Mechanics of sudden death. Can we link engineering and basic medical sciences?
R. Saumarez
Papworth Hospital
Many heart diseases can cause sudden death due to an abnormal rhythm
of the heart. In normal hearts there is fast and highly ordered
activation leading to effective contraction and ejection of blood into
the rest of the body. In disease, abnormal activation of the heart can
occur which may degenerate into a series of random waves of activation
through its muscle causing ineffective contraction, failure to eject
blood into the body and death. Sudden death due to this rhythm,
ventricular fibrillation (VF), can now be prevented by a device
(implantable cardioverter-defibrillator - ICD) which is implanted in
the body and will detect and correct abnormal rhythms when they
occur. A major problem is to determine if a patient with a particular
disease is at risk of sudden death and should receive an ICD.
The conditions in diseased heart muscle which allow VF to develop are
known as the 'substrate'. One component of the substrate for VF can be
shown to be different conduction delays through heart muscle. We have
developed methods of measuring activation delays, and presence of a VF
substrate, in patients with diseases that place them at risk of sudden
death. There is a very strong association between the risk of sudden
death and the presence of delayed activation. This effect is seen in
all the diseases which we have studied and may be a universal marker
of a risk of sudden death.
Experiments in isolated animal hearts have reproduced some of the
effects seen in patients by using drugs to manipulate conduction
through the heart. Some features of animal and human data have been
reproduced using a mathematical model of conduction and electrical
properties of cardiac cells. Development of these approaches in unison
may lead to better understanding of the mechanisms of sudden death and
its prevention.
Finally, the general approach to mathematical models of the heart will
be discussed with reference to measurable data and goals of models to
study cardiac disease.
