biochemical changes in atrial fibrillation 2

  • Research type

    Research Study

  • Full title

    Defence mechanisms against oxidative stress in atrial fibrillation

  • IRAS ID

    234855

  • Contact name

    Chris Peers

  • Contact email

    c.s.peers@leeds.ac.uk

  • Sponsor organisation

    University of Leeds

  • Duration of Study in the UK

    2 years, 11 months, 30 days

  • Research summary

    Atrial fibrillation (AF) is the most common form of disturbed electrical activity (arrhythmia) in the heart. It leads to stroke, heart failure and other life-threatening cardiac complications particularly in the elderly and middle-aged. AF-associated mortality is 3.5% per year. Disruption of electrical activity arises partly by changes in the activity and levels of specific proteins called ion channels which control electrical activity. Research by a number of groups including my own has shown that changes in channel activity seen in pathological conditions causing cardiovascular diseases such as arrhythmias can be significantly reduced by agents known as gasotransmitters. These are naturally occurring gases which, although best known as toxic agents, are actually generated inside most cells of the body. These gases include carbon monoxide and hydrogen sulfide, and each is produced by specific proteins (enzymes).
    Using a cell culture system, we have recently discovered that one of the key ion channel proteins controlling electrical activity in the heart is regulated by both carbon monoxide and hydrogen sulfide. Furthermore, our work indicates that these gases may protect this channel from the damage of AF. This is an exciting discovery, since it could ultimately lead to the use of drugs which release these gases in a controlled manner being employed as a means of treating AF. To advance our studies, we need to know if the same enzymes are present in human atrial tissue of the heart, and whether the levels of these enzymes are in any way affected by AF. Similarly we need to know how the ion channels controlling electrical excitability are compromised in AF. We have the expertise to do this, using atrial tissue samples obtained during cardiopulmonary bypass surgery, samples which would otherwise be discarded. We are therefore seeking ethical permission to use these samples.

  • REC name

    North West - Liverpool Central Research Ethics Committee

  • REC reference

    17/NW/0555

  • Date of REC Opinion

    21 Sep 2017

  • REC opinion

    Further Information Favourable Opinion