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Can I Avoid a Heart-attack?

THE LANCET

TAKING stock should be a regular exercise in ourmedical endeavour; and the reckoning must in partbe made by our patients, for only through the eyesof the customer can the value of the goods be finallyagreed. In heart-disease attention is easily drawn todramatic achievements in diagnosis and surgery-butthe major part of heart-disease in the Western worldis less tangible, and often makes its presence knownonly late in its progress, through acute myocardialinfarction or sudden death. It is in the area ofischaemic heart-disease that we need particularly toquestion medicine’s contribution. Within the pastdecade the prospect for the patient with ischaemicheart-disease has been much improved by the intro-duction of beta-adrenergic antagonists in the treat-ment of angina pectoris and by striking changes inthe practical management of acute myocardialinfarction. Yet, notwithstanding all the improvementin the clinical care of established illness, the mostimportant question-" How can I avoid a heart-attack ?"-remains as a sardonic commentary on ourperformance in preventing heart-disease.What are the facts in terms that the ordinary person

can understand, and what should he do to safeguardhis health now and for the future ? ? Another natural

question is " What are we trying to prevent ?", and

around this lies much of the uncertainty in our

thinking. The mechanism or mechanisms precipi-tating acute myocardial infarction are unknown. Thepseudonym

"

coronary thrombosis " reflects the

frequent finding of fresh thrombus in coronaryarteries of patients dying from infarction; but wedo not know whether this precedes or follows theinfarction. 1 The lower incidence of thrombus inpatients dying early in the acute illness 2,3 and thestill smaller incidence in patients dying suddenlysuggests that thrombus may not be quite so impor-tant 4 as was thought during the era of anticoagulants.Unfortunately, the unpredictability of the event inthe individual patient and its inaccessibility inanatomical location have denied us information on theearliest stages of a coronary attack.

Great store has been laid on the study of " risk

factors " associated with a high incidence of heart-attacks, the hope being that eliminating risk factors

1. Ehrlich, J. C., Shinohara, Y. Archs Path. 1964, 78, 432.2. Meadows, R. Med. J. Aust. 1965, ii, 409.3. Kagan, A., Livsic, A. M., Sternby, N., Vihert, A. M. Lancet, 1968,

ii, 1199.4. Spain, D. M., Bradess, V. A. Am. J. med. Sci. 1960, 240, 701.

will eliminate the associated disease. Animal-fatdiet, obesity, too little exercise, striving, fatigue,emotional deprivation in terms of success, cigarettesmoking, and various other supposed sins of our timehave all been upheld as the modern horses of theApocalypse. Organic disease such as hypertensionand diabetes mellitus also figure.5 One thing is clear:statistical association must not be immediatelyequated with cause and effect. To give proof ofcause and effect between one risk factor and disease

requires its isolation as a cause, and proof of benefitthrough its elimination. Thousands of patients needto be involved, the time scales are very long, evenup to a lifetime, the factors to be controlled are

multiple, and people are human. Any interferenceneeds to be undertaken as an act of scientific inquiry-but is it really practicable ? So far, despite all theeffort and money that has been spent, the evidencethat eliminating risk factors will eliminate heart-disease adds up to little more than zero in terms of

preventing heart-disease on a public-health scale.The only unassailable criterion of preventive successis a reduction in the number of deaths, so we

urgently need a new working standpoint. Do we

accept the case as proven, and so advise our patients,recognising the immense problems of absolute proofand sacrificing critical insight and scientific standards?Or do we start again, adopting a nihilistic attitudewhile awaiting the proof that may not come in ourtime ? ’;)

-

A simple answer cannot be given, for the evidenceis of different weight according to the "risk"selected. Obesity, exercise, blood-lipids, and diethave held the stage for many years-at one time

instilling such conviction that some believers longpast their prime were to be seen in public parks inshorts and singlets, exercising in their free time,later returning home to a meal of indescribablecaloric severity in pursuit of the cult of physicalfitness, low plasma-lipids, and avoidance of heart-disease. There is no proof that such activity offsetscoronary disease. However, gross obesity is dele-terious in terms of average prognosis for life, accord-ing to actuarial reports. Regular exercise of quitelow intensity certainly improves mental well-beingand resistance to mental depression. In the absenceof detectable heart-disease there is no special risk ofheart-attacks during minor exercise, and much canbe said for it on general grounds. 6Much more problematic is the question of blood-

lipids and diet. Here is a vast investment in termsof academic interest, epidemiology, and public-healthresponsibility. Serum-cholesterol, for instance, in-creases progressively with age in men and women.Men sustain an increase in total serum-cholesterol ofabout 25% between ages 20 and 50. Women show

5. Research on Acute Myocardial Infarction. Am. Heart Ass. Monogr.1969, no. 27.

6. Hellerstein, H. ibid. p. 124.

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a more striking increase from initially lower levels toabout the same as men at 50 years. Serum-cholesterolcorrelates positively with the incidence of clinicalevents linked with atherosclerosis.7-9 Cause andeffect is inferred, but is as yet unproven on a largescale. A key test is to show that electively reducingserum-cholesterol reduces clinical atheroscleroticcardiovascular disease. The evidence in man 10-15 is

hopeful, but miniscule in comparison with the generalaura of faith in such therapy. We should recognisethat serum-cholesterol is often very high even whendemonstrably reduced by diet and drugs, and a

magical halting of the complications of atherogenesiswould not necessarily be expected within a shorttime. Even if the reasoning that the greater theconcentration of blood-lipid the faster the onset ofdisease were correct, deferred onset might well bethe only legitimate expectation of blood-lipid reduc-tion. If so, benefit is likely to be very difficult toprove. Radical test of the blood-lipid hypothesis islikely to be possible only through drastic reductionof serum-lipids, and this is rarely achieved except insmall numbers of almost fanatically determined

patients. Sometimes surgical means of reducingcholesterol absorption need to be resorted to, thusavoiding the vagaries of diet and personal discipline.Partial ileal bypass 16,17 has its risks and is not

universally appealing. However, a thorough studyin patients accepting all such measures may be theonly way of estimating the order of benefit to beexpected at best through metabolic intervention.Trials of cholesterol-lowering drug therapy 18,19 haveyielded equivocal results, and diet studies are almostunmanageable in large numbers of patients over manyyears. However, despite these reservations aboutthe clinical profit in reducing plasma-lipids, it is truethat almost all patients dying from myocardial infarc-tion or sudden death do have at least a moderate

degree of atherosclerosis. It would be unfair to

deny atherosclerosis a basic role in clinical disease,since infarction and sudden death without tangibleexplanation is very rare in the presence of normal

7. Dawber, T. R., Moore, T. E., Mann, G. V. Am. J. pubi. Hlth,1957, 47, part II, p. 4.

8. Doyle, J. T., Heslin, A. S., Hilleboe, H. E., Formal, P. F., Korns,R. F. ibid. p. 25.

9. Chapman, J. M., Goerke, L. X., Dixon, W., Loveland, D. B.,Phillips, E. ibid. p. 33.

10. Leren, P. Acta med. scand. 1966, suppl. 446, p. 5.11. Turpeinen, D., Miettinen, M., Karvonen, M. J., Raine, P.,

Pekkarinen, M., Lehtosuo, E. J., Alivarta, P. Am. J. clin. Nutr.1968, 21, 255.

12. Christakis, G., Rinzler, S. A., Archer, M., Winslow, G., Jampal,S., Stephenson, J., Friedman, G., Fein, H., Kraus, A., James, G.Am. J. publ. Hlth, 1966, 56, 299.

13. Bierenbaum, M. L., Green, C. P., Florin, A., Fleischman, A. I.,Caldwell, A. B. Circulation, 1965, 32, suppl. II, p. 3.

14. Rinzler, S. H. Bull. N.Y. Acad. Med. 1968, 44, 936.15. Dayton, S., Pearce, M. L., Hashimoto, S., Dixon, W. J., Tomiyasu,

U. Circulation, 1969, 39, suppl. II.16. Buchwald, H. Surgery, 1965, 58, 22.17. Buchwald, H., Moore, R. B., Lee, G. B., Baltaxe, H., Amplatz, K.,

Frantz, I., Varko, R. L. Proc. I Vth Asian Pacific Congr. Cardiol.1968, p. 318.

18. Arthur, J. B., et al. Br. med. J. 1971, iv, 767.19. Research Committee of the Scottish Society of Physicians, ibid.

p. 775.

coronary arteries. On the other hand, severe coronaryatherosclerosis post mortem is compatible with a fullthree-score years and ten and more of symptom-freelife. In farming communities subject to prolongedexposure to diets dominated by dairy produce and,therefore, on the current thesis severely at risk ofatherosclerosis and heart-disease, the expectation forlife is good or better than average.20 Clearly it isnot a simple matter of one cause and one effect.

Stress, fatigue, frustration, depression, and otheradverse psychological situations rank highly in

popular acclaim as harbingers of cardiac disaster, andit would seem that there is something in this.21,22Myocardial infarction and sudden death is signifi-cantly increased among the recently bereaved.23Myocardial infarction rapidly following announce-ments to industrial staff of impending redundancyduring industrial strife has been observed but as

yet not collectively documented. General clinicalexperience is not short of such impressions, but thisapproach is often derided by those whose interestsare more easily quantified. They should not beunaware that animals deprived of nervous influenceson the heart by surgical denervation and adrenergicblocking drugs are remarkably resistant to majorcoronary occlusion, and lethal arrhythmias are rare.24More easily measured is cigarette consumption.Cigarette smoking is clearly related to the develop-ment af ischaemic heart-disease. 25, 26 Men, especially,are at risk. Giving up smoking is absolute and ismuch easier tested than changes in diet or mood.In limited groups who have given up the habit thereis definite evidence of a reduction in future risk ofheart-disease. The additional risk from smoking ismore striking in the younger sections of the coronary-risk age-group; about three times that of a non-smoker.

Ischaemic heart-disease is statistically linked withhypertension and diabetes, and the hypertension linkmay illustrate the fallacy in equating statisticalassociation with cause and effect. Hypertension ismore common in patients subject to ischasmic heart-disease than in others. Removal of excess arterial

pressure might be expected to result in a reductionin clinical heart-disease, but this does not happen.27,28Naturally, there are qualifying remarks such as, didtreatment begin early enough and was blood-pressureeffectively controlled?; and such questions lead on

20. Registrar General Decennial Supplements and Tables on Occu-pational Mortality. H.M. Stationery Office.

21. Wolfe, S. Am. Heart Ass. Monogr. 1969, no. 27, IV, 74.22. Bruhn, J. G., McGrady, K. E., Du Plessis, A. L. Psychiat. Dig.

1968, 29, 34.23. Rees, W. D., Lutkins, S. G. Br. med. J. 1967, iv, 13.24. Schaal, S. F., Wallace, A. G., Sealy, W. C. Cardiovasc. Res. 1969,

3, 241.25. Royal College of Physicians, Smoking and Health Now. London,

1971.26. Surgeon General. The Health Consequences of Smoking. U.S.

Department of Health, Education and Welfare, 1971.27. Hodge, J. V., McQueen, E. G., Smirk, H. Br. med. J. 1961, i, 1.28. Breckenridge, A., Dollery, C. T., Parry, E. H. O. Q. Jl Med. 1970,

34, 411.

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to more ethical debate about the case for interveningin the lives of individuals who are clinically well onthe basis of evidence which is suggestive, associative,but not provenly causative. Again, such evidence iscollective, grouped and averaged but not necessarilypertinent to the individual. This last point is

especially important. All that is known from

epidemiology and group studies which depend onstatistical expression of mean differences should beemphasised as representing just that, a mean differencebetween compared groups. Identification of a

susceptible individual has never really been achievedexcept through a gross averaged assessment ofaccumulated risk factors, and MEADE and CHAKRA-BARTl 29 point out that " a prediction within a highrisk group on the basis of multiple factors still

produces incorrect forecasts more often than correctones ".

So what do we do ? It may be that total eliminationof risk factors at an early stage should be our goal,and that we should accept the hotchpotch of hardevidence, suggestion, and faith as our guideline. 30For those who have not the time to wait for proofthere is much merit in the motto " Act now, thinklater ". Advice to our patients must be reasonableas well as objective, since only a proportion are futurebeneficiaries-the rest merely subjects. The cureshould not be worse than the disease. Smoking is ahazard to health and can be positively discouraged.Specifically it increases the risks of heart-attack andlung cancer to a degree which is unacceptable formany. Obesity is bad for general health and canlegitimately be attacked. Some degree of physicalfitness is an aid to general health. Diets high inanimal fats cannot be said to be so certainly causativeof heart-disease that they should be vetoed-butequally palatable alternatives are sensible. It is fairthat life should be enjoyed and rewarding, and thatmatters governing emotional wellbeing should be

consciously safeguarded. And the protection all thisgives ? We cannot say. The important thing is tomake a reasonable investment at a reasonable price.Perhaps the objective interest and care in the qualityof life will provide the best guarantee against a heart-attack.

Conquest of Malaria: the Art of theFeasible

" We like progress, but it must commend itselfto the Common Sense of the People." SAMUELBuTLER’s comment on the Erewhonian common-wealth, where machines would be acceptable onlyif they do not become masters of men, shows a

remarkable foresight into some aspects of today’sworld. It could very well be used as a prefix to a report29. Meade, T. W., Chakrabarti, R. Lancet, 1972, ii. 913.30. Turner, R., Ball, L. ibid. 1973, ii, 1137.

of the World Health Organisation’s interregionalconference on Malaria Control in Countries WhereTime-Limited Eradication is Impracticable at Pre-sent. 1 This report incorporates the collective

opinion of representatives of 31 countries andterritories of Africa, the Middle East, and theWestern Pacific, who gathered in 1972 in Brazzaville.

In 1955 the World Health Assembly adopted theprinciple of global malaria eradication, 2 and a

year later its concept was defined as " the end of the

transmission of malaria and the elimination of thereservoir of infective cases in a campaign limited intime and carried out to such a degree of perfectionthat, when it comes to an end, there is no resumptionof transmission ".3 This definition stresses un-

ambiguously the contrast between the " once-and-for-all " concept of eradication and the indeterminedduration of malaria control. The early results of thecampaign, waged mainly in Europe, Asia, and severalcountries of the Americas, were remarkable. Withinten years over 1000 million people living in the

originally malarious parts of the world were relievedof the enormous burden of this disease, and this wasoften followed by striking socioeconomic advance.Nevertheless, with a few exceptions, there has beenlittle progress in the tropical core of the geographicaldistribution of malaria. The initial credo of malariaeradication seems to have been copied from Silvius’sdeclaration to Phoebe in As you Like It: " all made of

passion and all made of wishes, all adoration, dutyand observance ". However, a decade after theofficial launching of the world-wide programme ofmalaria eradication the World Health Organisationrecognised the obstacles that lay ahead. A remarkablyfrank and realistic assessment of the situation was

presented before the 22nd World Health Assembly.-1This report pointed out that, during the first decade,too much confidence and emphasis was placed onthe use of residual insecticide spraying as the mainmethod of attack on the anopheline vector. On theother hand, the importance of all the administrative,socioeconomic, financial, and other factors so

prominent in tropical developing countries was

underestimated.5 Difficulties that had slowed the

early advance of malaria eradication were obvious,yet many countries with slender resources continuedrather wearily to fulfil their contractual obligations.Moreover, technical obstacles arose in the shape ofinsecticide resistance and drug resistance. When in1969 the future strategy of malaria eradication under-went its painful reappraisal, the need for an alterna-tive to the unfulfilled dream was evident but the newtactics were uncertain. The Brazzaville reportprovides much background for a less ambitious but

1. Tech. Rep. Ser. Wld Hlth Org. no. 537, 1974.2. World Health Organization, Proceedings of the 8th World Health

Assembly. Off. Rec. Wld Hlth Org. 1955, no. 63.3. Tech. Rep. Ser. Wld Hlth Org. no. 123.4. Off. Rec. Wld Hlth Org. no. 176, annex 13.5. Bruce-Chwatt, L. J. Bull. N.Y. Acad. Med. 1969, 45, 999.