LMITransactions&Report2014-15

LMI Transactions and Report 2014 - 2015
components of cardiac output to improve heart
failure. Most devices were battery operated with
leads to the appropriate areas of the heart. The leads
were able to sense cardiac electrical impulses and
deliver an appropriate electrical stimulation.
The majority of pacemakers inserted are dual chamber
with leads to both atria and ventricle. Single chamber
pacing is occasionally indicated in the atrium for sinus
node dysfunction with normal atrio-ventricular
conduction or ventricular pacing only for ventricular
rate control resistant atrial fibrillation. Cardiac
function is best maximised by efficient synchronised
atrial and ventricular activity. The existence of an
intraventricular bundle branch block results in
dysfunctional ventricular activity, in particular a left
bundle branch block gives rise to a dysfunctional left
ventricular contraction. In the past, pacing of the
right ventricle mimicked a left bundle branch block
and subsequent inefficient activity. This could be
overcome by pacing the posterolateral wall via the
coronary sinus requiring a 3 lead pacemaker.
Ventricular tachycardia or ventricular fibrillation is
amongst the commonest cause of sudden cardiac
death. Modern devices are able to sense ventricular
tachycardia or ventricular fibrillation to terminate it
and pace the ventricles. Unfortunately this technique
does not work for atrial fibrillation. Ventricular shock
so delivered can be painful but this is a relatively small
price. Dr Snowdon continued by briefly describing the
technique involved in the insertion of such devices.
The heart is approached from the systemic venous side
and a subcutaneous pocket is developed for the device
itself. Leads are of either a corkscrew or a grappling
hook type of end, which engages with the
trabeculations within the heart. Subcutaneous
defibrillation devices for ventricular tachycardia or
ventricular fibrillation have no intracardiac lead.
Intracardiac leads are continually moving and
therefore can become broken or moved from the
implanted position. Such devices will deliver a shock
to revert VT or VF but can only give rescue pacing.
Sudden cardiac death is usually of arrhythmic origin.
Implanted defibrillators do make patients live longer
but the anxiety about such attacks of VT or VF does
remain. In the presence of known episodes the risk of
death in five years, if untreated, is around 50%, and
the chance of surviving cardiac death outside hospital
is around 5%. In the presence of a known chance of
catastrophic arrhythmia implanted defibrillators
present a significant risk improvement. Life
expectancy is improved. Inappropriate shocks are
rare. Battery life of such devices is 5-8 years.
Indications for such devices are a known arrhythmic
problem, either familial or acquired with improved
long term survival following surgery for congenital
heart disease. Right ventricular failure can also present
an arrhythmic risk. The long term outcomes for the
different groups are obviously variable.
In the investigation of arrhythmias and syncope
attacks, external monitoring devices have a limited
use. Implantable loop recorders are capable of
monitoring for up to three years and usually record a
7-10 minute cycle overwritten if no event occurs. They
may be interrogated transcutaneously by telephone
without the necessity for visiting the monitoring
centre.
In recent years there have been significant
advancements in the scope of the use of such devices.
The risk of lead failure is now very low, battery life is
extended considerably and sophisticated electronics
are capable of sophisticated tasks. Although the
presence of an implanted device does improve patient
outlook, it is apparent that not all anxiety from
knowledge of the underlying condition is removed,
and patients continue to need significant
psychological support which at present is ill resourced.
The President thanked the two speakers from the
Liverpool Heart and Chest Hospital.
R Franks
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