Scientists find missing piece in sudden cardiac death puzzle
28 Jul 2010 by Evoluted New Media
Genetic mutation in a protein is responsible for disrupting the electrical activity of the heart and causing sick sinus syndrome – a form of sudden cardiac arrest often during sleep.
Genetic mutation in a protein is responsible for disrupting the electrical activity of the heart and causing sick sinus syndrome – a form of sudden cardiac arrest often during sleep.
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Scientists unravel the puzzle of sudden cardiac death |
Sick sinus syndrome occurs when the electrical activity of the sinoatrial node – the heart’s pacemaker – is impaired. Sudden cardiac death occurs after an abrupt loss of consciousness within an hour of the onset of acute symptoms – often at night when the heart rate slows dramatically – and can affect the healthy elderly and well-trained athletes.
The protein SCN5A is involved in the generation of electrical activity in the heart, and scientists at the Universities of Manchester and Bristol found that mutation in this gene disrupts the heart’s normal rhythm.
“We did not know why some people with sick sinus syndrome would die suddenly, but now we know why risk can increase at night during sleep. Our findings may be an important step towards ways of preventing this,” said Professor Henggui Zhang from Manchester.
Scientists used experimental measurements from the sinoatrial node together with computer models to simulate electrical activity in cardiac tissue. They found a chemical which, when present in the nervous system of healthy people, acts to slow heart rate. In sick sinus syndrome patients, it may entirely prevent electrical activity spreading across the heart and lead to cardiac arrest.
“The computer models we have made have created the effects of the chemicals on the heart and we then tested this experimentally with results that supported the computer predications,” said Zhang, “We are now in a position to test other forms of sick sinus syndrome so we can hopefully identify common features that can lead us to more effective treatments.”
Professor Jules Hancox from the University of Bristol said the insights into the condition from this study are of great importance: “If other forms of sick sinus syndrome that involve mutation to different proteins in the heart are affected by nerve activity in the same way, this may identify a common target to reduce or eliminate risk of dangerous arrhythmia.”
Zhang hopes it may be possible to influence nerve activity in sick sinus syndrome patients via drugs or pacemaker devices.
