Imperial college. UK: Scientists at Imperial College London have
developed a model that helps explain why we are more likely to develop
an abnormal heartbeat with age. The simple mathematical model also suggests why current treatments for the condition are not always successful.
The
model mimics how heart muscle tissue changes as we get older, focusing
on how the muscle cells in the heart link together to pass electrical
signals that create the heartbeat. Simulating these processes in the
model has suggested new avenues for treating abnormal heart rhythms, but
the results will need to be confirmed in experiments.
The research, published today in Physical Review Letters, is a collaboration between Imperial physicists and Nicholas Peters, Professor of Cardiology at Imperial’s National Heart and Lung Institute.
As
we age, we develop fibrosis, which is when connective tissue grows
within the heart muscle, cutting off the connections between the muscle
cells. Our risk of atrial fibrillation - the most common abnormal heart
rhythm and the single biggest cause of stroke – also increases with age,
but the mechanism of how this develops is still not understood.
The
model represents how cells are organised and connected within heart
muscle tissue and how that changes with age. It was able to show that
when fibrosis caused the ‘uncoupling’ of the muscle cells to reach a
critical point, then atrial fibrillation would occur. The model also
mirrored what’s known to happen in patients – that atrial fibrillation
initially occurs for very short periods, which gradually get longer as
the condition progresses.
Professor Kim Christensen, from Imperial’s Department of Physics,
said: “The model we’ve created is a very simple representation, yet it
is able to reproduce the behaviour of a very complex condition. It
showed that atrial fibrillation only occurred when fibrosis within the
heart muscle had reached a particular tipping point. This might offer a
way in the future to assess the risk of developing the condition as well
as inform possible treatments.”
One common treatment for atrial fibrillation is a technique called
ablation, where areas of the heart are destroyed by radiofrequency
energy to prevent the disorganised signals occurring. However, there is
limited evidence showing which areas should be targeted for ablation and
the treatment is not always successful.
The model showed that if
ablation was targeted at regions where the fibrosis had caused extensive
uncoupling of the muscle cells, then the atrial fibrillation would
stop. Although it’s possible to identify fibrotic regions in MRI scans, Kishan Manani, a PhD student from Imperial’s Department of Physics, stresses that simply targeting any kind of fibrosis isn’t the answer.
“Only
a certain type of fibrosis, where the cells were structured in a
certain way, appeared to cause atrial fibrillation in our model and it
was only when these areas were targeted that the fibrillation would
stop,” he explains. “Unfortunately, it’s not currently possible to
identify cellular structure at this level within patients, but our
findings do highlight where future research could be targeted. Our work
is a prime example of how a real, complex phenomenon can be studied with
a simple model. What we’ve essentially provided in the model is a
hypothesis that now needs to be tested experimentally.”
Reference:
'Simple Model for Identifying Critical Regions in Atrial Fibrillation'
by Kim Christensen, Kishan A. Manani and Nicholas S. Peters, Physical Review Letters, 16 January 2015. DOI: http://dx.doi.org/10.1103/PhysRevLett.114.028104