A m e r i c a n H e a r t J o u r n a l February, 1976, Volume 91, N u m b e r 2

Editorial

The cardiologist's responsibility for preventing coronary heart disease

Richard Turner Edinburgh, Scotland

Keith Ball London, England

Coronary heart disease (CHD) is the commonest cause of premature death in the western world today and in many countries its incidence is increasing. In America it is said that one man in five will develop symptoms before the age of 60 and one in three will have some form of sympto- matic arterial disease. Early death from acute myocardial infarction amounts to about 40 per cent. Four times as many men as women die from CHD before the age of 65, resulting in a large number of widows and fatherless children caused each year by CHD alone. Most deaths occur outside hosptial and too rapidly for medical care. In many cases sudden death is the first, and consequently the last, manifestation.

There is no prospect of spontaneous improve- ment in this situation.

That environmental factors are largely respon- sible is indicated by the increasing incidence, especially in younger men, by the wide variation in prevalence of CHD between countries and between different regions of the same country, by the development of CHD in migrants from poor

From the Department of Medicine, University of Edinburgh, Edim burgh, Scotland, and the Central Middlesex Hospital, London, England. Received for publication Dec. 2, 1974.

Reprint requests to: Dr. Richard Turner, Department of Medicine, University of Edinburgh, 12 George Square, Edinburgh EH8 9JZ, United Kingdom.

to relatively affluent countries, and by the war- time decline of CHD in food-restricted Europe. It follows that CHD should largely be prevent- able.

At present there is too little relevant action. Time, effort, and money are mainly s p e n t on coronary-care units, coronary ambulances, and even coronary arterial surgery and cardiac trans- plantation-although, when symptoms first ap- pear, the underlying disease is likely to be far advanced.

Secondary prevention, although often ne- glected, is second best.

Only primary prevention could be really effec- tive and, since coronary arterial disease often starts in youth and is of slow development, prevention should start early in life.

Although there are gaps in our knowledge, we believe that enough is already known not only for any doctor to apply a rational program of preven- tive treatment for his patients and their close relatives, but to warrant examining apparently healthy persons to detect those at high risk. 1

Epidemiologists, nutritionists, and others prin- cipally interested in research can perhaps view the situation with relative equanimity, hopefully awaiting positive results from more research and further trials, but physicians with clinical respon- sibilities must give advice on the balance of

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T u r n e r a n d Bal l

current evidence. Where probability of benefit is strong and the advice unharmful, they are surely failing in their duty not to take appropriate action.

Certain risk factors which have been identified are almost certainly causal and preventable. We therefore recommend regular health examina- tions for their detection. This is surely as reasonable as going to the dentist and much more important. At present automobiles get better service.

High-risk groups

High-risk groups include all patients with symptomatic disease and their near relatives, all with hypertension or diabetes, or with a strong family history of hypertension and/or atheroscle- rotic disease, and all found on examination to have hyperlipidemia or a combination of several risk factors.

We have found that about 20 per cent of middle-aged men fall into these categories.

Risk factors

Smoking. About one half of the excess deaths in cigarette smokers are cardiovascular in origin, and many of them are sudden. 2 In the U. K. deaths from CHD in men aged 35 to 44 almost doubled between 1950 and 1967, 3 which parallels the rapid increase in smoking between 1930 and 1945. Heavy smoking is especially frequent in relatively young men who die from myocardial infarction.

The mortality rate from CHD 40 years ago was far higher in the professions than in unskilled laborers, but since then the lowest paid have developed the highest mortality rate. 4 This may in part reflect changing smoking habits. Whereas cigarette smoking from 1955 has fallen consider- ably in the better educated, it has risen in the others.

Recent work has emphasized the importance of carbon monoxide (CO) in the development of CHD in smokers. 5 Carboxyhemoglobin levels up to 15 per cent have been found. CO not only induces hypoxia but also increases endothelial permeability and may thus enhance atherosclero- sis. We have found tha t many cigarette smokers who change to cigars continue to inhale and maintain raised COHb levels. 6

We have also found that smokers who change to very low tar and nicotine cigarettes may smoke more but their COHb levels are lower than when

they smoked medium tar and nicotine cigarettes. ~ Smokers with COHb levels over 5 per cent have been found to have more than 20 times the incidence of CHD than those with levels below 3 per cent2

Several studies have shown the benefit of stop- ping cigarette smoking. A rapid fall in death rates from CHD occurs in the first year and after 10 years rates approach those of life-long nonsmok- ers.

In the combined results from Edinburgh and London we have found that about 60 per cent of 243 male survivors of acute myocardial infarction who had been smokers and advised to stop were still nonsmokers one or more years later2

Prevention must start before the age of 10. Children are unimpressed by the chances of cancer or a coronary by the age of 50, but are influenced by example and by the antisocial aspects of smoking. Herein lies the opportunity. Doctors should understand the scientific basis for linking smoking and CHD, and this we have recently reviewed. 1~

Hypertension. There is epidemiological, clini- cal, pathological, and experimental evidence that hypertension accelerates the development oi ~1, 1~ atherosclerosis and that this is increased if hyper- lipidemia is present. There is a nearly linear relationship between the height of the blood pressure and the risk of CHD. It is a powerful predictor.

The lipid concentration of the arterial wall is related to that in the blood, the filtration pressure {blood pressure), and the permeability of the wall, which may be increased by the hypoxia which results from smoking.

Experimentally it has been shown that lower- ing raised blood pressure retards the development of atherosclerosis. ~

Although it has not yet been demonstrated that the treatment of hypertension will reduce the incidence of CHD, the at tempt has not been made in its early stages. It is reasonable to expect that benefit would result if t reatment were begun much earlier than is usually the case. However, since the incidence of hypertensive heart disease and stroke can be greatly reduced by treatment, the detection of hypertension is in any case important.

The bulk of the hypertensive problem lies with the many individuals who are unknown to their practitioners and can be detected only by health examinations. There is no escape from this

140 February, 1976, Vol. 91, No. 2

dilemma. We believe that there are needless fears that anxiety and introspection would often be induced or that the numbers found to have hypertension would be too great for management. Following an initial medical assessment by the physician, much of the management could be supervised by community nurses working with family doctors.

Treatment of other coronary risk factors, to- gether with the elimination of added salt from the table and in cooking, may alone suffice to control the blood pressure in those with borderline or mild hypertension. Others, including most with severe and moderately severe hypertension, re- quire drug therapy which will largely protect them from hemorrhagic strokes, left ventricular failure, and acceleration of renal failure. How- ever, since they still tend to die prematurely from CHD, attention to all risk factors is very impor- tant. This especially applies to hyperlipidemia and smoking.

The control of blood pressure without signifi- cant side effects is usually possible if an appro- priate combination of drugs is used, and those with a relatively high incidence of side effects, such as guanethidine, methyl dopa, rauwolfia and clonidine, are avoided. Oral diuretics are essential only for the control of fluid retention. They are often used in hypertension but the long-term effects of induced hypokalemia are unknown and some develop hyperglycemia or hyperuricemia.

We think a beta blocker should nearly always be given either alone or in combination, since the 51ood pressure is thereby reduced in both lying and standing postures. Side effects are uncom- mon and rarely severe, postural hypotension does not occur, and there are many potential advan- tages in reducing catecholamine secretion.

Most patients with more severe hypertension will in addition require another drug. For the last 10 years we have found that debrisoquine has many advantages and is the best of the adrenergic blockers. It is remarkably free from side effects and, provided tha t the initial dose is small and only slowly increased, postural symptoms can usually be avoided.

New methods of drug therapy are under study but not established.

Hyperlipidemia, atherosclerosis, and diet

Population studies have shown that there are close links between hyperlipidemia, atherosclero- sis, CHD, and diet. 13, 1~ Their interrelationships

Cardiologist's role in prevention of CHD

are complex and, since there is considerable vari- ation between individuals, other factors must be involved. The evidence suggests, however, tha t there are basically nutritional disorders.

Secondary thrombus formation and its compli- cations vary considerably despite similar severity of atherosclerosis so that the latter is more an index of susceptibility to CHD than to its inci- dence and the factors responsible are not identi- cal. 1~

There is also a vast amount of epidemiological, clinical, pathological, and experimental work to indicate that hyperlipidemia, influenced by inher- ited predisposition and habitual diet, not only has a high association and hence is a strong predictor, but is a causal factor in the etiology of atheroscle- rosis and CHD.

Nevertheless, there are gaps in knowledge and the crucial evidence that the incidence, extent, and mortality rate of CHD can with certainty be reduced by dietary means alone is not at present available. The trials which have been reported are promising but have had imperfections of design and so are not accepted as conclusive. Ideally they should begin in childhood before atheroscle- rosis is advanced, as it often is in middle age, but this would add to the difficulties referred to below.

In the absence of proof and in such a serious situation, decisions must be made and advice given or withheld on the basis of probability. Paradoxically, far stronger evidence is often demanded for preventive measures that is ever considered necessary for giving drugs or advising surgical treatment.

The evidence supporting a causal relationship between hyperlipidemia and CHD, and hence justifying dietary advice, includes the following facts:

CHD is rare in populations with low mean plasma cholesterol levels;

CHD at a relatively young age is common in patients with familial hyperlipidemia.

There is an almost linear relationship between plasma cholesterol levels above 200 mg. per 100 ml. and the incidence of CHD.16

Recent studies suggest that hypertriglyceri- demia is probably an independent risk factor.

Plasma lipids are mainly derived from the food and can be raised or lowered by changing eating habits.

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The hallmark of the atheromatous plaque is the accumulation of cholesterol in it.

The concentration of cholesterol in the arterial wall is in proportion to that in the plas- ma. ~

It has been repeatedly shown that atheroscle- rosis can be produced in many species by feeding a high fat ,high cholesterol diet but, most impressively, in primates nearest to man atherosclerosis and its complications of myocardial infarction and peripheral gan- grene has been induced by feeding a Western- type diet28

Furthermore, the pathological changes in the arterial wall regress on changing back to a natural diet. 19

The clinical counterpart in man is regression in cutaneous manifestations of hypercholeste- rolemia after treatment by diet or drugs.

Finally, as mentioned above, recent dietary trials in man are encouraging. 2~

Variation in plasma lipids. Although it is clear that atherosclerosis and plasma lipids are mainly nutritionally determined, lipid levels vary in populations and in individuals living on a similar diet and even between those kept on an identical diet in a metabolic unit. Consequently, there must be variable inherent Susceptibility to develop atherosclerosis. Nevertheless in all people lipid levels are much influenced by diet.

Not only is there considerable variation between individuals, but in the same individual from time to time and even from day to day; The reasons for this are not fully understood but include dietary and nondietary factors. Dietary factors include total calories, total fat, saturated and unsaturated fat, refined and unrefined carbo- hydrate, cholesterol, sugar, and alcohol. Nondie- tary factors include smoking, ' exercise, stress, season, posture, changes in weight, recent myocardial infarction, and drugs.

It is clearly important that measurement of cholesterol and triglycerides should be accurate but this is far from being the case in many laboratories. Quality control studies have shown remarkable variation in the reported results from different laboratories on the same specimen of blood.

These are unfortunate facts, but they must be kept in mind. Nevertheless, in the vast majority of patients and in population studies, only a

single measurement is made and more than this may not be practicable.

Plasma lipoproteins and lipids. The classifica- tion of plasma lipoproteins introduced by Fredrickson, Levy, and Lees ~ and the modifica- tions suggested by others were based on studies of familial hyperlipoproteinemias. They are impo r - tant for the understanding of metabolic abnor- malities and for research but, unfortunately, have been inappropriately applied to the general popu- lation.

Measurement of lipoproteins are unnecessary for the management of the great majority of coronary patients and those at high risk from developing the disease. They are needed only for the few with true familial hyperlipoproteinem- i a - tha t is, with a clear family history, and where eating habits have not been the main factor, and for the few who fail to respond to simple treat- ment. The facts that inherited predisposition and habitual diet are important for all with hyperli- pidemia does not mean that they can be classified into Fredrickson's types of familial hyperlipopro- teinemia. At present there is no evidence tha t measurement of lipoproteins is a better guide to prognosis or treatment than that of plasma lipids.

Diet. Reduction in lipid levels is likely to have a favorable effect in all at high risk, but most of them are unknown to their practitioners. Conse- quently it is reasonable to advise some modifica- tions in diet for the population as a whole, many of whom have relatively high lipid levels by ideal standards, that is to say, above those in Countries with little or no atherosclerosis. If regular health examinations were accepted and lipid levels known, advice could be given on an individual basis, but at best it will take some years before such routine screening can be introduced.

The principles of diet are not difficult to learn nor does adherence to them entail much hardship. Habits can often be changed if the reasons are appreciated. There need be no absolute taboos and general rules can be forgotten when dining out or on other special occasions.

In the obese, calorie restriction should include reduction in total fat and carbohydrate intake. Saturated fat, sugar, and salt should be reduced, with a switch from saturated to polyunsaturated fat at table and in cooking.

The same basic diet for lowering plasma lipids can be advised for all coronary patients and those

142 February, 1976, Vol. 91, No. 2

at high risk, with modifications for particular circumstances.

Obesity, hypercholesterolemia, and hypertri- glyceridemia are undesirable. The aim should be to eliminate adiposity and maintain cholesterol and triglyceride levels in the lower physiological range.

If cholesterol levels are inadequately reduced there must be greater emphasis on avoidance of saturated fat and eggs, and if triglyceride levels are inadequately reduced, on avoidance of sugar and alcohol. The benefits of increasing energy expenditure by regular exercise should also be explained.

Should this regime be inadequate, the next step is to give clofibrate, which is tolerated by almost all, without side effects of any kind.

Only a few require more detailed laboratory investigation of lipoproteins and individual drug therapy.

Obesity

All insurance statistics have shown that obesity is adverse to health, mainly from cardiov- ascular and cerebrovascular diseases, and that life expectancy improves with its reduction. I t is probably not so much obesity itself, however, which is a high-risk factor as the often-associated hypertension, hyperlipidemia, and impaired glu- cose tolerance, all of which improve with its reduction. In addition, obesity discourages the taking of exercise.

In treatment it is important that emphasis should be laid on regular exercises as well as diet because of its intrinsic benefits. One hundred calories less consumed and 100 more expended each day would lead, over the course of a year in an obese person, to the loss of about 20 pounds in weight.

Exercise

There is much to indicate that physical inac- tivity is one important factor in the high preva- lence and increasing incidence of CHD. Man did not evolve as a sedentary being, and lack of regular exercise is of recent development. The physiological responses to regular exercise, the value of training in rehabilitation after myocar- dial infarction, and in improving exercise capacity in patients with angina of effort all support its role in the primary prevention of CHD.

Between the pioneer studies of Morris and

Cardiologist's role in prevention of CHD

associates 2~ more than 20 years ago and their most recent paper ~ there have been many reports on the value of exercise. Conclusions based on retrospective analyses can be criticized owing to inherent defects which cannot be avoided. Almost all observational studies ~ which include leisure activities have shown a beneficial effect from exercise in reducing the incidence, severity, and morbidity of CHD. Further work of a similar kind is unlikely to bring stronger evidence. Only controlled prospective intervention studies could produce a conclusive answer but there would be great difficulties in carrying them out and, as in the case of dietary trials, expense alone would probably be prohibitive.

Regular exercise, if sufficiently vigorous, great- ly improves cardiopulmonary function and exer- cise tolerance in healthy individuals. ~7 Maximum oxygen uptake and its transport, together with oxygen extraction by the tissues, are increased, myocardial oxygen economy is improved with less oxygen required for a given amount of work, and myocardial vascularization is almost certainly increased. ~8 Peripheral mechanisms also play a part in improving regional blood flow.

Most coronary-risk factors are favorably mod- ified by exercise. Hyperlipidemia, postprandial lipemia, and hyperglycemia are all reduced. On the same calorie intake there is weight loss in the obese. Peripheral vascular resistance is lowered so that blood pressure is reduced. Fibrinolytic activity is increased and platelet aggregation reduced so that thrombus formation is likely to be impeded.

All forms of rhythmical dynamic exercise are beneficial if sufficiently Vigorous to cause sustained tachycardia. Walking, running, jogging, and climbing stairs or hills can be carried out throughout the year without expense or special facilities. Swimming and cycling are excellent for improving exercise tolerance. Half an hour's brisk walk each day, together with more vigorous exer- tion for half an hour three times a week, can greatly improve cardiopulmonary fitness. The major problem is that of motivation.

Although older subjects and those at high risk may need a medical examination before under- taking an exercise program, most healthy people do not, provided they start gently and gradual ly increase the vigor of activity.

All forms of exercise are useful for energy expenditure.

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Exercises (calisthenics) are useful for warming up and for improving muscle tone and joint mobility to avoid soft tissue injuries, but only sustained tachycardia for ten minutes or more will improve exercise tolerance and cardiopul- monary fitness to a degree which is likely to be protective to the myocardium. All these aspects have been reviewed. ~7

Exercise has to be built into our way of life, seeking every opportunity throughout each day.

Stress

Many workers have shown associations be- tween CHD and emotional stress. Angina, myocardial infarction, pulmonary edema, and sudden death can be precipitated by arguments, driving an automobile, excitement, or bereave- ment. These effects are thought to be due to catecholamine secretion.

The ambitious, aggressive, competitive way of living may, over the years, lead to CHD, although stress can also lead to other risk factors such as smoking and overeating. We have found that our coronary patients cannot be conveniently clas- sified into personality types because patients and controls each include a variety of characteristics in varying proportion. It is the reaction to stress which is important.

It has often been noted that preceding a myocardial infarction there have been weeks or months of unusual stress. A direct relationship between stress, atherosclerosis, and thrombus formation is more difficult to prove, but is supported by the known mechanisms of catechol- amine secretion which include increase in blood pressure, heart rate, circulating lipids, and platelet aggregation.

Advice relating to the reduction of sympathetic overactivity should be undertaken by personal counselling on avoiding unduly stressful situa- tions, including conflicts and confrontations at home and at work, on stopping smoking, and on the importance of regular exercise which im- proves autonomic balance. Beta-blocking drugs are useful while personal readjustments are being made.

Other risk factors

Most Other risk factors which have been consid- ered do not at present have practical implications other than the measures discussed above. They include diabetes and subclinical carbohydrate intolerance, hyperuricemia and various trace

elements. Diabetes in particular requires a very vigorous approach against the recognized risk factors.

Additive factors

Risk factors are not only individually adverse but often interrelated, cumulative, and possibly synergistic. This has been shown for various combinations of hypertension, hyperlipidemia, smoking, obesity, and physical inactivity. A strong family history of relevant disorders is also important because it reflects inherited predisposi- tion.

These facts should be kept in mind, particu- larly when making decisions on whether to treat borderline conditions, such as hypertension. In a multifactorial disease control of a single factor is unlikely to have a major impact, and it is clearly important to aim at controlling them all.

Vigorous approach to secondary prevention

The physician should regard each new patient with symptomatic CHD as one in whom primary prevention has failed, usually through not having been tried. Such a person should be accepted as an opportunity and a challenge for a vigorous and even aggressive approach to secondary preven- tion. In addition, each patient provides access to the family, who are also likely to be at high risk, in order to screen for coronary-risk factors and give appropriate advice on primary prevention. The aim should be to eliminate or greatly reduce each coronary-risk factor.

Myocardial infarction. Vigorous secondary pre- vention after myocardial infarction should be a major responsibility for every cardiologist. Such an approach is warranted because the prognosis is relatively poor in survivors of reinfarction. Conventional advice often amounts to little more than, "Cut down on smoking, lose some weight, and otherwise take it easy." Rather we should aim to eliminate smoking, hyperlipidemia, hyper- tension, and obesity, encourage a program of regular exercise, and pay individual attention to avoidable stress. Most patients should feel much fitter 6 months after their at tack than they did before.

We have found that acceptance of advice given in hospital is assisted by an explanatory booklet, by regular follow-up interviews, and by visits from a community nurse acting as a link between hospital and home. Not only can she ensure tha t the patient understands what should be done, but

144 February, 1976, Vol. 91, No. 2

she can give further advice on details, advising the wife on the optimum diet for her husband and children, and emphasizing the importance of a smoke-free home and of regular exercise.

Angina of effort. Most patients with angina of effort can be much improved by proper medical management, which is too often neglected. Surgical treatment is needed only in the small number who fail to respond. Unless it can be shown in properly controlled trials tha t the expectation of life is thereby improved, these hazardous investigations and palliative opera- tions should not take precedence over well-tried medical management. The risks and complica- tions of surgical treatment would certainly not be acceptable to the FDA if a drug rather than an operation were under consideration.

The cornerstone of management is a definitive exercise program, gently begun and gradually increased, short of pain, dyspnea, or fatigue. This is facilitated by the invariable use of prophylactic trinitrate and the routine use of a beta-blocking drug, such as propranolol or oxprenolol, up to at least 800 mg. daily if necessarY. At the same time there should be a vigorous attack on all asso- ciated coronary-risk factors.

We have found that this approach is successful in the great majority of patients.

Although these aspects of secondary preven- tion in treatment are important, the real answer to the coronary problem lies in primary preven- tion.

Primary prevention

Health examinations. The concept that pre- vention is better than palliation or cure is univer- sally held, but often little more than lip service is paid to this obviously sensible principle.

The detection of those at high risk with the object of giving preventive advice can be done only by screening, but this term has led to misunderstanding. Mass population screening is a formidable concept suggesting publicity and considerable expenditure on facilities and person- nel, with the problem of dealing with the large numbers detected. Rather do we recommend regular health examinations carried out by personal physicians as part of normal health care, needing few extra facilities, although assistance would be required from health workers.

We have found that community nurses are interested, keen, and capable of helping with the initial health examination and in the giving of

Cardiologist's role in prevention of CHD

advice and sometimes treatment, such as for hypertension. In addition, by visiting the home they can advise on food, smoking, exercise, and stress.

Nurses can also form an invaluable link between hospital and home in rehabilitation and secondary prevention after acute myocardial infarction and in extending advice to primary prevention in the family.

Some contend that health examinations are not indicated at the present time because: (1) The evidence that risk factors are causal is only circumstantial. (2) Prediction is not yet suffi- ciently accurate. (3) There is no proof that inter- vention would reduce the incidence of CHD. (4) Unwarranted anxiety might be induced. (5} Facil- ities will not always be available for dealing with conditions found. (6) Some conditions would be disclosed for which as yet no adequate t reatment exists. Consequently, it is considered tha t action should await more research and further trials.

Our viewpoint is that although more research is certainly needed, especially as regards better predictors of CHD and underlying mechanisms which might be influenced by treatment, enough is already known to justify preventive action.

In the United States much is being done by the example and enthusiasm of individual physicians and research teams. In the United Kingdom a little is being done by a few. However, the problem is a public health problem of national dimensions. There are immense implications for reorientation, including acceptance of the prin- ciple of regular health examinations followed by the giving of informed advice.

Periodic health examinations are made more often in the U. S. than in the U. K. After this has been done, however, advice on primary preven- tion should be given by physicians who are aware of the facts and have learned how best to put the message across. Most doctors are not motivated toward preventive medicine, are unfamiliar with the evidence justifying action, and may consider that they cannot afford the necessary time. In the U. K, the basis of health care is general practice and almost all are registered with a family doctor; routine health examinations could be introduced without need for special facilities, undue extra time, or the fear that anxiety and introspection would be engendered. An initial health examina- tion when registering with a family doctor would soon be accepted as normal practice.

The essential prerequisites are motivation, an

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up-to-date age-sex register, one or more commu- nity nurses, and secretarial help.

In the U. K. more than 60 per cent of patients consult their doctor each year and the average turnover of new patients and those dying or leaving the district is about 10 to 15 per cen t per annum. Within five years few would not have consulted their doctor and these could be visited by the community nurse.

No proof. "No proof- the evidence is only circumstantial" is the cry too often heard with regard to prevention. A growing number of physi- cians believe, however, that the risk factors discussed are almost certainly causal and that benefit would result from their reduction. As in many areas of medical practice, strong proba- bility rather than proof must govern action. The effectiveness of many treatments lacks proof yet they are widely prescribed.

Large-scale prospective intervention studies which alone could bring proof are unlikely to reach conclusions, at any rate for many years. Owing to great difficulties and cost, single-factor trials of adequate size may never be carried out. The case of dietary trials may be taken as an example. Recently it was estimated that a satis- factory full-scale trial would require between 24,000 and 115,000 participants, would need to last for 7 to 10 years, and would cost between $500 million and $1,000 million. ~9 It was considered that there would be great problems because of dropouts, the fact that about 20 per cent of Americans change their place of living each year, that participants would probably be motivated to change other risk factors and controls to modify their habits owing to a change in the climate of opinion and thus influe~ice the study. Also the trial might never be finished and, if it were, the results might be inconclusive.

For similar reasons conclusive evidence on the value of regular exercise might be even harder to obtain and a trial in relation to stress would be impossible.

There is no need for stronger evidence that smoking, hypertension, and obesity are adverse to health.

Prevention in childhood

Since atherosclerosis frequently starts in youth, preventive measures should begin early. Children could be brought up virtually free from coronary-risk factors. The first step lies in infant

feeding. There are many advantages in breast milk but in the coronary context most important are the avoidance of obesity (which is easier than when substitutes and supplementary foods are given), of hyperlipidemia, and of a taste for sugar and salt.

Obesity in infancy frequently precedes that in childhood and adult life, yet still it is the tradi- tional "bonny" baby who gets the prize rather than the parents who should be allotted the booby prize.

Babies vary in their requirements as do adults, and excessive weight gain should be immediately countered.

Breast milk has been gradually evolved toward perfection over millions of years and for a normal baby born to a healthy mother is an all-sufficient food for the first few months.

Cow's milk is unnatural, except for calves. The fat is more saturated than in human milk and less well absorbed. The sodium content is much higher and this could be a factor in later hyper- tension. Recently it has been suggested that cow's milk protein has antigenic properties which, for some, may be a causal factor in atherosclero- sis. 30

Appropriate weaning should include limitation of saturated fats and their partial replacement with polyunsaturated fat with a high linoleic acid content, together with avoidance of added sugar and salt. A taste for healthy foods should be inculcated early, since good feeding habits are likely to persist.

School meals require review with the same principles in mind. All this implies a changed attitude by nutritionists and all concerned with health education.

Summary,

The recent increase in coronary heart disease is real and the causes must mainly be environment- al. Consequently the condition should largely be preventable. The application of what is already known is likely to be a far more effective way of reducing the mortality rate than all a t tempts at palliative treatment, but vigorous action will be necessary. Much greater sums are being expended on coronary-care units and cardiac surgery than in preventing the need for them, although there is little evidence that they have significantly lowered the over-all mortality rate.

Conventional treatment is immensely expen-

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Cardiologist's role in prevention of CHD

sive. P r e v e n t i o n cou ld in t he long r u n be m u c h cheaper.

Cardiologis ts on the i r own are u n l i k e l y to succeed in a p r o g r a m of p r e v e n t i o n . T h e y n e e d the help of m a n y others , i n c l u d i n g c o m m u n i t y nurses , nu t r i t i on i s t s , pub l i c h e a l t h workers , soci- ologists, a n d of course gene ra l p r ac t i t i one r s , b u t t hey have r e spons ib i l i ty for l eade r sh ip a n d for p rov id ing b a c k g r o u n d knowledge .

For the de tec t ion of c e r t a i n r isk factors , h e a l t h e x a m i n a t i o n s are neces sa ry a n d s h o u l d be p a r t of genera l pract ice. Also, advice is bes t g iven on a n ind iv idua l basis. T h e ch i e f -known r isk fac to rs (hyper l ip idemia , h y p e r t e n s i o n , smoking , phys i ca l

inac t iv i ty ) could be con t ro l l ed .

C H D occurs in a d u l t s b u t a the rosc le ros i s s t a r t s m a n y years before. P r e v e n t i o n s h o u l d begin w i t h appropr i a t e i n f a n t feeding, w h e n e v e r poss ib le wi th b reas t milk, a n d c o n t i n u e i n to ch i ldhood, when hab i t s are fo rmed a n d a t t i t u d e s to life c a n

best be inf luenced. I t shou ld be possible to b r i ng u p ch i l d r en

v i r t u a l l y free f rom risk factors .

I t m a y never be possible to prove the effective- ness of such a m u l t i f a c t o r i a l p r o g r a m by prospec- t ive con t ro l l ed i n t e r v e n t i o n s tudies , b u t t he evidence ind ica tes s t r o n g p robab i l i t y . T h e s t akes are too high to de l ay a c t i o n a n y longer . Phys i - cians da i ly give advice in a reas where the ev idence is m u c h less cer ta in .

Such a p rog ram for the c o n t r o l of c o r o n a r y a r te ry disease is u r g e n t l y needed a n d cou ld become one of the m o s t r e w a r d i n g ac t iv i t i es for

the med ica l profession.

REFERENCES

1. Turner, R., and Ball, K.: Prevention of coronary heart disease, Lancet 2:1137, !973.

2. Fletcher, C. M., and Horn, D.: Smoking and health, Report to World Health Organisation, 1970.

3. Diet and coronary heart disease. Department of Health and Social Security, Health and Social Subjects No. 7, London, HMSO 1974.

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