Research Johan Saenen

Abstract

Cardiac arrhythmias are the result of disorganised electrical signalling in the heart, affecting up to 33.5 million people worldwide and about 1-3% of the Belgian population. Moreover, as the prevalence of atrial fibrillation is expected to double the next 20 years, the clinical and economic impact of the disease is huge. The goal of the project is two-fold: (1) Establish a new and innovative tool for the synchronous stimulation of cardiomyocytes using light and circumventing the need for genetic manipulation and (2) Provide a proof of concept and initial protocol for a safer alternative for RF/cryo balloon cathether ablation. Both aims will be achieved by using a gold nanoparticle label, which specifically targets a cardiomyocyte surface marker. The gold nanoparticle will absorb LASER/LED light and produce heat. Depending on the rate of change in temperature, either photothermal stimulation or photothermal ablation is accomplished.

Researcher(s)

• Promoter: Labro Alain
• Co-promoter: Saenen Johan
• Co-promoter: Snyders Dirk
• Fellow: Coonen Laura

Research team(s)

Project type(s)

• Research Project

Abstract

Torsade de pointes (Tdp ), one of the most feared cardiac arrythmias is associated with QT prolongation on surface Ecg. This disease already known for some years as long QT syndrome (LQTS) is caused by underlying acquired or congenital disturbances in myocardial transmembrane ion channels causing action potential duration (APD) prolongation. At least six loci (LQTl-6) have already been identified causing congenital LQTS. Although a widespread variety of drugs have QT prolonging properties, many underlying causes for acquired LQTS still have to be identified. Moreover at the level of the cardiac ion channels many biophysical, cell biological and pharmacological mechanisms underlying QT prolongation stili remain unclear. Therefor, the purpose of this research is to study the electrophysiological characteristics of LQT-related cardiac ion channels and the cell biological processes necessary for functional expression to identify the pathogenesis of both acquired and congenital LQTS. The studies are conducted through Whole cell Patch Clamp techniques and if necessary during pharmacological incubation. Confocal microscopy is used to study possible trafficking deficiencies in LQTS.

Researcher(s)

• Promoter: Snyders Dirk
• Co-promoter: Raes Adam
• Co-promoter: Vrints Christiaan
• Fellow: Saenen Johan

Research team(s)

Project type(s)

• Research Project

Abstract

Torsade de pointes (Tdp ), one of the most feared cardiac arrythmias is associated with QT prolongation on surface Ecg. This disease already known for some years as long QT syndrome (LQTS) is caused by underlying acquired or congenital disturbances in myocardial transmembrane ion channels causing action potential duration (APD) prolongation. At least six loci (LQTl-6) have already been identified causing congenital LQTS. Although a widespread variety of drugs have QT prolonging properties, many underlying causes for acquired LQTS still have to be identified. Moreover at the level of the cardiac ion channels many biophysical, cell biological and pharmacological mechanisms underlying QT prolongation stili remain unclear. Therefor, the purpose of this research is to study the electrophysiological characteristics of LQT-related cardiac ion channels and the cell biological processes necessary for functional expression to identify the pathogenesis of both acquired and congenital LQTS. The studies are conducted through Whole cell Patch Clamp techniques and if necessary during pharmacological incubation. Confocal microscopy is used to study possible trafficking deficiencies in LQTS.

Researcher(s)

• Promoter: Snyders Dirk
• Co-promoter: Raes Adam
• Co-promoter: Vrints Christiaan
• Fellow: Saenen Johan

Research team(s)

Project type(s)

• Research Project