circulatory homeostasis. Patients with acute myocardial infarction (AMI) experience both physical and psychological stress, accompanied by its physiological manifestations. Conclusion: SNPs of the NR3C2 gene appear to correlate with better ventricular remodeling and a reduced rate of arrhythmias post-AMI, possibly by limiting the deleterious effects of cortisol on cardiomyocytes. The rs5522 TT genotype was associated with a higher frequency of arrhythmias, while the presence of at least one rs5522 C allele was associated with a lower risk of arrhythmias. Results: The rs2070950 GG genotype and rs4635799 TT genotype were most common in patients who had LV end-diastolic volume increase < 20% and the same or increased LV ejection fraction, indicating a possible protective effect of these SNPs. A total of 127 AMI patients underwent transthoracic echocardiography follow-up after 72 h and 6 months. Methods: A cohort of 301 AMI patients who underwent revascularization was included. Objective: To study the impact of the NR3C2 rs2070950, rs4635799 and rs5522 gene polymorphisms on left ventricular (LV) remodeling, rhythm and conduction disorders in AMI patients. Prior studies reported an association between the presence of NR3C2 single-nucleotide polymorphisms (SNPs) and an increased cortisol production during a stress response such as acute myocardial infarction (AMI), which may lead to adverse cardiac remodeling. ![]() Background: The NR3C2 gene encodes the mineralocorticoid receptor, which is present on cardiomyocytes. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |