﻿ ﻿﻿ Atrial Fibrillation caused by Mutations – Methods for Recognition of Conditions when Genetic Predisposition becomes Reality
 Articolul precedent Articolul urmator 282 0 SM ISO690:2012CAPCELEA, Svetlana; SIDORENKO, Ludmila. Atrial Fibrillation caused by Mutations – Methods for Recognition of Conditions when Genetic Predisposition becomes Reality. In: NANO-2019: Limits of Nanoscience and Nanotechnologies. 24-27 septembrie 2019, Chişinău. Chișinău, Republica Moldova: 2019, p. 50. EXPORT metadate: Google Scholar Crossref CERIF DataCiteDublin Core
NANO-2019: Limits of Nanoscience and Nanotechnologies 2019
Conferința "SPINTECH Summer school “S/F Hybrid Structures for Spintronics”"
2019, Chişinău, Moldova, 24-27 septembrie 2019

 Atrial Fibrillation caused by Mutations – Methods for Recognition of Conditions when Genetic Predisposition becomes Reality

Pag. 50-50

 Capcelea Svetlana, Sidorenko Ludmila ”Nicolae Testemițanu” State University of Medicine and Pharmacy Disponibil în IBN: 23 ianuarie 2020

Rezumat

More and more studies research genetic mechanisms of heart rhythm control and constitutional arrhythmia [1]. These tendency has started after publishing the results of CASTII study [2]. As shown in the CASTII study pharmacotherapy of atrial fibrillation is quite problematic regarding the proarrhythmic effects of the antiarrhythmical drugs of class I antiarrhythmics (Vaughan Williams classification). But even such a modern non-pharmacologic method method as PVI has a high rate of recurrence, about 60% and an amount of non-responders about 15-25% [2]. So with non-responders, other pathomechanisms are responsible. There are more than 100 genes effecting the heart rhythm [1]. Mutation in any of these genes leads to arrhythmia. Arrhythmias are very heterogenouse, but still atrial fibrillation is the most common sustained arrhythmia in cardiology, it is an arrhythmia which affects about six million people in the EU [3]. Majority of inherited arrhythmias are autosomal dominant, thus have familial characteristic and the risk to inherit the disease is 50%. The aspect which could be influenced by medicine is recognition of circumstances which ensure the realisation of genetic predisposition into arrhythmia. Genetic predisposition is not expressed into disease until the compensatory mechanisms of the functional systems in the organism function properly. The main feature which represents the compensatory capacity of functional systems is parasympathetic part of the vegetative nervous system [4]. As shown in the study of Sidorenko L. et al. patients had atrial fibrillation recurrence after the parasympathetic steering systems of the heart were broken down [5]. It happens even in patients who are non responder to several treatment methods, so probably, with a genetic predisposition to atrial fibrillation. In this study methods for recognition of parasympathetic insufficiency are described. These methods are very sensitive, allowing recognition of early stages of parasympathetic insufficiency. So this can be applied for prediction of the atrial fibrillation onset. It means, it could be the moment when doctors can interfere with, in order to prevent atrial fibrillation’s onset, applying methods for restoring the parasympathetic functional capacity. This should be researched on a clinical study, checking the possibility of the found methods for preventing the atrial fibrillation onset and prolonging the time of conversion of the genetic predisposition to atrial fibrillation into its clinical manifestation.

### Dublin Core Export

<?xml version='1.0' encoding='utf-8'?>
<oai_dc:dc xmlns:dc='http://purl.org/dc/elements/1.1/' xmlns:oai_dc='http://www.openarchives.org/OAI/2.0/oai_dc/' xmlns:xsi='http://www.w3.org/2001/XMLSchema-instance' xsi:schemaLocation='http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd'>
<dc:creator>Capcelea, S.V.</dc:creator>
<dc:creator>Sidorenko, L.</dc:creator>
<dc:date>2019</dc:date>
<dc:description xml:lang='en'><p>More and more studies research genetic mechanisms of heart rhythm control and constitutional arrhythmia [1]. These tendency has started after publishing the results of CASTII study [2]. As shown in the CASTII study pharmacotherapy of atrial fibrillation is quite problematic regarding the proarrhythmic effects of the antiarrhythmical drugs of class I antiarrhythmics (Vaughan Williams classification). But even such a modern non-pharmacologic method method as PVI has a high rate of recurrence, about 60% and an amount of non-responders about 15-25% [2]. So with non-responders, other pathomechanisms are responsible. There are more than 100 genes effecting the heart rhythm [1]. Mutation in any of these genes leads to arrhythmia. Arrhythmias are very heterogenouse, but still atrial fibrillation is the most common sustained arrhythmia in cardiology, it is an arrhythmia which affects about six million people in the EU [3]. Majority of inherited arrhythmias are autosomal dominant, thus have familial characteristic and the risk to inherit the disease is 50%. The aspect which could be influenced by medicine is recognition of circumstances which ensure the realisation of genetic predisposition into arrhythmia. Genetic predisposition is not expressed into disease until the compensatory mechanisms of the functional systems in the organism function properly. The main feature which represents the compensatory capacity of functional systems is parasympathetic part of the vegetative nervous system [4]. As shown in the study of Sidorenko L. et al. patients had atrial fibrillation recurrence after the parasympathetic steering systems of the heart were broken down [5]. It happens even in patients who are non responder to several treatment methods, so probably, with a genetic predisposition to atrial fibrillation. In this study methods for recognition of parasympathetic insufficiency are described. These methods are very sensitive, allowing recognition of early stages of parasympathetic insufficiency. So this can be applied for prediction of the atrial fibrillation onset. It means, it could be the moment when doctors can interfere with, in order to prevent atrial fibrillation&rsquo;s onset, applying methods for restoring the parasympathetic functional capacity. This should be researched on a clinical study, checking the possibility of the found methods for preventing the atrial fibrillation onset and prolonging the time of conversion of the genetic predisposition to atrial fibrillation into its clinical manifestation.</p></dc:description>
<dc:source>NANO-2019: Limits of Nanoscience and Nanotechnologies () 50-50</dc:source>
<dc:title><p>Atrial Fibrillation caused by Mutations &ndash; Methods for Recognition of Conditions when Genetic Predisposition becomes Reality</p></dc:title>
<dc:type>info:eu-repo/semantics/article</dc:type>
</oai_dc:dc>