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.

Angina through increased sympathetic drive

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.

Stress and angina
Next therapy
Authors

Robert J P Lewin (University of York) and David A Brodie (University of Liverpool).

References
  1. Smith, T.W., Follick, M.J. and Korr, K.S. Anger, neuroticism, Type A behaviour and the experience of angina. British Journal of Medical Psychology 1984; 57: 249-252.

  2. Jenkins, D.C., Stanton, B.A., Klien, M.D., Savageau, J.A. and Harken, D.E. Correlates of angina pectoris among men awaiting coronary artery bypass surgery. Psychosomatic Medicine, 1983; 45: 141-153.

  3. Williams, R.B., Haney, T.L., McKinnis, R.A., Harrell, F.E., Lee, K.L., Pryor, D.B., Califf, R., Yi-Hong Kong, Rosati, R.A., Blumental, J.A. Psychosocial and physical predictors of anginal pain relief with medical management. Psychosomatic Medicine, 1986; 48: 200-210.

  4. Channer, K.S. and Rees, J.R. Affect and angina. Stress Medicine, 1987; 3: 141-146.

  5. Channer, K.S., O'Connor, S., Britton, S. (1988) Psychological factors influence the success of coronary artery surgery. Journal Royal Society Medecine, 11, 629-632

  6. Zigmond, AS, Snaith, RP. The Hospital Anxiety and Depression Scale. Acta Psychiatrica Scandinavica: 67: 361 - 70

  7. Deanfield, J.E., Shea, M. and Kensett, M. Silent myocardial ischaemia due to mental stress. Lancet 1984; 2: 1001-1004.

  8. Deanfield, J.E., Maseri, A., Selwyn, A.P., Ribeiro, P., Chierchia, S. and Morgan, M. Myocardial ischaemia during daily life in patients with stable angina: Its relation to symptoms and heart rate changes. Lancet, October 1, 1983: 753-758.

  9. Maseri, A., Mimmo, R and Chierchia, S. Coronary artery spasm as a cause of acute myocardial ischaemia in man. Chest 1975: 68: 625-629.

  10. Rozanski, A, Bairey, C.N. and Krantz, D.S. Mental stress and the induction of silent myocardial ischaemia in patients with coronary artery disease. New England Journal of Medicine, 1988; 318: 1005-1012.

  11. Neill, W.A., Pantley, G.A. and Nakornchai, V. Respiratory alkelemia during exercise reduces angina threshold. Chest,1981; 80: 149-153.

  12. Heberden, W. Some account of a disorder of the breast. Med. Transactions 1772; 2: 59-67.

  13. Lewin, B. The psychological and behavioural management of angina. Journal of Psychosomatic Research 1997; 43: 5: 453-462.

  14. Appels, A., Bar, F., Lasker, J. Flamm, U., Kop, W. The effect of a psychological intervention program on the risk of a new coronary event after angioplasty: A feasibility study. J Psychosom Res 1997; 43: 209-217.

  15. Wynn, A. Unwarranted emotional distress in men with ischaemic heart disease. Med J Aust, 1967; 2: 847-851.

  16. Havic & Maeland suppl Scand J of ??

  17. Weinman and Petrie

  18. Lewin, B., Cay, E.L., Todd, I., Soryal, I., Goodfield, N., Bloomfield, P. and Elton, R. The angina management programme: A rehabilitation treatment. British Journal of Cardiology 1995; September: 221-226.

  19. Thompson, D.R., Bowman, G.S., Kitson, A.L., De Bono, D.P., Hopkins, A. Cardiac rehabilitation services in England and Wales: A national survey. Int J Cardiol 1997; 59(3): 299-304.

All pages copyright © angina.org. Last Revision: August 15 2002