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Chronic Refractory
Angina
Cardiac
Rehabilitation for Refractory Angina: PART 2:
PSYCHOLOGICAL ASPECTS (authors)
Patient version (English)
A number of studies have shown that the degree of occlusion
of the patient's coronary arteries is not related
to;
-
the self report of the frequency, severity or
duration of angina,
-
the degree to which it impairs the patient's
life,
-
the degree to which patients report
'satisfactory' outcome from medical treatment.
In these studies it was psychological features such as
anxiety, depression, neuroticism and hypochondriasis that
were the best independent predictors of symptom report
and treatment success (typically at around the r=0.5
level)1,2,3,4,5.
Co-existing psychiatric illness.
Perhaps the most obvious psychological mechanisms
underlying undue symptom reporting are depression and
somatisation disorder. Anxiety, depression, neuroticism
and hypochondriasis are known to be predictors of
patients who will `fail' medical treatment3,
report more angina (despite having no worse CAD) or
report a less satisfactory outcome from coronary artery
bypass surgery5. It is important to remember
that psychological distress is not related to the
extent of CAD in angina patients or to residual
physiological impairment following MI. In coronary artery
disease there may also be a psycho-biological interaction
between depression and ischaemia5. These facts
suggest that it would be advisable to screen patients for
anxiety and depression and where these exist, to attempt
to treat them before resorting to more expensive and
invasive treatments. A simple measure such as the
Hospital Anxiety and Depression Scale6 is
acceptable to the vast majority of medical patients,
takes only a couple of minutes to complete and score and
has no insultingly psychiatric items. It was designed as
a screening tool for this purpose and patients scoring
above the norm should be referred to a clinical
psychologist (or liaison psychiatrist) for advice and
possible treatment.
Approximately 30% and 50% of anginal and ischaemic
episodes respectively are induced by emotion arousal7,8,
probably through dynamic factors such as coronary artery
spasm and possibly hyperventilation9,10,11.
Angina was named after the strangling sensation of
acute fear it evokes12 and it seems likely
that in anxious patients this increase in autonomic drive
may itself increase the ischaemic burden. Both relaxation
training and stress management have been shown, in a
number of trials, to reduce angina13.
Psychological treatment has also been shown to reduce
further acute events, mostly coronary artery bypass
surgery (by 50%) in angioplasty14 patients.
Patients who report that most of their angina is related
to emotional arousal, or who come close to panic during
an episode may greatly benefit from referral to a
psychologist. All too often these frequently admitted
patients are told that they have `unstable angina' as a
euphemism for panic or acute hyperventilation. Many are
aware how dangerous unstable angina is and are made more
anxious, compounding the problem. Most of these patients
will admit that `stress' may have something to do with
heart disease and/or bringing on their angina and will be
prepared to see a psychologist on an `exploratory basis'
to examine the possibility of learning to control stress.
They should be reassured that no one thinks they are
`mad' or `making things up'.
The role of health beliefs
The patient's beliefs about the illness may also
influence the amount of symptoms experienced. This is
because they can lead to increased anxiety and unhelpful
ways of coping. Health beliefs have been shown to predict
both the use of health services and poor recovery after
MI15,16,17. For example, many patients believe
that angina is a lesser kind of heart attack and that
each episode further damages the heart. Or, that rest is
the cure for angina, rather than a temporary
reliever of it. These beliefs, often unwittingly
reinforced by health professionals15, usually
lead to a significantly reduced activity level and an
almost phobic avoidance of anything that might provoke
angina. This in turn may lower the ischaemic threshold
and lead to a morbid preoccupation with any sensations
from the chest. Both reduce the patient's quality of life
and may lead to dissatisfaction with treatment and a
demand for `something more' to be done.
Cognitive-behavioural treatment
A similar lack of relationship between impairment (the
lesion) and disability (disease burden) is common in
other chronic illnesses and has led to
cognitive-behavioural `disease management' programmes
being developed for complaints such as chronic pain. We
have developed and evaluated a similar programme for
patients with angina that attempts to address the
psychological factors described above18. It
was assessed in a trial, involving 80 patients, 40% of
whom were awaiting coronary artery bypass grafting
surgery (CABG) the others had already had surgery or
angioplasty but still had significant angina or, had been
considered for an interventional treatment but were
technically unsuitable. At one-year post treatment,
patients showed a mean reduction in episodes of angina of
70% with 30% per cent reporting no angina, a 65%
reduction in the use of nitrates and a 73% reduction in
self-reported disability. Of the 28 patients who were
awaiting elective coronary artery bypass surgery, 50%
were subsequently removed from the list following a
review by their cardiologists as it was felt that they
were unlikely to receive any further symptomatic
improvement. We have since gone on to compare this
treatment with patients randomly allocated to the
treatment, an exercise programme of the same duration or
to routine medical care. The results are to be published
elsewhere but they reinforce the treatment
recommendations presented in this article.
Unfortunately, in the UK, few patients with angina
receive cardiac rehabilitation19, indeed in
some centres it is used as an exclusion criterion! Even
fewer receive appropriate psychological interventions.
Conclusions
There are many psychological factors that can produce
or exacerbate angina. These factors help to explain why
some patients appear to cope with extensive disease and a
low ischaemic threshold and others find it intolerable
and demand further treatment. It may often be more
profitable to address these factors than to proceed to
more invasive, expensive and less proven remedies.
Cognitive-behavioural rehabilitation treatments have
demonstrated beneficial results and a clinical
psychologist with a cardiac interest can also be helpful;
unfortunately both are scarce resources. The guidelines
for refractory angina recognise the need for early and
continuous cardiac rehabilitation. The process should be
multi-disciplinary and involve careful assessment of
psychological status and suitability for appropriate
cognitive-behavioural treatment in combination with all
of the features of comprehensive CR.
Robert J P Lewin (University of York) and David A
Brodie (University of Liverpool).
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