Gene-guided therapy for catheter-ablation of atrial fibrillation: are we there yet?

Huang, Henry; Darbar, Dawood

doi:10.1007/s10840-015-0086-1

Cited by 3 publications

(3 citation statements)

References 27 publications

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“…Этот аллельный вариант также связан с увеличенным диаметром правого предсердия, при этом полиморфизмы rs2106261 и rs7193343 в гене ZFHX3, также являющиеся факторами риска идиопатической ФП и анализируемые в нашей работе, не связаны с риском рецидива аритмии. В любом случае все эти полиморфизмы можно рассматривать и как критерий при выборе тактики лечения фибрилляции предсердий, и как прогностический фактор результата лечения [24], но при этом анализировать полиморфизмы в генах транскрипционных факторов следует независимо друг от друга, поскольку их взаимное влияние не подтверждается [25].…”

Section: Discussionunclassified

Genetic aspects of lone atrial fibrillation in patients without structural heart disease

et al. 2019

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Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia. Among patients with AF the subgroup posessing AF without traditional risk factors is differentiated. Such patients are commonly referred as having lone AF and comprise 1020% of all cases. A number of studies have demonstrated that the background of AF, and in particular lone AF, have a substantial genetic component. Aims: To evaluate the influence of gene polymorphism to the development of atrial fibrillation in patients without concomitant valvular pathology and coronary artery disease. Materials and methods: The study included 174 patients with atrial fibrillation and 124 controls without any cardiovascular pathology. All patients were divided into two subgroups: with lone AF (n=94) and with concomitant arterial hypertension (n=80). All patients underwent a complex of clinical, instrumental (ECG, echocardiography, computed tomography of the pulmonary veins) and laboratory tests (thyroid hormones, inflammatory markers, fibrosis), as well as genetic analysis (determination of single nucleotide polymorphisms described as AF risk factors in genes AGXT2, PDE4D, SLN, SCN5A, PITX2, PRRX1, ZFHX3, TBX5, CAV1 и HCN4). Results: For the rare polymorphisms rs12291814 (SLN) and rs137854601 (SCN5A) wasnt found anyone carrier of the minor allele (C and A, respectively). In the both patient subgroups the minor allele T of rs2200733 in PITX2 (OR=3.18, p0.0001), minor allele G of rs3903239 in PRRX1, and minor alleles A of 2 polymorphisms rs2106261 and rs7193343 in ZFHX3 gene were revealed as risk factor of AF (OR=2.96, p0.0001, OR=2.02, p=0.0045, OR=1.64, p=0.04, respectively). We also revealed significant difference between AF and control groups for rs3807989 in CAV1: homozygotic state of minor allele A has a protective effect on the development of arrhythmias (OR=0.39). Conclusions: We revealed the association between the polymorphisms in genes regulating transcription and the development of atrial fibrillation. These polymorphisms have already described but their frequencies have never investigated in Russian population. But the polymorphisms influence to gene functions stays unclear, although attempts to investigate relationship between genotype and gene expression have been made. When the relationship will be discovered it can help us to modify our approach in treatment to patients with atrial fibrillation.

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Genetic aspects of lone atrial fibrillation in patients without structural heart disease

et al. 2019

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“…Initial observations suggest that the haplotype of common AF‐related variants modifies the outcome of anti‐arrhythmic therapy (Parvez et al . ; Huang & Darbar, ), suggesting that rhythm control therapy could benefit from precision and personalisation based on genomic information.…”

Section: Introductionmentioning

confidence: 99%

PITX2‐dependent gene regulation in atrial fibrillation and rhythm control

Syeda

Kirchhof

Fabritz

2017

The Journal of Physiology

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Atrial fibrillation (AF) is a common arrhythmia. Better prevention and treatment of AF are needed to reduce AF‐associated morbidity and mortality. There are several major mechanisms that cause AF in patients, including a genetic predisposition to develop AF. Genome‐wide association studies have identified genetic variants associated with AF populations, with the strongest hits clustering on chromosome 4q25, close to the gene for the homeobox transcription factor PITX2. The effect of these common gene variants on cardiac PITX2 mRNA is currently under study. PITX2 protein regulates right–left differentiation of the embryonic heart, thorax and aorta. PITX2 is expressed in the adult left atrium, but much less so in other heart chambers. Pitx2 deficiency results in electrical and structural remodelling, and impaired repair of the heart in murine models, all of which may influence AF through divergent mechanisms. PITX2 levels and single nucleotide polymorphisms on chromosome 4q25 may also be a predictor of the effectiveness of anti‐arrhythmic drug therapy.

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“…In suggesting that these SNPs may relate to the observations in the clinical laboratory, their insights may help reconcile the many and varied electrophysiologic and disease state findings associated with this arrhythmia. In a prescient editorial, Huang and Darbar place these new observations in perspective, and how they can potentially fit into the embryology and development of the arrhythmia substrate as well as the electrophysiology of sinoatrial and atrial arrhythmias [6].…”

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confidence: 99%

Tailoring interventional arrhythmia therapy to individual patients: seeking the Art and the Science of Cardiac Electrophysiology in 2016

Saksena

2016

J Interv Card Electrophysiol

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Gene-guided therapy for catheter-ablation of atrial fibrillation: are we there yet?

Cited by 3 publications

References 27 publications

Genetic aspects of lone atrial fibrillation in patients without structural heart disease

Genetic aspects of lone atrial fibrillation in patients without structural heart disease

PITX2‐dependent gene regulation in atrial fibrillation and rhythm control

Tailoring interventional arrhythmia therapy to individual patients: seeking the Art and the Science of Cardiac Electrophysiology in 2016

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