Personalized Medicine in the Treatment of Atrial Fibrillation: Myth or Reality?

Abstract

Due to the spectacular progress made in human genomic studies, molecular biology and genetics have become an essential part of modern medicine making it possible to early detect the risk factors and select the personalized treatment. The genetic studies have been widely used in the diagnosis and treatment of arrhythmias. Significant advances in the study of electrophysiological and genetic mechanisms of life-threatening arrhythmias have been achieved through studies of familial conditions with high risk of sudden cardiac death. However, the area of special interest for a practitioner is the identification of mutations associated with atrial fibrillation (AF). The novel methods enable us to study histological, structural, cellular and molecular causes of this arrhythmia. The two main directions of molecular genetic studies of AF are the identification of genetic mutations causing familial atrial fibrillation and the study of different genes polymorphism predisposing to arrhythmia in general population. Gene polymorphism screening helps both identify AF risk factors and predict its evolution from paroxysmal to chronic type. Emerging genetic studies provided explanation for the variable efficacy of antiarrhythmic drugs. It can be assumed that the clinical use of genetic methods will allow accurate and personalized selection of antiarrhythmics. Currently, therapeutic drug monitoring is widely recommended for a number of medications including cytostatics, aminoglycosides, anticonvulsants, and, by some researchers, antiarrhythmic and anticoagulant drugs. Medicine from the very beginning was intended to be personalized, but until recently it was a little more than a myth. The discovery of the human genome makes it possible to choose the most effective treatment with minimal adverse drug reactions for a particular patient.

Role of genetic research in the prevention of life-threatening rhythm and cardiac conduction disorders in young people

“…Частота случаев ВСС среди пациентов с синдромом WPW составляет от 0,15 до 0,39% [2,28]. При коротком антеградном рефрактерном периоде пучка Кента проведение импульсов на желудочки с высокой частотой во время ФП может привести к фибрилляции желудочков [29][30][31]. В рутинной клинической практике не используется генетическая диагностика [29].…”

“…У противоположного пола такой взаимосвязи не обнаружено, что, возможно, обусловлено гормональными влияниями [28]. Мутация гена KCNA5 приводит к увеличению длительности потенциала действия кардиомиоцитов предсердий и значительно увеличивает риск развития ФП [30]. Кроме того, при ФП была выявлена гетерозиготная мутация в гене NPPA, кодирующем предсердный натрийуретический пептид [30].…”