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Thesis topic proposal
 
Mechanisms and novel pharmacological treatment options in atrial fibrillation

THESIS TOPIC PROPOSAL

Institute: University of Szeged
theoretical medicine
Doctoral School of Multidisciplinary Medical Scienses

Thesis supervisor: István Baczkó
Location of studies (in Hungarian): Department of Pharmacology and Pharmacotherapy, Faculty of Medicine
Abbreviation of location of studies: SZTE


Description of the research topic:

Atrial fibrillation (AF) is the most common sustained arrhythmia and it is associated with significant morbidity and mortality, especially due to the increased risk of heart failure and stroke. The prevalence of AF increases with age, with 0.5% of patients affected in the 50 year old range, ~10% over the age of 80 and the prediction is that it would increase in the future. State-of-the-art invasive electrophysiological intervention and current pharmacological treatment of AF have limited efficacy in a number of patients with remodeled atria and persistent/permanent AF. Moreover, traditional antiarrhythmic drugs used for AF treatment were originally developed for ventricular arrhythmias leaving a clearly unmet need for better pharmacological management of AF.
In this program, the student gains insight into the mechanisms underlying different clinical forms of AF and into novel trends and current efforts for improved future pharmacological management of AF. The candidate will master in vitro and in vivo experimental techniques in cardiac electrophysiology and experimental AF, and contributes to the identification of novel pharmacological modalities of the treatment of AF.

Required language skills: English B2
Number of students who can be accepted: 1

Deadline for application: 2023-06-12


2024. IV. 17.
ODT ülés
Az ODT következő ülésére 2024. június 14-én, pénteken 10.00 órakor kerül sor a Semmelweis Egyetem Szenátusi termében (Bp. Üllői út 26. I. emelet).

 
All rights reserved © 2007, Hungarian Doctoral Council. Doctoral Council registration number at commissioner for data protection: 02003/0001. Program version: 2.2358 ( 2017. X. 31. )