Q J Med 1999; 92: 81-86
© 1999 Association of Physicians
Group psychological treatment for chest pain with normal coronary arteries
From the University Department of Psychiatry, Royal Edinburgh Hospital, Edinburgh, UK
Received 3 August 1998
Dr S.G. Potts, Department of Psychological Medicine, Royal Edinburgh Hospital, 1 Lauriston Place, Edinburgh EH3 9YW
 |
Summary |
|---|
 Top Summary IntroductionMethodsResultsDiscussionReferences |
|---|
We used a psychological treatment package (education, relaxation, breathing training, graded exposure to activity and exercise, and challenging automatic thoughts about heart disease) to treat 60 patients who had continuing chest pain despite cardiological reassurance following haemodynamically normal angiography. The treatment was delivered in six sessions over eight weeks to groups of up to six patients. The patients kept daily records of chest pain episode frequency and nitrate use. Questionnaires were used to assess anxiety, depression and disability. Exercise tolerance was tested by treadmill electrocardiography, with capnographic assessment of hyperventilation. The results were compared with waiting-list controls. Treatment significantly reduced chest pain episodes (p<0.01) from median 6.5 to 2.5 per week. There were significant improvements in anxiety and depression scores (p<0.05), disability rating (p<0.0001) and exercise tolerance (p<0.05), and these were maintained at six month follow-up. Treatment reduced the prevalence of hyperventilation from 54% to 34% (p<0.01) but not the prevalence of ECG-positive exercise tests. Patients continuing to attribute their pain to heart disease had poorer outcomes. Group psychological treatment for non-cardiac chest pain is feasible, reduces pain, psychological morbidity and disability, and improves exercise tolerance.
|
Introduction |
|---|
|
TopSummaryIntroductionMethodsResultsDiscussionReferences |
|---|
As many as 20% of patients investigated for chest pain with coronary angiography have normal or near-normal coronary arteries.1 Long-term follow-up studies of this group reveal a low mortality2 but high morbidity in terms of chest pain and other physical symptoms.3 They are much disabled and make heavy use of medical resources;4 yet little is known about how to treat them. Psychological studies have consistently demonstrated levels of anxiety and depression which are higher than in comparable patients with proven coronary artery disease at angiography,5 and which persist at follow-up.6 It is therefore likely that these symptoms are not purely reactive, but operate as causal or maintaining factors, suggesting a role for psychological intervention. Klimes et al.7 have shown that individual cognitive behavioural psychotherapy improves symptoms and disability in non-cardiac chest pain, but scant resources limit the availability of such labour-intensive treatment. A programme which is similar in outline but delivered in groups has been shown to be effective in chest pain with definite coronary artery disease.8 We therefore compared the effect of group psychological treatment in patients with chest pain and normal coronary arteries against waiting-list controls.
|
Methods |
|---|
|
TopSummaryIntroductionMethodsResultsDiscussionReferences |
|---|
Recruitment
Potentially eligible subjects were identified via records of recent coronary angiograms in the Departments of Cardiology of the Royal Infirmary and Western General Hospitals in Edinburgh. Eligibility was confirmed by obtaining their medical records and applying the following criteria. Inclusion criteria: (i) aged 18–70; (ii) recent (within the last year) coronary angiography for the investigation of chest pain revealed coronary arteries which were either normal or <50% stenosed;3 (iii) chest pain continuing at least twice weekly after angiography, despite reassurance by the cardiology team; and (iv) residence within easy travelling distance of Edinburgh. Exclusion criteria: (i) past history of myocardial infarction; or (ii) serious concurrent physical or psychiatric illness.
Permission to approach subjects was sought from their general practitioners or consultant cardiologists as appropriate. Subjects were then contacted in writing, with follow-up telephone calls to those expressing interest.
Design
The study design is summarized in Figure 1
. Subjects were randomized to two groups: one entered treatment immediately after initial assessment, while the control group was assigned to a waiting period before being reassessed and then entering treatment. All subjects were reassessed after treatment finished, and then again a further six months later. This design allows a controlled comparison of treatment versus a waiting period; and, since all subjects were treated eventually, it also allows an uncontrolled comparison of pre- and post-treatment status.
|
Assessment
After documenting informed consent, subjects underwent a structured assessment comprising an interview, pain diaries, questionnaires, exercise tolerance testing, and capnography.
Initial interview
Demographic details, medical and psychiatric history and cardiac risk factors were recorded in a standardized way. Clinical features of chest pain were recorded with a modified version of the Master questionnaire.9
Attributions
Subjects attributions of the cause of their pain were recorded on a five-point Likert scale, responses ranging from `definitely cardiac' to `definitely not cardiac'.
Questionnaires
The following self-report questionnaires were administered. (i) Hospital Anxiety and Depression scale.10 A 14-item inventory covering non-somatic symptoms of anxiety and depression, intended for use in medical populations. It yields separate scores for anxiety and depression, with cut-offs indicating caseness above 11. (ii) The Nijmegen hyperventilation scale.11 A 16-item inventory of physical symptoms associated with hyperventilation, yielding a numerical score, values above 22 indicating probable abnormal breathing patterns. (iii) The Sickness Impact Profile (SIP).11 A 136-item inventory yielding measures of the impact of illness on various domains of everyday life, as well as an overall disability score. (iv) The Nottingham Health Profile (NHP).12 A 24-item inventory quantifying the impairments due to illness in six areas.
Diaries
Subjects were asked to complete chest-pain diaries for two consecutive one-week periods. They were asked to record, for each episode of pain, its duration, its severity (on a scale of 1–100), and the number of doses of nitrate they took in response.
Exercise electrocardiography
All subjects underwent exercise ECG testing using the modified Bruce protocol13 on a treadmill. A positive test was defined as one where ST depression >2 mm occurred, accompanied by typical pain. The test was ended once unequivocally positive, or when the subject reached either their age-predicted maximum heart rate, or the limit of their exercise tolerance. Test duration was recorded in all cases.
Capnography
Subjects were fitted with a face mask attached to a portable CO2 monitor with which end-tidal PACO2 was recorded at rest, throughout exercise testing, and for 5 min of recovery afterwards. Hyperventilation was defined as a sustained end-tidal PACO2 of <4.0 kPa.14
On subsequent assessments, all measures except the initial interview were repeated, and, for the post-treatment assessment, subjects were asked to rate any changes in their general health and chest pain on a five-point Likert scale, responses ranging from `Much better' to `Much worse'.
Treatment
Treatment took place in small groups with a maximum of six subjects. Groups met weekly for 4 weeks, then every two weeks for a further 4 weeks. Each session lasted 2 h, with a short break. Subjects were asked to practice various exercises at home between sessions, and to report their progress at the beginning of subsequent sessions. Treatment was broadly behavioural in orientation, based on a manual developed via an initial pilot group, and was supplemented by written material given to subjects at each session.
Components of treatment included: (i) opportunities for subjects to recount their experiences of pain and its management; (ii) education about heart disease and other causes of chest pain; (iii) relaxation exercises, supplemented by the use of relaxation tapes, galvanic skin response biofeedback devices, and alarm watches to cue rapid relaxation exercises through the day; (iv) breathing retraining (including hyperventilation provocation tests); (v) light physical exercise; (vi) graded exposure to activities avoided because of pain; and (vii) the use of thought diaries to record and challenge assumptions about heart disease triggered by episodes of pain.
Analysis
Categorical variables were analysed using 
2 tests. Because nearly all continuous variables were highly dispersed and/or heavily skewed, non-parametric tests were used throughout, with values expressed in medians. The Mann-Whitney test was used to compare changes during treatment with changes during the control waiting period, and the Wilcoxon signed rank test to compare pre- and post-treatment values.
|
Results |
|---|
|
TopSummaryIntroductionMethodsResultsDiscussionReferences |
|---|
Demographics
60 patients were randomized (34 to immediate treatment, 26 to waiting control). Two subsequently dropped out from each group. The treatment and control groups did not differ as to age (mean 52.8 years (SD 8.6) vs. 55.4 (7.7) respectively, NS) or sex (59% and 63% female, respectively, NS). Nor did they differ on baseline variables of chest pain episode severity, frequency, duration or nitrate use, or any of the psychological or functional measures.
Controlled comparison
Table 1 summarizes the comparison between the changes occurring with treatment and the changes occurring during the control waiting period. Treatment was associated with a significantly greater reduction in chest pain episode frequency, and a greater increase in pain-free days per week, than waiting. There was no significant difference between the treatment and control groups in changes in chest pain severity or duration, although there were non-significant trends to improvement in the treatment group, and the range of variation was very wide.
|
Treatment was also associated with significant reductions in both the anxiety and depression subscales of the HAD, the total disability score of the SIP, and two of the four sub-scales of the NHP (pain and energy). Exercise tolerance improved significantly, but the Nijmegen hyperventilation score did not.
Pre- and post-treatment comparison
Table 2 summarizes the overall changes with treatment for all 56 subjects. There were significant improvements in chest pain episode frequency, nitrate use, and pain-free days per week, as well as in the HAD, all subscales of the NHP, the SIP, the hyperventilation score, and exercise duration. Ten patients were pain-free after treatment. One patient in the control group became pain-free during the waiting period, but pain returned following treatment, although at a lower frequency (2.5 episodes/week) than when first assessed (6.5 episodes/week). Thirty-eight patients (76%) reported improvement in chest pain after treatment, while 10 (20%) said it was unchanged and two (4%) said it was worse. As for general health, 42 (84%) reported improvement, seven (14%) no change, and one (2%) a deterioration.
|
There was no significant change in the proportion of exercise tests which were positive, but the proportion of subjects with capnographic evidence of hyperventilation did improve with treatment (30/56 hyperventilating before treatment, 19/56 after,
2=7.0, p<0.01).
Subjects were significantly less likely to believe they had heart disease after treatment (11/56, 20%) than before (25/56, 45%, 2=10.9, p<0.05). Those who maintained this belief (or remained uncertain, n=4) had significantly fewer pain-free days per week than those who did not (median 3.5 vs. 5.5, Mann-Whitney z=-2.1, p<0.05). They also had higher problem scores on the NHP subscales for pain (median 29.2 vs. 0, z=-2.2, p<0.05) and energy (60.8 vs. 0, z=-2.8, p<0.01). There were non-significant trends to worse outcomes for SIP disability (p=0.06), NHP sleep problems (p=0.08), and change in general health (p=0.07). On all other measures, patients who continued to believe they had heart disease did worse, but the differences were not significant.
Follow-up results
Figure 2 shows the typical pattern of change with waiting, treatment, and follow-up, for selected variables (pain episode frequency, exercise tolerance, disability ratings, and combined anxiety and depression scores) in the treatment and control groups. There was little change during the 2-month control waiting period, but on all four variables there was a substantial improvement with treatment, which was maintained during the 6-month follow-up. Similar patterns were observed for other variables. Five of the ten patients who were pain-free after treatment remained so on follow-up, mean episode frequency amongst the remainder rising to two episodes/week, as compared with 2.2 before treatment. Six other patients (whose episode frequency had been 2.8/week after treatment) became pain-free during the follow-up period.
|
|
Discussion |
|---|
|
TopSummaryIntroductionMethodsResultsDiscussionReferences |
|---|
These results provide preliminary evidence that, in this patient population, group psychological treatment is effective in improving both physical and psychological symptoms and associated disability. Further work is required to establish which elements of the treatment package are the most effective, and the mechanisms by which they operate, although the model underpinning the treatment approach postulates a set of complex interactions between physiological, affective, cognitive, behavioural and iatrogenic factors. The patient group is heterogenous,14 which is to be expected, since it is defined purely in terms of physical symptoms and negative investigations: individual elements of the treatment may therefore be most appropriate for particular subgroups, such as breathing exercises for the hyperventilators, or relaxation for those with anxiety disorders. The occurrence, and indeed persistence, of abnormal exercise ECG tests in one subgroup, albeit with improved exercise duration after treatment, requires further explanation, which this study cannot provide.
The degree of improvement observed, in terms of chest pain symptoms, is broadly comparable to that produced by individual psychological treatment,7 and by imipramine in analgesic, rather than antidepressant, doses,15 although there is little evidence about relapse rates following drug discontinuation. However, the much larger improvement in disability ratings may be of greater significance: it suggests that some patients experience pain as frequently after treatment as before, but are less anxious and less likely to limit their activity, perhaps because they no longer believe their pain to come from the heart. The tentative evidence of an association between poorer symptomatic and functional outcome and a continuing attribution of pain to a cardiac cause would support this.
There is now a need for further studies to compare the effects of psychological treatment with drugs, and with both combined, on symptoms, disability, and medical resource use, both acutely and in the long term.
|
Acknowledgments |
|---|
We thank the patients, their GPs and consultants, as well as Kathryn Watt and Zoe Clyde for their invaluable contribution. The study was funded by the Cohen Bequest and the Scottish Office, Home & Health Department.
|
References |
|---|
|
TopSummaryIntroductionMethodsResultsDiscussionReferences |
|---|
1. Chambers JB, Bass C. Chest pain with normal coronary anatomy: a review of natural history and possible etiologic factors. Prog Cardiovasc Dis 1990; 33:161–84.
2. Proudfit WL, Bruschke AVG, Sones FMJ. Clinical course of patients with normal or slightly or moderately abnormal coronary arteriograms: 10 year follow-up of 152 patients. Circulation 1980; 62:712–17.
3. Papanicolau MN. Prognostic implication of angiographically normal and insignificantly narrowed coronary arteries. Am J Cardiol 1986; 58:1181–7.
4. Potts SG, Bass CM. Psychosocial outcome and use of medical resources in patients with chest pain and normal or near-normal coronary arteries: a long-term follow-up study.Q J Med 1993; 86:583–93.
5. Bass C, Cawley R, Wade C, Ryan KC, Gardner WN, Hutchison DCS, Jackson G. Unexplained breathlessness and psychiatric morbidity in patients with normal and abnormal coronary arteries. Lancet 1983; i:605–9.
6. Potts SG, Bass CM. Psychological morbidity in patients with chest pain and near-normal coronary arteries: a long-term follow-up study. Psychol Med 1995; 25:339–47.
7. Klimes I, Mayou RA, Pearce MJ, Coles L, Fagg JR. Psychological treatment for atypical non-cardiac chest pain: a controlled evaluation. Psychol Med 1990; 20:605–11.
8. Lewin R, Cay E, Todd I, et al. The angina management programme: a rehabilitation treatment. Br J Cardiol 1995; 2:219–26.
9. Master AM. The spectrum of anginal and non-cardiac chest pain. JAMA 1964; 187:104–9.
10. Zigmond AS, Snaith PR. The Hospital Anxiety and Depression Scale. Acta Psych Scand 1983; 67:361–70.
11. van Doorn P, Folgering H, Colla P. Contribution of end-tidal PACO2 in the hyperventilation syndrome: effects of biofeedback and breathing instructions compared. Bull Eur Physiopathol Resp 1982; 18:829–36.
12. Hunt SM. A quantitative approach to perceived health status: a validation study. J Epidemiol Comm Health 1980; 34:281.
13. Bruce RA, Clarke LJ. Exercise stress testing. In: Fishman AP, ed. Heart Failure. New York, McGraw Hill, 1978.
14. Cooke RA, Chambers JB, Anggiansah A, Henderson RA, Sowton E, Owen W. Chest pain and normal coronary arteries: a clinical evaluation with oesophageal function tests, exercise ECG, end-tidal CO2 measurement and psychiatric scores. Eur Heart J 1991; 12 (suppl):103.
15. Cannon RO, Quyyumi AA, Mincemoyer R, Stine AM, Gracely RH, Smith WB, et al. Imipramine in patients with chest pain despite normal coronary angiograms. N Engl J Med 1994; 330:1411–17.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  A. Sumathipala What is the Evidence for the Efficacy of Treatments for Somatoform Disorders? A Critical Review of Previous Intervention Studies Psychosom Med, November 1, 2007; 69(9): 889 - 900. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. D. Rosen Hearts and minds: psychological factors and the chest pain of cardiac syndrome X Eur. Heart J., October 1, 2004; 25(19): 1672 - 1674. [Full Text] [PDF]
|
|
|
|
|
|
E. A. Asbury, F. Creed, and P. Collins Distinct psychosocial differences between women with coronary heart disease and cardiac syndrome X Eur. Heart J., October 1, 2004; 25(19): 1695 - 1701. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Gilbert Clinical Applications of Breathing Regulation: Beyond Anxiety Management Behav Modif, October 1, 2003; 27(5): 692 - 709. [Abstract] [PDF]
|
|
|
|
|
|
J. C. Kaski and L. F. Valenzuela Garcia Therapeutic options for the management ofpatients with cardiac syndrome X Eur. Heart J., February 2, 2001; 22(4): 283 - 293. [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||