Cardiac arrhythmias occur in millions of people worldwide and have been related with sudden cardiac death not only of heart failure patients but of healthy individuals as well. The existing pharmacological treatments focus mainly on the prevention of the symptoms rather than the pathogenetic mechanisms of arrhythmias. Additionally, drugs used to prevent arrythmias sometimes might have the opposite effect: they can cause arrhythmias.
In order to develop new specific drugs with greater and long-term effectiveness, it is required: i) in depth understanding of the molecular mechanisms of pathogenesis; ii) selection of the appropriate pharmaceutical compounds that might prevent the dysfunction of these mechanisms; iii) preclinical studies for the evaluation of the specific pharmaceutical compounds using an appropriate experimental model of cardiac arrhythmias.
Taking advantage of the new data that our research group had previously discovered regarding the molecular mechanisms that participate in physiological and pathological cardiac function, as well as the new, valuable for studying cardiac arrhythmias, genetically modified mouse model that we had created (junctin knockout, JKO), we performed a detailed characterization of two novel pharmaceutical compounds that were selected for their action on the molecular mechanisms of pathogenesis. Specifically, arrhythmias were induced in the JKO mice followed by administration of either of the two compounds. Extensive in vivo (intact mice) and in vitro (isolated cardiomyocytes) analysis demonstrated that one of the two substances significantly reduced arrhythmias at both levels (in vivo and in vitro). These findings suggest that the specific chemical compound could have a promising role in combating arrhythmias in the long run and merits further in depth analysis.
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