Brock, J.F.

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Suid-Afrikaanse Tydskrif vir Geneeskunde South African Medical JournalTHE MANAGEMENT OF ISCHAEMIC tCORO ARY) HEART DISEASE*i<aapstad, 23 Januarie 1960 Deel 34 No. 4 Volume 34 Cape Town, 23 January 1960J. F. BROCK, M.D., F.R.C.P., University of Cape TownWithout belittling in any way the valuable contribution whichcan be made in the management of ischaemic heart diseasethrough therapeutics, it is still true that the most importantaspect of management is what is said to the I?atient and hisrelatives by the doctor in charge. "There is a great deal ofiatrogenic heart disease resulting from errors of commissionand omission on the part of the medical practitioner in theverbal management of ischaemic heart disease. These errorsarise in part from uncertainty as to the prognosis in tl:Je indi-vidual case, either in terms of natural history or in terms ofthe modification of natural history which can be achieved bymedical management or therapy. It will probably always bedifficult to assess .individual prognosis, as in many otherdiseases; the best that can be done is to form a judgment ongroup prognosis and., assume that the patient may well dobetter than the average. This optimism is better for thepatient than the reverse pessimism.Few doctors now make the mistake of attributing thepain of myocardial ischaemia to indigestion, but manypatients make this mistake and do not report to their doctors.Furthermore, there is more and more evidence for infarctionwithout pain. For these reasons unexplained breatWessnessor arrythmia among the classes of people defined later asbeing 'at risk' of ischaemic heart disease justifies carefulexamination and electrocardiography.This commendable consciousness of the wide prevalenceand potential severity of the disease leads some doctors togive the patient an exaggerated impression of the potentialseverity during the period of diagnostic uncert.ainty which isoften unavoidable. Patients are often unnecessarily frightenedby the opinion given by the doctor at the first consultation.In doubtful cases some such words as 'I believe' or 'I hopethat this is not a coronary h,eart attack but I can't afford totake the risk of not confining you to bed until electrocardio-graphy and two or three days of observation have excludedthe condition' will save patients much unnecessary worry.When the diagnosis is establish~d it is much easier to correctth,e preliminary opinion in a direction of greater gravitythan to dispel unnecessary and unjustified fears which havebeen raised in the patient's mind.For practical purposes, ischa~mic heart disease is the resultof atheroma or'atherosclerosis of the coronary arterial trunks.Other rare causes will be ignored in this discussion. Athero-sclerosis may be very local and may in some cases beprecipitated into occlusion by subintimaf haemorrhage orother mechanisms which are at present obscure. In general,however, both coronary trunks are considerably ocCludedbefore infarction occurs. The cause of the infarction isoften obscure, but in the majority of cases it is due to throm-bosis of blood in a small segment of one trunk (coronary* Paper presented at the Plenary Session on Heart Diseaseduring the 42nd South African Medical Congress (M.A.S.A.),East London, c.P., September-<:>ctober 1959.thrombosis from occlusive thrombogenesis). Myocardialinfarction without coronary thrombosis is stiU a littlemysterious; in some cases it is undoubtedly due to effort ofsufficient intensity to render the blood flow through narrowedarteries inadequate for the oxygen requirement of the veryactive myocardium. This variety of cau ation will befacilitated by myocardial hypertrophy a in hypertension, orby failure of the oxygen-carrying capacity of the bloodresulting from anaemia or methaemoglobinaemia. In othercases it is not UJl.feasonable to assume that the coronarysystem, or a small segment of one of these trunk , undergoesfunctional narrowing of the lumen through va oconstriction.Such precipitating events as exposure to a cold wind, excite-ment and anger, or effort on a full stomach, are suspectedto operate in this way. In the last resort, however, we mustrecognize that a certain proportion of cases of infarctionare not explainable in terms of coronary occlusion by throm-bosis or of any other mechanism which is at present under-stood.Any pathologist will confirm that severe coronary atherO-sclerosis is often seen at autopsy in the absence of any clearevidence of infarction. Indeed, Morris ha deduced fromthe evidence of the Bernard Baron Institute of Pathologythat the extent and severity of coronary athero clerosis hasnot increased in the London population over the last 3.decades although there has been a great increase in myo-cardial infarction in the same population over the same'period of time. Unless Morris's deduction is refuted we mustconclude that the modern epidemic of myocardial infarctionis determined by an increase in those factors which precipitateinfarction as opposed to those factors which cause athero-sclerosis; in other words, the study of occlusive thrombo-genesis may be more rewarding than the study of atherogenesisin explaining the increasing prevalence of myocardial in-farction. It is admitted that the mechanisms through whichblood is caused to coagulate within a segment of a narrowedcoronary artery (occlusive thrombogenesis) are not at presentunderstood and may not represent all the mechanismswhereby myocardial infarction is precipitated; nevertheless,they must be very important for study. By the same token,therapy through anticoagulant drugs may have a soundbasis in theory.The encouraging feature in the outlook of the last decadeis the epidemiological demonstration that myocardial in-farction, as diagnosed, is increasing in prevalence among theprivileged group of the more developed races. If it beaccepted that this is not due to better diagnosis, then wemust c{)nclude that it is due to recently operating and,therefore, remediable aspects of the environment of theseprivileged group . This view is supported by the orwegianstatistics for mortality from myocardial infarction duringand shortly after the Second World War. It also gives reason-6162 S. A. MED I C A L J 0 U R N"A L 23 January 1960able hope for an improvement in the next decade in what has. been a deteriorating trend in the last decade.If the factors responsible for the recent increase are con-cerned with the mechanisms of occlusive thrombogenesis,we might expect a distinct difference between White andBantu blood in South Africa in respect of coagulationmechanisms and fibrinolysis. The disappointing resultsreported by Merskey et al. do not necessarily negative thetheory of increased thrombogenesis. It may be that we havenot yet developed techniques of in vitro study adequate forthe recognition of disturbed coagulation mechanisms in vivo.This possibility is a challenge to haematologists who areinterested in this field. There is considerable evidence thatpostprandial lipaemia from fatty meals may be connectedwith some form of increased in vivo tendency to coagulation.Turning to the consideration of atherogenesis, althoughMorris's figures do not support the idea of increasing severityof atherosclerosis in the London ~pulations affected by thegreat increase in myocardial infarction, we can neverthelesspoint to the considerable difference between South AfricanWhites and Bantu in respect of atherosclerosis of the aortaand coronary trunks. There can be no doubt that there is avery considerable difference between the two races in theextent and severity of atherosclerosis in these two regions,although the Bantu is by no means in such a favoured positionin respect of cerebral atherosclerosis. This dissociation in theextent and severity of atherosclerosis between the aorta andcoronary trunks on the one hand and the cerebral arterieson the other hand has also been observed in Japan. It isextremely puzzling but does not concern us in the presentdiscussion.Disturbed Lipid MetabolismThe most hopeful aspect of the study of the epidemiologyof ischaemic heart disease is the link between disturbed lipidmetabolism and myocardial infarction.In general those diseases which are associated with hyper-cholesterolaemia (e.g., diabet~ and familial xanthomatosis)show a high prevalence of ischaemic heart disease.Apart from such diseases, the privileged groups whosuffer from the increasing prevalence of myocardial infarctionare the groups who have high levels of total serum cholesterolin their blood, and who consume large quantities of. fat,especially saturated fat, in their diets. The evidence for thisassociation has been fully reviewed elsewhere. The linkbetween dietary fat and serum-eholesterollevels is now clear.The link between high serum cholesterol and myocardialinfarction might be through either or both of the mechanismsdescribed above as thrombogenesis and atherogenesis. Ifthe link is through thrombogenesis there is great hope forimmediate reduction of mortality from myocardial infarction.If it is also through the mechanisms of atherogenesis, thereis reasonable hope that this pathological process, for so longregarded as an inevitable result of aging, may be in partpreventable.Applying these principles to the management of coronaryheart disease we have felt that a diet which reduced serumcholesterol is likely to favour prognosis in general in thosewho are at risk of coronary heart disease. This term 'at risk'will include those who have already had symptoms, thosewho have a strong family history, and those whose serumcholesterol is consistently high. We do not yet know thenormal range for men of 40-50 years, but in general 275 mg. %may be taken as too high and figures between 275 and 225as worth trying to reduce. We have shown that the majorityof men with serum cholesterol figures above 225 will droptheir level towards or to below 225 mg. % for: as long a timeas they consume 50-75 g. daily of an unsaturated oil such llSsunflower-seed oil. The same result can probably be obtainedby reducing dietary fat calories to 30% and substitutingunsaturated oils for at least half of the total. This dietaryadjustment can be made without undue discomfort to thepatient and his household.. Jolliffe et al.4 have confirmedthese findings in New York with his 'prudent diet'. In thepresent uncertain state of our knowledge we have not feltjustified in making recommendations for populations ingeneral or for people not at risk. There are many other waysin which the diets of populations with high prevalence ofmyocardial infarction differ from those of populations withlow prevalence. These differences have been reviewed andin the present state of our knowledge the quantity andquality of dietary fat appears to ·be of greatest relevance.Advancing knoWledge, however, may bring other factors tolight.The application of these dietary principles Can be combinedwith any other method of therapy, induding the short-tennor long-term use of anticoagulants which will be reviewedby Dr. Suzman.* This appears to be the most promisingline of drug therapy at present. Its value for periods up to2 years after the last infarction has been supported by acareful study by the Medical Research Council of Britain,although there are still many dissenting voices.Oestroien therapy has given conflicting results in the handsof Oliver and of Katz. In full dosage the-discomforts anddisadvantages are such that a stronger case is required tosupport their use. A recent report with doses much smallerthan conventional is encouraging, but will require criticalexamination and confirmation. In my opinion, oestrogentherapy cannot at present be recommended.TreatmentIn practical management coronary heart disease can bedivided into 4 grades of severity. The management will bediscussed in relation to these 4 grades.1. Angina pectoris on effort without infarction and withnormal electrocardiograph. ~ the ECG can be decisivelyaltered by effort, then the patient is at risk. If the ECG isnot altered by effort, the patient is nevertheless at risk if thesymptomatology is clear cut. The explanation given to thepatient is of paramount importance. It must be a$pted tothe patient's personality and circumstances. It is preferableto err on the side of optimism because angina pectoris canso easily be complicated by anxiety neuroses. On the otherhand, the diagnosis must not be taken lightly. Physicaleffort should be maintained to the limit of capacity withoutpain, but the limit must definitely not be exceeded andnitroglycerine should not be used to achieve greater physical-effort performance. The use of that drug for the relief orprevention of angina resulting from motional strain andcauses other than effort is however entirely legitimate andoften constitutes the only effective therapy. Rest should im-mediately be enforced and· anticoagulants used if the angina* Dr. M. M. Suzman contributed a paper at the Congress onthe u e of anticoagulants.23 Januarie 1960 S.A. TYDSKRIF VIR GENEESK1J DE 63~hould develop crescendo qualities not related to effort;this sequence suggests impending infarction. The patient~hould avoid heavy meals and particularly exertion soon aftermeals. If he is over-weight, his calories should be reduced.His serum cholesterol should be determined by a reliable:laboratory with reasonable agreement between at least tworeadings. If the mean is above 275 mg. %restriction of totalfat and a swing towards unsaturated fats should be recom-mended as discussed above. The same recommendation isreasonable at mean levels between 275 and 225. At lowerfigures, the diet has less rationale but a case may still bemade on the assumption that the individual may have apostprandial lipaemic tide which encourages thrombosis.2. Patients who have survived mild infarction withoutarrythmia, angina decubitus or myocardial failure may betreated in exactly the same way as the group 1.3. Patients with persistent angina decubitus or those inwhom the angina is more related to tension and excitementthan to effort constitute a most difficult group. The treatmentsrecommended for groups I and n should be applied but inaddition special measures may have to be taken for intractablepain. The psychic and emotional aspects of this pain arewell appreciated but not easily handled. The most importantconsideration is to prevent a vicious circle by adequateexplanation and reassurance, with reasonable optimism andconviction. Once the vicious circle is established, psychichandling is, in my experience, not of great value. There arecertainly unexplained aspects of angina pectoris and it isunfair to attribute all of these to psychic mechanisms.Nitroglycerine and related vasodilators are the stand-byof treatment. If they fail, and life becomes intolerable, aftera long enough period of trial and adjustment it may" bedesirable to render the patient hypothyroid as the lesser oftwo evils. Many other treatments have been used, but nonehave stood the test of time and we have to confess that inthis group medical treatment is far from satisfactory.4. Patients whose infarction has been followed by perma-nent arrythmia and/or congestive cardiac failure. Thetreatments appropriate to these two complications will beof primary importance. At this stage, angina decubituswill seldom be a problem. Caloric restriction for weightreduction when indicated, or salt-restriction for the relief ofcongestive heart failure, will be the most important partsof dietary treatment. Exercise should not be unnecessarilyrestricted, although it is usually necessary to put a considerablebrake on physical activity and on strenuous and tiring days.The place of surgical treatment is not ignored but spacedoes not allow the necessary critical consideration. In myopinion, the case has still to be made for most forms ofsurgical correction. I do not decry carefully controlledsurgical experiments with adequate and prolonged follow-up,preferably by someone other than the operating surgeon.On the other hand, no surgical operation has yet fulfilledthe criteria for general application. Surgical techniques willinclude (l) interruption of pain fibres for intractable anginaand (2) various operations for the promotion of collateralblood flow. Thyroidectomy for the reduction of basalmetabolism tends to be replaced by thiouracil and relateddrugs or by radio-active iodine.ADDENDUMSince preparing this paper for Congres I have person-ally vi ited most of the group in the USA and Britain fromwhich important contribuhon; have been made, and haveattended the Gordon Lipid Conference (July 1959). It ipossible therefore to bring recent iews and trend right upto date.There is intense activity in many field, mo t of itrepresented at the Lipid Conference. A whole ses ion wadevoted to the lipid component of in vitro coagulationmechanisms. The tudy of lipids and their metaboli m willrapidly advance under the influence of the new techniqueof gas chromatography. A promising start has been made inthe study of in vivo thrombosis in isolated vein segments.There is further evidence for genetic variability in lipidmetabolism, and particularly in the response of total cholesteroland other lipid fractions of the serum, and in the duration of. the postprandial lipid tide, when groups of people are fed.with different quantities and qualities of fat.It is evident that total-serum-eholesterol levels in man canwhen they are too high, be reduced effectively by a greatvariety of methods. These include diet, oestrogen therapylarge doses of nicotinic acid, hydralazine, and neomycin.There is still no evidence that effective reduction can beachieved by any small-dose fraction of lipids or vitamin atpresent commercially available in South Africa. Dr. G. E.Burch has referred to certain new therapeutic preparationfor the reduction of serum cholesterol. They sound promisingbut are still under clinical trial in the USA.However there is still no direct evidence that mortality andmorbidity from ischaemic heart disease is favourably in-fluenced by these manreuvres even though they reducetotal serum cholesterol. e ertheless there must be few whwould not give their patients the benefit of the doubt andadvise reduction of immoderately high erum-eholesteroLlevels (see main text for figures) in people at ri k of i chaemicheart disease. The statistical association of these high levelwith ischaemic heart disease is too close to be ignored whenthere are so many possible mechanisms of cau al association.The American Council on Foods and Nutrition2 finditself at present unable to give advice on how reduction ofserum cholesterol should be achieved, but publishes 5 articleto illustrate current trends of thought. I have no doubtthat sensible dietary principles should always be recom-mended to people at risk whether or not other methods ofreducing serum cholesterol are added to the dietary regime.On the other hand I think some people are pres ing dietaryrestriction too severely. Our regime has been published as aguide. 3 Jolliffe et al.' have demonstrated effective reductionof serum cholesterol by a similar type of diet, which theycall 'prudent'.REFERE CESJ. A full list of reference is given in tbe following two publications:(a) Brock, J. F. "al. (1959): Poslgrad. Med. J., 35, 216.(b) Brock, J. F. (1959): 'utrition and the CliniciQ/l (Humpbry Davy RoUestonLectures to the Royal College of Phy icians). Lancet, in press.2. Council on Foods and utrition (1959): Symposium an Significance ofLowered Cholesterol Luds. J. Amer. Med. Assoc., 170,219 .3. Gordon. H. and Brock, J. F. (1958): S. Air. Med. l., 32, 907.4. Jolliffe, ., RinzlCT•. H. and Archer, M. (1959): Amer. J. CHn. utr., 7, 451.

The management of ischaemic (Conorary) heart disease

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The management of ischaemic (Conorary) heart disease

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