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Sudden Death From Stress Linked to Uneven Signals
Between Brain, Heart
Dec. 27, 2004 - Sudden cardiac death from emotional
stress, which kills about 60,000 each year in the U.S., may be triggered
by uneven signals from the brain to the heart, according to a study by
University College London scientists to be published in the January
issue of Brain.
UCL researchers have discovered that a system which
normally coordinates signalling from the brain to different parts of the
heart may be disrupted in some people, making them vulnerable to
potentially fatal abnormal heart rhythms during mentally taxing tasks or
emotional events such as family gatherings.
This is particularly true of people who already
have heart disease, but it is the brain that may be most responsible.
The new study suggests that uneven brain activity, in a region where
nerves link directly to the heart, seems to result in an uneven
distribution of signals across the heart, which stops the heart from
contracting normally.
Around a third of the 300,000 sudden cardiac deaths
which occur each year in the U.S. arise from a blood clot in a major
artery, which leads to a fatal heart attack. Mental stress is thought to
be responsible for a further 20 per cent of these deaths, but scientists
have been baffled by the exact mechanisms by which stress can bring on a
fatal short-circuiting of the heart.
In the UCL study, volunteers with a history of
heart disease were given stressful mental tasks while their brain
activity was monitored using PET imaging. Electrical waves travelling
across their heart were monitored using electrocardiogram analysis. The
study showed that stress-induced changes in electrical currents in the
heart were accompanied by uneven activity within the lower brain, in an
area known as the brainstem.
The brainstem is connected on the left and right side to the heart by
nerve pathways, known as autonomic nerves. These autonomic nerves
control heart rate during physical or mental activity.
To maintain a regular heartbeat, the electrical
currents that travel across the heart and initiate the heartbeat should
be smooth and even. If these electrical waves travel slower or faster in
parts of the heart, this can result in a short circuit which leads to
arrhythmia - an irregular heartbeat.
Normally, the output from the brainstem to the
heart via left and right autonomic nerves is symmetrical and does not
disrupt heart rhythm, even during stress. However, UCL scientists think
that, in some cases, the autonomic nerves fire unevenly during stress,
which disturbs the smooth electrical pattern across the heart and could
ultimately induce an irregular, and eventually fatal, heartbeat.
Dr Peter Taggart from UCL`s Centre for Cardiology
says: Some people are at risk of sudden death from stress, mainly
people who already have heart disease. In these cases the combination of
heart and brain irregularities means that heart failure could occur
during a stressful or emotional event like a family gathering or even a
boisterous New Year party.
Efforts to prevent the development of potentially
dangerous heart rhythms in response to stress have focused on drugs
which act directly on the heart, but results have so far been rather
disappointing. Our research focuses on what is happening upstream, in
the brain, when stress causes these heart rhythm problems. The results
so far are very encouraging.
It may soon be possible to identify which people
are particularly at risk and even to treat a heart problem with a drug
that works on the brain.
Dr Hugo Critchley from UCL's Institute of Neurology
says: The next stage of our research is to explore how signalling from
the brain becomes uneven. It seems that emotions and stress may
particularly activate the right hemisphere in the upper brain, but this
is usually balanced out into a symmetrical signal produced lower down in
the brainstem, possibly though a mechanism that works as a protective
balancing relay.
Some patients with epilepsy produce strong
one-sided brain activity during fits and may also show asymmetric
changes in the heart, suggesting that the relay system is by-passed. In
apparently healthy people, it is possible that massive amounts of stress
may also overload the system so that the brain's normal conversion to a
balanced symmetric heart response is overcome, leading to arrhythmia.
Ultimately we would like to establish whether
there might be a therapeutic target in the brain for people at risk of
stress-induced heart problems. Some medicines already reduce emotional
stress responses and help reduce the risk of sudden heart problems, but
we hope to develop more selective treatments that eliminate the need to
dampen emotional responses in order to reduce the risk of arrhythmia and
sudden death.
This study was funded by the Wellcome Trust (
http://www.wellcome.ac.uk/ ).
Mental stress and sudden cardiac death: asymmetric
midbrain activity as a linking mechanism, by Hugo D. Critchley, Peter
Taggart, Peter M. Sutton, Diana R. Holdright, Velislav Batchvarov,
Katerina Hnatkova, Marek Malik, and Raymond J. Dolan, will be published
in the January edition of Brain (http://www.brain.oupjournals.org/
).
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