Is the nervous system involved in abnormal heart rhythms in acquired long QT syndrome?
Dr James Winter (lead researcher)
University of Birmingham
Start date: 01 August 2016 (Duration 4 years)
Autonomic modulation of torsades de pointes in acquired long QT syndrome
BHF Intermediate Basic Science Research Fellow Dr James Winter is studying long QT syndrome, a disorder of the heart’s electrical system, characterised by a typical pattern on an electrocardiogram. Long QT syndrome can be inherited because of a faulty gene that affects ion channels, the structures that control the flow of electricity in the heart. But it can also be a side effect of drugs (acquired long QT syndrome). In both inherited and acquired long QT syndrome, the electrical disturbance can trigger a dangerous abnormal heart rhythm called torsades de points, which can become so severe that the heart stops beating, leading to sudden cardiac death. We know that the autonomic nervous system, which controls subconscious body functions such as breathing, digestion and the heartbeat, is important in sudden cardiac death in inherited long QT syndrome, but much less is known about its contribution to acquired long QT syndrome. In this project, Dr Winter will find out if stimulating autonomic nerves causes torsades de points in acquired long QT syndrome. To do this, he will develop a new laboratory model of torsade de points, where drugs are used to induce the abnormal heart rhythm. Dr Winter’s research will try to better understand how changing the activity of the autonomic nervous system affects susceptibility to this dangerous heart rhythm. Understanding how the autonomic nervous system is involved in acquired long QT syndrome may reveal new ways to prevent this dangerous side effect of drugs and could lead to new treatments for the inherited condition as well.
Project details
Grant amount | £493,874 |
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Grant type | Fellowships |
Application type | Intermediate Basic Science Research Fellowship |
Start Date | 01 August 2016 |
Duration | 4 years |
Reference | FS/16/35/31952 |
Status | In Progress |