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British Medical Bulletin 59:113-133 (2001)
© 2001 Oxford University Press

Later management of documented ischaemic heart disease: secondary prevention and rehabilitation

A A McLeod

Department of Cardiology, Poole Hospital NHS Trust, Poole, UK

	Abstract

Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 
Patients may present with a variety of syndromes related to ischaemic heart disease. These include unstable or stable angina pectoris, acute myocardial infarction, and occasionally cardiac failure without prior anginal pain or infarction. For the purposes of this review, it will generally be assumed that the condition has been stabilised, though one important aspect of the rehabilitation process is the recognition of continuing or recurrent problems such as angina pectoris and cardiac decompensation. This should then be followed by appropriate intervention. The key components of post-hospital management of such patients are: (i) support; (ii) education; (iii) assessment; (iv) intervention (if necessary); (v) therapy; and (vi) lifestyle modification.

	Introduction

Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 
A comprehensive programme of cardiac rehabilitation will contain all of these components, and will place varying emphasis on each one in a manner which is tailored to the individual patient. In the computer age, this could be called the ‘menu driven’ approach, in which the doctor or therapist chooses the most appropriate course of action for the ischaemic heart disease patient from a selection of options. Although many reviews and texts of cardiac rehabilitation exist, a brief summary of the process is appropriate.

	Cardiac rehabilitation

Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 
The definition of this process has altered subtly over recent years. The most commonly quoted definition is:

The rehabilitation of cardiac patients is the sum of activities required to influence favourably the underlying cause of the disease, as well as the best possible physical, mental and social conditions, so that they may, by their own efforts preserve or resume when lost, as normal a place as possible in the community. Rehabilitation cannot be regarded as an isolated form of therapy, but must be integrated with the whole treatment of which it forms only one facet¹.

The US Agency for Health Care Policy and Research expands this concept thus:

Cardiac rehabilitation services are an essential component of the contemporary management of patients with multiple presentations of CHD and with heart failure. Cardiac rehabilitation is a multifactorial process that includes exercise training, education, counselling regarding risk reduction and lifestyle changes, and use of behavioural interventions; these services should be integrated into the comprehensive care of cardiac patients. The objective of cardiac rehabilitation services is to improve both the physiologic and psychosocial status of cardiac patients. The physiologic outcomes targeted include improvement in exercise capacity and exercise habits and optimization of risk-factor status, including improvement in blood lipid and lipoprotein profiles, body weight, and blood glucose and blood pressure levels, and the cessation of smoking. Enhancements of myocardial perfusion and performance, as well as reduction in progression of the underlying atherosclerotic process, are additional goals. The psychosocial functioning of patients should be improved when needed, including reduction of stress, anxiety, and depression. Functional independence of patients, particularly the elderly, is an essential goal of cardiac rehabilitation services. Return to appropriate and satisfactory work could benefit both patients and society².

The WHO definition emphasizes a particular aspect of treatment for chronic diseases such as ischaemic heart disease, namely that improvements in health should be ‘by their own efforts’. In modern medical practice, the patient becomes a partner in a concerted effort to improve their health status. An exclusively paternalistic approach, where the doctor dictates the treatment that is followed by the patient, means that treatment for a condition where the patient can also help himself or herself is necessarily incomplete.

The phases of rehabilitation

These are commonly divided into four time periods.

Phase I: the in-hospital treatment phase

A variety of interventions, endorsed by a substantial evidence base, are applied in acute myocardial infarction. These include therapy with fibrinolytic drugs, beta-blocking drugs, and Angiotensin Converting Enzyme (ACE) inhibitors. The goals of rehabilitation in this phase are to speed recovery and to minimise risk from deconditioning and immobility such as muscle wasting and deep venous thrombosis. Although an extremely vulnerable phase psychologically, this period provides a valuable opportunity to begin imparting lifestyle advice such as the cessation of cigarette smoking. Studies indicate that uptake of health-related information during this phase is limited, and needs to be re-inforced during subsequent phases.

Phase II: the immediate post-hospital phase

A peak of anxiety is recorded at, or immediately after, hospital discharge. Poor resources or poor planning often mean that patients are not well supported during this period. Potentially life threatening problems such as early recurrent myocardial ischaemia, deterioration in or the emergence of heart failure symptoms, and occasionally the emergence of cardiac arrhythmias may jeopardise recovery at a time when the specialist cardiac services present in hospital are no longer available to provide support. This phase represents one where potentially the impact of a well organized cardiac support team can minimise anxiety and react to the development of the specific medical problems mentioned above.

Phase III: the formal rehabilitation programme phase

Many programmes of rehabilitation focus on the provision of services during this phase. The specialized skills of physiotherapists, exercise physiologists, occupational therapists, pharmacists, dieticians, cardiac nurses, and clinical psychologists may be used in educational and lifestyle modification programmes. Many programmes focus on exercise as a means of promoting both physical fitness and healthy behaviour in general. Unfortunately, many programmes are delayed until 6–8 weeks after the index cardiac event. Patient education (the re-inforcement of information already given in hospital) and progressive exercise rehabilitation should ideally start as soon as the patient leaves phase I.

Phase IV: the maintenance phase

After the formal intervention of phase III, this phase which is life-long focuses on the maintenance of a healthy lifestyle, and aims to avoid the loss of previously achieved goals such as improved physical fitness, the maintenance of weight loss, and continued abstinence from tobacco products. Many studies attest to the difficulties of long-term health maintenance.

	Post-hospital cardiac care

Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 
All rehabilitation phases after phase I can be thought of under the above heading. The original development of ischaemic heart disease can be thought of as the net result of the interplay of risk factors, and the impact of measures to reduce these after the acute phase of illness is known as secondary prevention. Before discussing pharmacological and non-pharmacological interventions, it is necessary to consider the optimum management of specific medical problems. Adjunctive therapy after myocardial infarction has been reviewed by multiple authorities³.

Myocardial ischaemia

An aggressive approach to the management of acute myocardial ischaemia is validated by the results of recent trials⁴ and by the knowledge that optimum flow in a coronary artery which has occluded and caused myocardial infarction is associated with reduced mortality. The degree to which a patient has been treated with interventional therapies during acute myocardial ischaemia or infarction varies substantially world-wide. However, a consistent goal for cardiologists, prior to a patient's discharge, is the abolition of evident ischaemia by intervention, or by ischaemia-reducing drugs. The efficacy of in-hospital therapy is often assessed by formal exercise testing on a stationary bicycle ergometer, or by motor-driven treadmill.

Unfortunately, treadmill testing, despite its simplicity and obvious relevance to physical stress in everyday life, has substantial limitations in practice. The Italian GISSI-2 study concluded that even being able to perform a treadmill test was a predictor of a good outcome after a myocardial infarct. The mortality of patients who were not subjected to treadmill testing or in whom treadmill testing was thought to be contra-indicated was 4-fold greater than those who undertook a treadmill test^5,6.

Substantial limitation on a treadmill test is associated with a poor outcome. Two major factors underlie this. The first is left ventricular impairment. The second is marked ischaemic limitation. Evidence of ischaemia at a low workload on exercise testing may indicate unresolved coronary flow limitation, or multivessel coronary artery disease. Some centres will further investigate these patients with a view to angioplasty or coronary artery surgery. There will always be some patients, however, in whom these problems are either unresolved or unavoidable. In such patients, it is important to check that the role of drug therapy has been fully explored. Exercise and other forms of stress testing are however relatively poorly predictive of re-occlusion in an infarct-related artery, and close surveillance is advised to detect recurrent ischaemia⁷.

Cardiac failure therapy

ACE inhibitors are the most obviously beneficial agents in this condition. A wealth of evidence supports their use in asymptomatic left ventricular dysfunction (LVEF 0.40 or less) or in overt left ventricular failure, even if the failure has been transient. It seems likely that the angiotensin (AT) II inhibitors are as beneficial, though at present none are licensed for this indication⁸.

ß-Blocking drugs are also valuable in patients with cardiac impairment. A paradox exists, however, in this form of therapy. When ACE inhibitors are given, it can immediately be appreciated that their actions are likely to be beneficial. Sudden loss of left ventricular pump function results in a substantial stimulus to the renin-angiotensin axis. The deleterious effects of ACE and angiotensin activation such as salt and water retention, and increased left ventricular afterload are blocked by ACE inhibitors and ATII antagonists. In acute cardiac failure, however, there is substantial stimulation of adrenergic activity, primarily through sympathetic nerves (noradrenaline), but also through the adrenal medulla (adrenaline) if the stress is severe enough. Acute blockade of this response is dangerous. Nonetheless, in chronic stable cardiac impairment, considerable evidence for deleterious effects of chronic sympathetic stimulation exists. A large number of trials have been conducted with ß-adrenoceptor antagonists following myocardial infarction, with a consistent indication of benefit to both reduction of re-infarction risk, and also to mortality. An interesting feature of these studies has been that the more severe or damaging the infarct, the greater the evidence of benefit. For example the Beta Blocker Heart Attack Trial (BHAT) showed that the mortality reduction with propranolol when compared with placebo was most substantial in the group of patients who had either suffered electrical complications (such as cardiac arrest) or cardiac failure during their index infarct⁹. In clinical practice, it is common to control overt cardiac failure with an ACE inhibitor and if necessary a diuretic, but to try and introduce a ß-blocker before hospital discharge. The long-term benefit of ß-blockade in chronic heart failure is also incontestable. Many studies, however, show that all too often drugs such as ß-blockers are not given to patients who could benefit from them. There is a particular bias in this respect against the elderly, and a national bias is also evident. ß-Blockers are less commonly prescribed in the UK than in Scandinavia, Italy and the US. Some physicians point to the real adverse effects of these drugs such as fatigue. This is not a reason for not trying the agents in the first instance, however, particularly when the mortality benefits are so striking. Although ß-blockers experimentally show an antifibrillatory action, it is unclear if this is important in clinical practice. Some evidence exists, however, to show that there is less ventricular irritability when patients receive these drugs in the post-infarction period. There is little evidence for such a role for any other purely anti-arrhythmic drugs. Although some evidence of benefit for amiodarone has been found in several studies, no other anti-arrhythmic drugs have been shown to be beneficial and most have shown increased mortality. An interesting case in point is sotalol, a non-selective ß-blocker with class III (action potential and refractoriness prolongation) anti-arrhythmic effect. Commercially available sotalol is a racemic mixture, but its ß-blocking effect resides in the l-isomer. When d-sotalol (only class III action) was tested in the Survival With Oral d-sotalol (SWORD) trial, increased mortality in the active treatment group was found¹⁰.

Anticoagulation with warfarin or other drugs has also been tested after myocardial infarction. There is considerable heterogeneity in the studies (some are in heart failure, some post-infarction) though overall a meta-analysis found a reduction in mortality when patients with coronary artery disease were treated with high-intensity warfarin therapy¹¹. An excess of major bleeding events is to be expected with this treatment strategy. In addition, the possible complementary roles of anticoagulant drugs such as warfarin, and antiplatelet drugs such as aspirin, remains to be determined. Aspirin is routinely prescribed to most patients with chronic coronary artery disease. It does appear to interact with ACE inhibitors reducing the efficacy of the latter. There is interest, therefore, in the thienopyridines – antiplatelet drugs with apparently similar efficacy to aspirin. At present, their use is generally short-term following coronary intervention, or when aspirin is genuinely contra-indicated¹².

Anti-ischaemic therapy

As discussed above, modern management of coronary artery disease attempts to eliminate ischaemia where possible, often using physical intervention techniques. Despite this, overt (symptomatic) ischaemia or silent ischaemia is often present and not amenable to angioplasty or coronary bypass techniques. Where treatment with ß-blockade is not possible, there is reasonable evidence to support the use of heart rate lowering calcium antagonists (diltiazem and verapamil) post-myocardial infarction. Their use appears deleterious when heart failure is present. The routine use of dihydropyridine calcium antagonists or of nitrates does not appear to add benefit, though they synergise well with ß-blockers in patients with symptomatic angina³.

Plasma lipid modification

Westernized populations have high circulating levels of plasma cholesterol when compared with countries whose food intake is closer to subsistence level. Although plasma cholesterol was considered a marker for increased coronary risk for many years, conclusive proof that manipulation of the circulating cholesterol level affected coronary heart disease risk was only obtained when the hydroxymethyl glutaryl coenzyme A reductase (HMGCoA) antagonists became available and were tested in large-scale clinical trials. These drugs act at an important rate-limiting step in cholesterol synthesis. Since the landmark 4S (Scandinavian Simvastatin Survival Study) was published in 1994, a wealth of evidence has confirmed the very substantial effect on coronary event rates and mortality that these compounds confer¹³. There is dispute (largely for economic reasons) over the use of these drugs in patients whose coronary risk is low, or in whom for reasons that are unclear, very low LDL cholesterol levels co-exist with coronary artery disease. The majority of patients with overt ischaemic heart disease, including unstable angina pectoris¹⁴, can benefit from therapy however. More recently, gemfibrozil, which has little effect on LDL cholesterol, but which increases HDL cholesterol and reduces triglycerides, has also been shown to be beneficial¹⁵. During the rehabilitation process, the key issue with these drugs (as well as with drugs such as ACE inhibitors and ß-blockers) is not whether they work, but how is it possible to ensure that patients receive them, and whether they should be titrated to produce optimal effect in the individual patient. Compliance with therapy is therefore a vital issue.

	Compliance and psychological issues in the rehabilitation process

Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 
Thus far we have focused on the classical ‘disease model’ of coronary artery disease, familiar to all doctors from their training in medical school. Firm evidence shows that implementation of specific therapies can make a major impact on the disease process. But there is another model of disease, the ‘illness perspective’. In this model, familiar to clinical psychologists, the subjective responses of patients, and indeed those close to them determine how they make sense of and respond to the symptoms. It is vital for the patient to overcome the psychological hurdles that the disease has placed in his or her path. Both the patient and the family must adapt to the illness, and also react positively to the advice given. It is of little import how great the P value of a trial indicating benefit from ß-blockade after myocardial infarction is if the patient does not comply with the therapy. If significant clinical depression, or poor understanding of the condition is present after infarction and is not addressed, then improvements in lifestyle behaviour such as smoking cessation, weight reduction, compliance with therapy, and modification of diet are unlikely. Skilled rehabilitation therapists can work with a patient to encourage positive change, and should be alert to the need to refer for appropriate clinical help where necessary. Other treatments such as better diabetic control and improved antihypertensive regimens may also be needed. The process of conveying information to the patient has recently been formally reviewed by Scott et al¹⁶.

Observations within and without cardiac rehabilitation programmes indicate that important lifestyle interventions are not adhered to long-term¹⁷. Three specific areas can be identified. These are: (i) patient-related factors – these can be predicted by the patient's initial adherence, their self-efficacy, and social support; (ii) regimen-related factors – a more complex treatment regimen predicts non-adherence; and (iii) provider-related factors – these relate to the empathic and communication and motivational skills of the healthcare professional delivering therapy.

As well as exploring the patient's readiness to change behaviour¹⁸, it is important to emphasise the concept of self-efficacy, where the power to change is seen to reside within the patient himself or herself. Other strategies include the involvement of partners, self-monitoring, re-inforcement, multiple contacts and goal setting. When lifestyle modification advice is delivered in a cardiac rehabilitation programme, extended-length participation predicts better control of body weight, physical fitness, and lipoprotein subfractions, and may be an argument for continuing centre-based programmes¹⁹. Lack of funding and other practical issues suggest, however, that strategies for enhancing adherence to home-exercise and dietary programmes will be needed.

	Lifestyle modification of coronary risk factors in the rehabilitation process

Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 
Although much emphasis is rightly placed on pharmacological therapy in ischaemic heart disease, many patients are reluctant to take drugs. Even when the patient accepts that appropriate medication is needed, many will also wish to try and avert further cardiac events, and will readily accept lifestyle change advice. The implementation of such advice is problematic. This section of the review now focuses on areas where patients can help themselves.

Physical inactivity and exercise

Physical inactivity continues to increase in Westernised populations and is associated with increasing levels of obesity²⁰. Physical inactivity is itself a risk factor for the development of coronary artery disease^21,22.

A number of studies link physical inactivity with increased risk of coronary artery disease. The largest single trial of exercise and its potential beneficial effects on coronary artery disease patients was the National Exercise and Heart Disease Project, sponsored by the National Heart, Lung, and Blood Institute (NHLBI) in the US²³. Premature withdrawal of funding compromised the conclusions of this study, which showed trends in favour of an intensive 1-year exercise programme compared with ‘usual care’. This study, however, was incorporated into both of the two substantial overviews of exercise and cardiac rehabilitation published within a short time of each other^24,25. These analyses independently reached broadly similar conclusions. After approximately 3 years, the reduction in risk of cardiovascular death following participation in a cardiac rehabilitation programme is of the order of 20–25%. But trials included were performed between 1972 and 1985, and the exercise intervention applied varied widely. Follow-up of more than 1 year was required for the O'Connor analysis and 2 years for the Oldridge analysis. Almost all trials recruited exclusively male patients under the age of 65 years. A more recent systematic review suggests that exercise trials per se have favourably influenced mortality²⁶. Recent data from the British Regional Heart Study also suggest that exercise in subjects with coronary artery disease is associated with reduced cardiovascular disease mortality²⁷.

Physical exercise can aid symptom management after myocardial infarction. The ‘training effect’ whereby the patient can achieve an external workload with reduced heart rate and blood pressure compared with the levels before training is valuable in clinical practice. Both heart rate and systolic blood pressure are important determinants of myocardial oxygen consumption²⁸. It follows that patients may achieve a level of external work after exercise training that they cannot achieve without experiencing angina pectoris prior to training. Myocardial function may also be improved after training in cardiac patients, particularly if prolonged and intensive²⁹. Much of the training effect, however, is due to enhanced oxygen extraction by exercising in the trained muscle groups (increased arteriovenous oxygen difference), and is, therefore, largely obtained at a reduced overall cardiac output³⁰. This training effect can be quite potent, comparable in clinical results with anti-anginal therapy^31,32.

Exercise is important life-long, but has particular and attractive benefits for the elderly. Longitudinal studies of the age-related decline in maximal aerobic performance, as assessed by maximal oxygen uptake (VO₂max), indicate that between 60–90 years minimal aerobic requirement for survival is reached. Exercise conditioning attenuates this decline³³. But exercise in older people brings other benefits too, some as apparently mundane as the prevention of disabilities caused by immobility – faecal impaction, incontinence, deep vein thrombosis³⁴. Exercise also increases safety for older people^35,36. Exercise and its contribution to lipid management is further reviewed below, but its continuation in a life-long pattern is important. Many exercise benefits are lost with discontinuation³⁷. Exercise is not ‘bankable’.

Exercise in heart failure

Exercise in this group of patients has evolved from complete contra-indication: ‘rest for the body; rest for the mind; rest for the heart’³⁸ to accepted practice³⁹. Although there is general agreement on rest for acute heart failure, patients with chronic left ventricular dysfunction can undergo exercise training safely and show benefit. Improvements in peak oxygen consumption and exercise duration are associated with reduced catecholamine levels and other neuro-endocrine responses, and improved heart rate variability. These latter markers are known to be associated with poorer prognosis in heart failure, though the conceptual leap between the observation of more favourable neuro-endocrine profiles, and improved prognosis has not been demonstrated in adequately sized trials as yet.

The US Agency for Health Care Policy and Research consensus document endorses the opinions expressed above². An independently constituted group has also endorsed the need for greater physical activity in the maintenance of cardiovascular health and prevention of recurrent disease⁴⁰.

Anxiety exists about the possible adverse effects of exercise. It is a common anecdotal experience that some people die suddenly during exercise, due to coronary artery disease, or sustain a heart attack shortly afterward. This phenomenon is sometimes called ‘triggering’. Current knowledge of acute coronary syndromes and myocardial infarction suggests that frequently this is triggered by rupture of a ‘vulnerable’ coronary artery plaque, though instantaneous death is more commonly due to arrhythmia⁴¹. During violent isometric exercise, substantial increases in cardiac afterload occur, and direct mechanical stress is imposed on the whole of the central vasculature. The phenomenon of ‘triggering’ has been explored in both Augsburg, Germany, and in Boston, USA⁴². Although a substantial amount of debate was engendered by the papers discussed by Curfman⁴² (see correspondence⁴³), the essential message is 2-fold: (i) exercise can act as a trigger of myocardial infarction; and (ii) paradoxically, perhaps, exercise taken regularly is nonetheless protective. The worst thing to do is never to exercise, and then to have to do so! Pushing a broken-down car, or shovelling snow, are not only fixed in the layman's mind as associated with heart attack, they are also borne out by the evidence. All exercise programmes with physiological demonstrable benefits to patients utilize an aerobic, graded, exercise programme with repetitive, rythmic exercise of large muscle groupos to steadily increase whole body oxygen uptake and cardiac output. In heart failure patients who may initially be very deconditioned and sedentary, this level of exercise may be very low indeed. In young uncomplicated, previously fit, post-myocasrdial infarction patients the level of exercise may be much greater than this. A safe starting point for most subjects ia approximately 50% of an individual's maximal oxygen uptake.

Smoking cessation

Cigarette smoking is the single largest avoidable environmental and behavioural cause of cardiovascular disease, and of course the cause of several forms of cancer⁴⁴. Its highly addictive nature can be seen in studies carried out in drug addiction clinics, in that opiate addicts generally find it easier to give up heroin than to give up smoking. Interventions to promote smoking cessation have been costed at less than £1000 per life-year gained, in contrast with over 310 other medical interventions with a median cost of about £17,000 per life-year gained. Smoking is, therefore, a ‘best buy’ target for healthcare professionals. Intensive support and nicotine replacement therapy are important components of any serious attempts to help heavy smokers, though even brief but assertive medical advice is helpful. Kottke and colleagues reviewed the attributes of successful smoking cessation interventions in medical practice⁴⁵. Programmes with multiple advisers in the team, multiple methods of approach, and sustained and regular contacts with clients were the most successful. Fiscal measures are also important⁴⁶. Full details of guidelines can be found elsewhere⁴⁷.

Dietary modification

Rigorous dieting can improve cholesterol levels, though generally only of the order of 0.3–0.6 mmol/l. It is noteworthy that in the Scandinavian 4S trial, although the placebo group was given advice on dietary modification, the run-in levels of cholesterol prior to initiation of randomized therapy showed no difference over several months, and continued without any real change on randomized placebo therapy for 5 years or more¹³. This, therefore, probably represents the ‘real world’ of treatment effect (or lack of it) with simple dietary advice alone. A systematic overview of dietary intervention trials indicated that diets equivalent to the American Heart Association Step 2 diet (vide infra) lowered blood total cholesterol by 6.1% and diets equivalent to the American Heart Association Step 1 schema lowered blood total cholesterol by 3.0% (P <0.0001)⁴⁸. Efficacy was limited by lack of compliance. Overviews of complex interventions, however, are fraught with statistical problems, and the paper by Tang and colleagues has been criticized for inappropriately excluding trials and for drawing conclusions when statistical testing reveals substantial heterogeneity between studies⁴⁹. Although there is little doubt that such interventions do good, the modest effects on plasma cholesterol should be compared with the 30–40% reduction in cholesterol achievable by HMGCoA reductase inhibitors.

In a number of small-scale studies, however, relatively large effects on plasma lipids have been found, and in some cases these have been associated with favourable angiographic changes. In the Lifestyle Heart Trial, Ornish and colleagues sought to modify risk in a multifactorial manner, though with an approach which eschewed drug therapy in favour of major dietary changes, meditation and relaxation therapy, and moderate physical exercise⁵⁰. Although the study populations were small, changes in LDL cholesterol were quite striking, and this was associated with improved coronary angiographic appearances. In the dietary component, however, only about 10% of total calories were made up of fat. This intake is very markedly below most dietary levels in the Western world. Current US fat intake is 33% of calories; the National Cholesterol Education Program recommends 30% (Step I) and 20% (Step II)⁵¹. Dramatic changes in fat intake as in the Lifestyle Heart Trial require very careful dietary planning. In this study there was one chef for every 8 patients enrolled! Another study incorporating diet in the management of coronary artery disease was the St Thomas' Atherosclerosis Regression Study (STARS)⁵². Although an examination of cholestyramine added to dietary treatment, the diet alone group in whom the primary aim was to reduce fat intake to 27% of dietary energy also showed significant falls in LDL cholesterol compared with a control group over 39 months. Triglyceride levels were also reduced. The dietary strategy also increased intake of -3 and -6 fatty acids. Plant-derived soluble fibre was also added. Weight did not change significantly. In addition to encouraging results obtained in plasma lipids, improved angiographic appearances were seen in patients treated with diet alone or diet plus cholestyramine in this study⁵².

The STARS study gives a clue to what is perhaps an important feature of successful dietary intervention studies. Not only may it be important to reduce saturated fat intake, but it might also be necessary to modify the composition of the ingested fats. A number of studies have examined this possibility. In the DASH study, the effect of dietary patterns on blood pressure was examined⁵³. A diet rich in fruits, vegetables, and low fat dairy products reduced blood pressure more than a control diet in 459 subjects with mild hypertension, independent of sodium or caloric intake. Similarly, in the Lyon Diet Heart Study, after approximately 4 years in a post-myocardial population, a ‘Mediterranean’ diet result in reduced cardiac events compared with control diet, though the numbers were relatively small⁵⁴. The Diet And Reinfarction Trial (DART) also modified diet, the most important component being the introduction of fatty fish, with beneficial results⁵⁵. It is notable that modest, if any, changes in the usual measured plasma lipids occurred in these studies, demonstrating the shortcomings of conventional lipid risk factor measurement. The very substantial GISSI-Prevenzione trial, in 11,324 post-myocardial infarction subjects in Italy investigated the addition of vitamin E and/or n-3 polyunsaturated fatty acids (PUFA) to the diet. Dietary supplementation with n-3 PUFA led to reduction in death or cardiac events by 10–20%⁵⁶. There is some evidence that the effects of n-3 (-3) fatty acids may be mediated by an electrophysiological effect in suppressing malignant ventricular arrhythmias⁵⁷. Finally, and most recently, a report from US women in the Breast Cancer Detection and Demonstration Project (BCDDP) indicated that women with better Recommended Food Score (RFS) have a lower than expected all-cause mortality, despite adjustment for confounding reductions in known coronary risk factors. Although not a clinical trial, this study is powerful because of the large number of events recorded (2065 deaths after a median follow-up of 5.6 years) from a total of 42,554 women who completed a food frequency questionnaire⁵⁸. The contrasting results of trials of saturated fat reduction and trials where intake of unsaturated fats has been the aim have been reviewed by Oliver⁵⁹.

Hypertension is an important risk factor for coronary artery disease. Although multiple studies attest to the importance of lowering blood pressure by pharmacological means in hypertensive subjects, salt restriction has a potentially important role to play in lowering blood pressure. The DASH study mentioned above has also studied the effects of modest salt restriction in lowering blood pressure. Even modest sodium restriction – to less than 100 mmol/day had significant beneficial effects on blood pressure, which were enhanced with the DASH diet for any given sodium intake over the control diet population⁶⁰.

Multifactorial intervention studies

Schuler and colleagues performed a randomised multifactorial intervention trial with an intensive physical exercise programme and a low-fat diet in 113 patients with coronary artery disease⁶¹. They used the American Heart Association Phase 3 diet with fat intake <20% of energy. Lipid lowering drugs were not prescribed. Intensive cardiac investigations were performed at 1 year of intervention. Coronary artery disease progressed at a slower pace in the intervention group. In the intervention group, body weight decreased by 5%, total cholesterol by 10%, LDL by 8%, and triglycerides by 24%. All changes were highly significant⁶¹. There are some inconsistencies here with regard to triglyceride levels, which fell in some studies, but failed to do so in others. This issue is partly addressed by Lavie and Milani⁶². In 313 patients not taking any lipid modifying therapy undertaking an exercise programme and an American Heart Association Phase I diet⁶³, the reductions seen in triglyceride levels were restricted to patients with high baseline triglycerides. This could, however, be an example in part of regression toward the mean.

Dietary additives

Phytosterols in the diet
Chisholm et al⁶⁴ studied the effect of replacing butter with margarine of canola (rape-seed like) oil. Concentrations of LDL cholesterol fell by about 10%. No adverse lipoprotein patterns were found. In addition to substitution of one fat by another, new approaches have been taken with the introduction of proprietary brands of margarine containing plant stanol esters. Plant stanol esters reduce cholesterol absorption and when incorporated into diets low in saturated fat and cholesterol have achieved reductions in LDL cholesterol of up to 24%⁶⁵. When plant fatty acids are added to the diet of animals, they can in turn modify the body composition of those animals. This approach has been applied to egg production and to some meats. When consumed by humans, these products appear to have the same beneficial effects as when the original plant fatty acids are eaten. Although entire populations have been treated with plant sterols (in Finland), it remains possible that adverse effects may occur in the long-term. Phytosterols, as these compounds are called, are remarkably similar to human sterols, and could potentially interact with steroid hormone biosynthesis⁶⁶.

Antioxidant vitamins
Considerable interest has been shown in dietary supplementation, particularly with antioxidant vitamins. Although oxygen is essential for life, it has been known for many years that excess oxygen has harmful effects. Oxidation of intrinsic structural molecules in the body may result in irreversible change, and there are numerous enzyme systems which protect against oxidation. It has been hypothesized that low density lipoprotein cholesterol, when oxidized, is particularly atherogenic, and that antioxidant vitamins might protect against this⁶⁷. Preliminary studies using -tocopherol and ß-carotene have been disappointing⁶⁸; although one study using vitamin E supplementation gave positive results, neither the GISSI-Prevenzione trial⁵⁶, nor the recent very large HOPE study showed benefit in patients at high risk for coronary artery disease events⁶⁹. The National Academy of Sciences Institute of Medicine has recently re-evaluated the Dietary Reference Intakes (DRIs) for antioxidant vitamins, selenium, and carotenoids and concluded that definite upper intake levels for these compounds exist, with lack of benefit for pharmacological levels of supplementation⁷⁰.

Alcohol
High levels of alcohol ingestion are directly damaging to myocardium, possibly through a mechanism involving the non-oxidative metabolism of ethanol to fatty acid ethyl esters⁷¹. In contrast, moderate alcohol consumption is associated with a lower risk of coronary heart disease⁷². Although there are potentially confounding reasons for this (in some Westernized countries higher alcohol intake is associated with greater wealth and higher socio-economic status), there is a plausible biological mechanism. Alcohol increases the serum concentration of high density lipoprotein cholesterol (HDL). The effect does not appear to be specific for any type of alcoholic beverage⁷³. It is unclear how much of the effect relates to the ethanol itself, or to congeners in alcoholic drinks, which have other potentially beneficial effects such as antioxidant activity. One interesting study from Copenhagen indicates that the association between alcohol ingestion and risk of an ischaemic heart disease event is highly dependent on concentration of LDL cholesterol. In other words, those with the highest baseline risk (high LDL cholesterol) benefit more from the effect of alcohol than those with lower LDL concentrations⁷⁴.

Weight reduction

Western populations continue to increase in weight. In the US, the 1990s saw the prevalence of obesity rise to one-third of the population. In the 1997 Health Survey for England⁷⁵, it was reported that 17% of men and 20% of women in the UK were obese. Obesity correlates with higher mortality and a higher incidence of chronic disease. Concerns have been raised, however, about the risks of losing weight, particularly rapidly. Dattilo has reviewed 70 studies on almost 1300 subjects and concluded that per kilogram excess weight loss the total cholesterol falls by 0.05 mmol/l, and that favourable influences are seen on glycaemic control in diabetes, lipid oxidizability status, haemostatic factors, left ventricular hypertrophy and blood pressure⁷⁶. Care should be taken to ensure that there is not just substitution of carbohydrate for fat. When study subjects are fed isocaloric diets in which the fat has been substituted by carbohydrate, serum triglycerides tend to increase, and HDL cholesterol levels tend to decrease⁷⁷. Where weight reduction accompanies changes in the energy source in the diet, any adverse changes appear to be lost. One of the clearest indications of the beneficial effects of weight reduction within a single trial is seen in the correlation observed in the MRFIT trial. Weight reduction showed a clear graded relation with total cholesterol reduction⁷⁸. Weight reduction and blood pressure reduction can also be seen in the context of a 3 year clinical trial⁷⁹. Control of obesity in itself has not been shown to lower morbidity or mortality in cardiac patients though the changes above clearly reduce risk, and reduction of excess body fat improves symptoms and lessens fatigue⁸⁰.

	Psychosocial intervention

Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 
Most patients (and indeed relatives of patients) when interviewed attribute their coronary artery disease event to stress. There is some evidence to support this view in terms, for example, of accumulation of stressful events such as divorce, bereavement, or unemployment⁸¹. Once coronary artery disease is established, there is firm evidence to indicate that stress is deleterious and may provoke ischaemic events^82,83. The most well recognized psychological component of coronary artery disease risk is the type A behaviour. The type A personality is hard-driving, competitive, aggressive and impatient. Following a number of studies with null findings in respect of this personality overall, adherents of type A behaviour as a coronary risk factor have pursued the possibility that the hostility element of such behaviour is the most dangerous, in that it promotes rebellion against advice, and continuation of adverse lifestyle traits such as cigarette smoking. The assessment of true type A personality is a skilled task, however⁸¹. Modification of life-long behaviour patterns is difficult, but there is some evidence that a programme of stress management incorporated within a cardiac rehabilitation programme may be beneficial⁸⁴. It is important to realise that, though type A behaviour may be a risk factor for coronary artery disease, once the disease is present, type A personality may predict a better survival, at least for some categories of patients who are at the highest risk. This paradox probably stems from the ‘driven’ characteristic of such patients, which may improve their adherence to treatment regimens⁸⁵. Exercise training per se does not appear to influence psychosocial functioning, though depressed patients improve⁸⁶. The literature on psychosocial interventions is extremely confused with passionately held views on all sides. A useful overview of cardiac rehabilitation, published by the NHS Centre for Reviews and Dissemination, University of York, discusses this issue⁸⁷. Drawing the threads of multiple papers together, it would appear that psychosocial and educational intervention might correct potentially harmful misconceptions about cardiac disease, improve compliance with recommended regimens such as non-smoking, dietary modification, and increase physical activity. It appears particularly important to include both patient and spouse or partner. Steptoe⁸³ has stated: ‘the recognition that an individual's circumstances and personality interact with biological risk factors may provide new opportunities for prevention, and for more refined risk stratification’.

Depression is a manifestation of the most adverse psychosocial reaction to myocardial infarction. In some patients, of course, depression is present beforehand. It is common, with 13–19% of patients exhibiting some features of the disorder. Importantly, it is correlated with substantially increased risk of mortality, angina, arrhythmias, rehospitalisation, prolonged disability and continued smoking⁸⁸.

Studies of rehabilitation in depressed patients probably suffer from the dilution of patients with major problems by patients who form the mass of people suffering from, and then recovering from, any major medical disorder. In addition, the interventions applied to the mass of recovering myocardial infarction patients may not be intensive enough or suited to significantly depressed patients⁸⁹. Although the major adverse impact on prognosis of significant depression is well documented by Creed⁸⁸, the evidence for benefit is not persuasive – at least in terms of subsequent cardiac morbidity. There can be few, however, who would deny patients adequate care when as many as one in six post-myocardial infarction patients are affected, and specialised help is available, and perhaps too rarely sought. Strategies for correcting the misapprehensions many patients have about their illness have been well reviewed by Thompson and Lewin⁹⁰.

	Conclusions

Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 
Treatments available for the cardiac patient range from complex surgical procedures to psychosocial interventions. Valuable guidelines exist and have been widely distributed⁹¹, but their real challenge is in their implementation. Although it is clear that some strategies can save more lives or relieve symptoms better than others, only a fully integrated cardiac team can realise the maximum benefits of the appropriate treatments for every patient.

	Footnotes

Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 
Correspondence to: Dr A A McLeod, Department of Cardiology, Poole Hospital NHS Trust, Longfleet Road, Poole, Dorset BH15 2JB, UK

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Top Footnotes Abstract Introduction Cardiac rehabilitation Post-hospital cardiac care Compliance and psychological... Lifestyle modification of... Psychosocial intervention Conclusions References

 

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