Ageing to arrhythmias: conundrums of connections in the ageing heart

Authors

  • Sandra A. Jones

    Corresponding author
    1. Institute of Membrane and Systems Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK. Sandra A. Jones
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Correspondence: Sandra A. Jones, Level 10, Worsley Building, Institute of Membrane and Systems Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK. E-mail: s.a.jones@leeds.ac.uk

Abstract

The proportion of the population that is elderly continues to increase, leading to an increasing need to address problems chiefly associated with old age. Progressive ageing of the heart is associated with an increasing incidence of arrhythmias and disorders of the normal origin of the heartbeat, the sinoatrial node. This intrinsic pacemaker of the heart has an increasing tendency with age to lose its dominant role in pacing the heart, and regulation of heart rate becomes erratic. This ‘sick sinus syndrome’ is associated with fainting, palpitations, shortness of breath and sudden death. Current treatment of this condition is by implantation of an artificial pacemaker, an intervention increasingly required with age. The current evidence suggests that the normal heartbeat fails due to changes in the expression of critical proteins that ensure the correct production and conduction of the cardiac action potential. Depletion of a protein directly responsible for providing electrical connections between the cells of the heart, connexin 43, appears to leave the normal cardiac pacemaker disconnected and unable to drive the heart. This process may be associated with age-dependent changes in stress-related signalling. Simple interventions such as exercise could impact on the processes hypothesized to be involved and may offer a means to preserve the stability of the electrical activity of the heart into old age without pharmacological manipulation.

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