SPINAL
CORD STIMULATION FOR THE TREATMENT OF REFRACTORY ANGINA
Contents
Introduction
Safety
Mechanism of action of SCS
SCS implantation
Treatment of patients who are
anticoagulated
Types
of devices
Patient
selection
Complications
What next
Editors
The first description of the use of electricity for
angina is found in John Wesley's journal of 1774. He
wrote of a patient who “was reported to be dying of
the gout of the stomach, but on observing the symptoms, I
was convinced it was not the gout but the angina pectoris
(well described by Heberden, still more accurately by Dr
McBride, Dublin). I advised him to take no more medicine
but to be electrocuted through the breast. He was so. The
violent symptoms immediately ceased and he fell into a
sweet sleep.”
The gate theory of pain1
led to the first
stimulator being implanted by Norman Shealy2
for cancer pain, and its use in angina was reported as a
chance finding in a patient who had a stimulator for
another reason in 1984.3 Spinal cord
stimulators were originally implanted specifically for
intractable angina in Australia in 1987.4
Since then there have been over 70 publications on SCS in
refractory angina. These studies have confirmed
improvement in quality of life of these patients,5 fewer
ischaemic episodes 6 7 and reduced frequency
of hospital admissions.8 Moreover these
effects are long lasting9 and obtained at
negligible risk.10
Clinicians are naturally concerned about the potential
risks of masking myocardial ischaemia by spinal cord
stimulation. Studies have demonstrated that spinal cord
stimulation decreases lactate production with pacing11
and total ischaemic burden,6 without an
increase in silent ischaemia. It does not mask the pain
of a myocardial infarction12 and mortality
rates in patients with stimulators are similar to those
of the general population of patients with coronary
artery disease. 13 14
Spinal cord stimulation has been demonstrated to
promote local blood flow and ischaemic ulcer healing in
patients with peripheral vascular disease.15 16
Positron emission tomography (PET) shows a more
homogenous pattern of coronary flow following spinal cord
stimulation in patients with myocardial ischaemia but no
increase in total flow.17 18 This
redistribution of flow to areas that were previously
ischaemic, may explain why there is an increase in
exercise capacity prior to the inevitable onset of
angina. To date there has been no proof of an increase in
coronary flow velocity when patients undergo pacing
stress with spinal cord stimulation.19
It has been suggested that spinal cord stimulation
might alter the sympathetic/parasympathetic balance, but
no change in heart rate variability has been shown in a
group of patients post spinal cord stimulation.20
However Meglio found a decrease in resting heart rate and
features suggestive of a functional sympathectomy in 25
patients without coronary disease.21 Cerebral
PET scanning of patients with a spinal cord stimulator
demonstrated changes in blood flow22 in areas
that are known to be related to pain perception in
angina.23
SCS implantation
Spinal cord stimulator implantation is a surgical
procedure requiring complete aseptic technique and
prophylactic antibiotics. The system has three
components: an epidural lead with a number of electrodes
over a variable length, an extension lead and an
implanted pulse generator. The patient lies prone on the
x-ray screening table and a Tuohy needle is placed
epidurally (using loss of resistance to confirm that it
is correctly sited) from a paramedian approach under
local anaesthetic at the level of T3-4 or T4-5. The
electrode is then fed through the needle and is
positioned in the midline at the appropriate level under
fluoroscopy. (For patients with angina this is usually
with the tip at C6/7 and the electrode at T1/3.) Then the
electrode is attached to an external stimulator which
produces paraesthesia. The final position of the
electrode is determined when the area of paraesthesia
produced matches that where pain is usually experienced.
The distance between the insertion point and electrode
tip should be as long as possible to minimise the risk of
dislocation.
The patient is then turned over and anaesthetised as
the remainder of the implantation can be painful. The
generator box (very similar to a pacemaker) is placed
subcutaneously in the left side of the abdomen (in a
comfortable position that has been determined prior to
the procedure with the patient standing) and it is then
connected to the electrode by an extension lead that is
also tunnelled under the skin. In some centres this is
performed on a different date to ensure the stimulation
achieved persists prior to the full implantation of the
device. At our centres, both steps are carried out at the
same time unless the area of pain is not covered by
paraesthesia. We justify this because of the increased
infection rate with two stage procedures means that some
patients might be denied the opportunity for quality of
life improvement simply because of infection.
Although epidural haematoma is a rare complication
following instrumentation of the epidural space, the
possible devastating consequences of this requires
serious consideration. Full anticoagulation has long been
considered a contraindication to epidural catheter
placement. However if this rule were to be applied
rigidly, many cardiac patients would be denied SCS, which
may represent their most promising therapeutic option.
Consultation with haematological colleagues is advised.
There are different indications for anticoagulation in
cardiac patients, which can be stratified into low-risk
e.g. atrial fibrillation with no previous embolic
history; and high-risk groups e.g. metal valve
replacement, when considering the temporary interruption
of their warfarin.
In the low risk group, anticoagulants can be stopped
and the stimulator implanted when the INR is <1.4.
This usually takes three days. In the high-risk group the
“therapeutic window” must be tightly controlled
to minimise the embolic risks to the patient without
exposing them to the risk of epidural haematoma. The
patient should be admitted five days prior to the
procedure, warfarin stopped and an intravenous infusion
of unfractionated heparin is commenced. Regular APTT
estimation is mandatory. On the day of implantation,
heparin is discontinued three hours prior to the start of
the procedure and APTT is checked once more to ensure
there is no coagulopathy. Following implantation, the
heparin infusion should be recommenced after 3 hours.
Warfarin can be restarted that same evening at the usual
loading dose and both drugs should run concomitantly
until full anticoagulation is achieved.
There is no evidence to suggest that the presence of a
catheter or wire stably located in the epidural space
exposes the patient to any additional risk.
There are two different sorts of generator. One type
has an internal power supply with an external antenna to
switch the device on and set the required amplitude. This
is less cumbersome but requires replacement usually after
4-6years. Another option is an internal receiver with an
external battery. An antenna is placed over the receiver
and connected to an external power supply. This
radiofrequency generator activates the implanted device,
producing stimulation. The battery can then be replaced,
thus avoiding box changes. At present a rechargeable
implantable device is in development.
All patients referred for spinal cord stimulators
should go through a pain management programme and have
experienced insufficient amelioration of their symptoms.
There is no evidence that stimulators are more beneficial
in patients without severe psychological difficulties.
Drug dependence is not a contraindication, but the
patients should be told prior to their implantation that
their opioids will be slowly withdrawn once adequate
analgesia has been achieved.
As with all interventional procedures there is a steep
“learning curve” and training is essential. All
operators are urged to attend one of the organised spinal
cord stimulator courses.
The greatest risk in these patients is of infection
that results in the system having to be removed. In
Taunton the infection rate is 3% if the procedure is done
over two stages and is lower if the entire procedure is
done at one sitting.
Lead displacement requiring re-exploration is
relatively common, but might be improved with newer lead
designs. Lead fracture is rare.
Epidural haematoma is a rare but severe acute
complication occurring in about 1/2000 according to the
total number of implants and anecdotal complications
reported. Local nursing guidelines should acknowledge the
possibility of this and the appropriate action that
should be taken.
Registry
An international registry is being pilotted at present
and all practitioners will be asked to contribute to the
dataset.
Spinal cord stimulation or surgery?
Spinal cord stimulation has been compared to coronary
artery bypass surgery in high-risk patients who were
undergoing intervention for symptomatic reasons only and
an expected increased risk of surgical complications.10
In this study there was a significant decrease in
frequency of angina attacks and use of short-acting
nitrates that was the same in both groups. The primary
aim of both treatments is to improve quality of life by
reducing symptoms. In this regard, both SCS and CABG
produced similar benefits. Surgery produced an additional
improvement in ischaemia on exercise testing at 6 months,
but this “bonus” was paid for at a high price
in that 4 patients died perioperatively.
SCS will not produce a satisfactory
result in a small proportion of patients in whom the
subsequent stages of the algorithm should be considered
after a full clinical and psychological reappraisal.
Conclusions
Spinal cord stimulation is a safe and effective
treatment in patients where neither CABG or PTCA are
possible. It may be an alternative to redo coronary
artery surgery or intervention in high risk patients.
SCS discussion page
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Clare Hammond MB ChB MRCP
Research Fellow in Cardiology*
PD Collins MB BS FRCA
Consultant Anaesthetist and Pain Specialist
†
Austin A Leach MB BS FFARCS
Consultant Anaesthetist and Pain Specialist*
Michael R Chester MB BS MRCP
MD Consultant Senior Lecturer in Cardiology*
*National Refractory Angina
Centre, Mersey Regional Cardiothoracic Centre,
Thomas Drive, Liverpool L14 3PE
†Taunton and Somerset
Hospital, Musgrove Park, Taunton, Somerset TA1
5DA
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