Detection of Subclinical Paroxysmal Atrial Fibrillation and Its Correlation with Candidate Genes in Patients with Cryptogenic Ischemic Stroke and TIA

A. Petrovičová, E. Kurča, A. Andrášová, J. Bernatova, P. Blaško, T. Burjanivová, T. Duris, M. Grendár, J. Hasilla, B. Malicherová, V. Nosáľ, P. Obona, L. Pátrovič, Š. Sivák, P. Snopek, M. Svetlosak, P. Vahala, D. Čierný
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引用次数: 0

Abstract

Abstract Introduction: Cardioembolic etiology is assumed to be the most frequent cause of cryptogenic strokes. The detection of subclinical paroxysmal atrial fibrillation (AF) is important in the correct choice of preventive treatment. The aim of this prospective study was to detect the incidence of AF in patients with a cryptogenic stroke or transient ischemic attack (TIA) and to evaluate the association between the presence of AF and selected single-nucleotide polymorphisms (SNP). Methods: Patients with a cryptogenic stroke/ TIA (n=100) and a control group (n=15) of volunteers without significant cardiovascular disease were included in the study during the period of 2014 to 2019. To detect AF they underwent 12 months of ECG monitoring using an implanted loop recorder (ILR). Genotyping for SNPs rs10033464, rs2200733, rs225132, and rs2106261 was performed by a high resolution melting analysis. Results: We found AF to be present in 24 (24%) patients with a cryptogenic stroke/TIA, versus no subjects in the control group. The SNPs rs2106261, rs2200733, rs225132, and rs10033464 were not found to be associated with AF in our study (p=0.240; 1.000; 0.887; 0.589). However, a weak trend for a higher frequency of rs2106261 risk allele A homozygotes was observed in the patients with AF compared to the patients without AF (0.416 vs. 0.263, p=0.073). Homozygotes for allele A of rs2106261 were also present in a significantly higher frequency in AF patients compared to the controls (0.416 vs. 0.133, p = 0.012). Conclusion: In our study paroxysmal AF was a probable etiological factor in 24% of patients with cryptogenic ischemic stroke / TIA during the 12 months of monitoring. The homozygous allele A of rs2106261 was identified to be the possible genetic risk factor of AF, but this should be verified in larger cohorts. The study has been registered at www.clinicaltrials.gov, identifier NCT02216370.
隐源性缺血性脑卒中和TIA患者亚临床发作性心房颤动的检测及其与候选基因的相关性
摘要简介:心脏栓塞病因被认为是隐源性中风最常见的原因。亚临床阵发性心房颤动(AF)的检测对于正确选择预防性治疗至关重要。这项前瞻性研究的目的是检测隐源性中风或短暂性脑缺血发作(TIA)患者的房颤发生率,并评估房颤的存在与所选单核苷酸多态性(SNP)之间的关系。方法:2014年至2019年期间,将患有隐源性脑卒中/TIA的患者(n=100)和没有严重心血管疾病的志愿者对照组(n=15)纳入研究。为了检测房颤,他们使用植入的环路记录器(ILR)进行了12个月的心电图监测。通过高分辨率熔解分析对SNPs rs10033464、rs2200733、rs225132和rs2106261进行基因分型。结果:我们发现24例(24%)隐源性脑卒中/TIA患者存在房颤,而对照组中没有受试者。在我们的研究中,未发现SNPs rs2106261、rs2200733、rs225132和rs10033464与房颤相关(p=0.240;1.000;0.887;0.589)。然而,与非房颤患者相比,房颤患者rs2106261危险等位基因a纯合子的频率呈微弱趋势(0.416 vs.0.263,p=0.073)。与对照组相比,房颤动患者rs2106.261等位基因的纯合子频率也明显更高(0.416 vs 0.133,p=0.012)。结论:在我们的研究中,阵发性房颤可能是在监测的12个月内,24%的隐源性缺血性脑卒中/TIA患者的病因。rs2106261的纯合等位基因A被确定为AF的可能遗传风险因素,但这应该在更大的队列中得到验证。该研究已在www.clinicaltrials.gov上注册,标识符为NCT02216370。
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来源期刊
自引率
0.00%
发文量
11
审稿时长
14 weeks
期刊介绍: Acta Medica Martiniana is a medical scientific journal, first published in print form in December 2001. It is a continuation of the journal / almanac Folia Medica Martiniana (1971 - 1996). The journal‘s owner is the Jessenius Faculty of Medicine, Comenius University, Slovakia. Dissemination of research results and scientific knowledge from all areas of medicine and nursing. Stimulation, facilitation and supporting of publication activity for the young medical research and clinical generation. The contributions of young novice authors (PhD students and post-doctorials) are particularly welcome. Acta Medica Martiniana is an open-access journal, with a periodicity of publishing three times per year (Apr/Aug/Dec). It covers a wide range of basic medical disciplines, such as anatomy, histology, biochemistry, human physiology, pharmacology, etc., as well as all clinical areas incl. preventive medicine, public health and nursing. Interdisciplinary and multidisciplinary manuscripts, including papers from all areas of biomedical research, are welcome.
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