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longitudinal study that has revealed an association betweenpattern of individual fat intake and coronary mortality, thedietary assessment was likewise very detailed."The Western Electric study shows three things-firstly, an

inverse association between coronary mortality and con-sumption of polyunsaturated fat, significant at the 1% level;secondly, a positive association of coronary mortality withdietary cholesterol and with the Keys and Hegsted "scores"(which are combined measures of the amount of saturated fat,polyunsaturated fat, and cholesterol in the diet); but, thirdly,no association of CHD with saturated fat intake itself. Theseresults are similar to those of the London study of Morris,Marr, and Clayton which disclosed an inverse associationbetween P:S ratio (polyunsaturates: saturates in the diet) andcoronary incidence-the higher this ratio the lower therate-and hinted at an inverse association with "marine and

vegetable fats and oils".11 The latter was not significant, butthe association with P:S ratio was, both in the first five yearsof observation, and in the latest follow-up.12 The WesternElectric study also showed that changes from one year to thenext in dietary intake of saturated fatty acids and cholesterolwere related to changes in serum cholesterol.These results may be assessed in relation to theories of

aetiology of coronary heart disease and to current dietaryrecommendations. First the theoretical aspect: the WesternElectric study showed that, although there was a correlationbetween dietary fat and serum cholesterol, there was anassociation between dietary fat and coronary mortality thatwas independent of the level of serum cholesterol and of othercoronary risk factors. Lately, there has been renewed specula-tion as to the importance of thrombosis in the aetiology ofcor-onary heart disease. The thrombotic tendency of the blood isreported to be increased by some saturated fatty acids andreduced by certain polyunsaturated fatty acids-the essentialfatty acids.13,14 An effect on thrombosis may be one of themechanisms underlying the results from both Chicago andLondon.With respect to dietary recommendations, we should not

ask too much of a single study. Nearly all the committees thathave reported on this subject recommend reduction in totalfat in the diet. Unfortunately Shekelle and co-workers did notreport any results for total dietary fat, and their negativeresults for saturated fat, by themselves, provide no en-couragement in that area. Their results are consistent withrecommendations to increase polyunsaturates in the diet andthe P:S ratio. It must be remembered, however, that thedietary assessments were made on the Western Electric menin the late 1950s and their mean percentage of dietary caloriesfrom polyunsaturates was 3-9. Recent American nationaldata put the figure at 7 - 8%.’ The data supplied’" can do nomore than strengthen the speculation’that this higher intake isprotective. On the question of safety of the diets, the figuresare not presented but the Western Electric investigators tellus, that there was no significant association between anyaspect of dietary fat and other causes of death. Theinvestigators did not report on two other features of diet thathave been shown to be positively associated with coronarymortality-a low intake of cereal fibre, 11 and low calorie in-

11. Morris JN, Marr JW, Clayton DG. Diet and heart: a postscript. Br Med J 1977; ii:1307-14.

12. Lewis B. Dietary prevention of ischaemic heart disease—a policy for the ’80’s: Br Med J1980; 281 177-180.

13. Sinclair HM. Dietary fats and coronary heart disease. Lancet 1980; i: 414-15.14. Vane J. Fats and atheroma: an inquest. Br Med J 1979; i: 484-85.15. Page L, Marston RM. Food consumption patterns—U.S. diet. In: Havlik RJ, Feinleib

M., eds. Proceedings of the Conference on the Decline in Coronary Heart DiseaseMortality US. DHEW N.I.H. Publication 79-1610, 1979; 236-43.

take,r,16 the latter possibly indicating the detriment of lowlevels of physical activity.The great importance of the Western Electric findings is in

demonstrating, within one population, a link between thediet of individuals and those individuals’ risk of coronarydisease. The findings should give new impetus to research onthe possible protective effects of essential fatty acids.

Inevitably, the evidence in favour of dietary recommenda-tions to prevent coronary heart disease will again come underreview. In Britain the D.H.S.S.’s Committee on Medical

Aspects of Food Policy is reconvening its panel on this sub-ject. These latest results will help strengthen the case forrecommending a change in the type of fat consumed. Thosewho are ready to perform inquests on the diet-heart theoryshould pause to consider this important study.

BETA-BLOCKADE AND CONGESTIVECARDIOMYOPATHY

To give a beta blocker to a patient in heart failure is aperverse form of treatment. Yet a group in Sweden has beendoing just this for the past 5 years with apparent successYThey have given beta-blocking drugs (mainly metroprolol) to28 patients with heart failure caused by congestive (dilated)cardiomyopathy, for between 6 and 62 months. The

symptoms were lessened in 15, unchanged in 12, and worse inonly 1. During this period, 10 of the patients died, a mortalityrate lower than might be expected in a group of patients withsevere congestive cardiomyopathy. In 3 of the 4 patients whohad invasive haemodynamic measurements, there was

improvement in left ventricular performance. In the

remainder, left ventricular function was assessed mainly byechocardiography, which can be unreliable if the leftventricle is very large.3 An important practical point is thatthe beta blocker had to be started in a low dose and slowlyincreased, otherwise breathlessness tended to get worse

initially. When the beta-blocking drug was withheld from thepatients who improved, there was obvious deterioration in 6and evidence of a decline in left ventricular function in theother 9.

Why should a drug with a strong negative inotropic actionhelp patients with heart failure. Swedberg and co-workersfavour the notion that beta blockade prevents the damagedone to myocardium by circulating catecholamines. In

animals high concentrations of isoprenaline can cause

myocardial necrosis and Fleckenstein et awl.’* have shown thatdamage of this sort is due to a flood of calcium ions into cells,with excessive activation of the calcium-dependent intra-cellular ATPases, energy depletion, mitochondrial damage,and finally cell necrosis. This can be prevented by slow-channel calcium blocking agents such as verapamil as well asbeta-blocking drugs, and both of these also prevent the

development of cardiomyopathy in the Syrian hamster. 5

16. Yano K, Rhoads GG, Kagan A, Tillotson J. Dietary intake and the risk of coronaryheart disease in Japanese men living in Hawaii. Am J Clin Nut 1978; 31: 1270- 79

1. Swedberg K, Hjalmarson A, Waagstein F, Wallentein I Beneficial effects of long-termbeta-blockade in congestive cardiomyopathy. Br Heart J 1980; 44: 117-33

2. Swedberg K, Hjalmarson A, Waagstein F, Wallentein I. Adverse effects of beta-blockade withdrawal in patients with congestive cardiomyopathy Br Heart J 1980.44: 134-42.

3 Fortuin NJ, Pawsey CGK. The evaluation of left ventricular function by echocardio-graphy. Am J Med 1977; 63: 1-9.

4. Fleckenstein A, Janke J, Döring HJ, Pachinger O. Calcium overload as the determinantfactor in the production ofcatecholamine induced myocardial lesions. Rec Adv StudCardiac Struct Metab 1973; 2: 455-66.

5. Jasmin G, Solymoss B. Prevention of hereditary cardiomyopathy in the hamster byverapamil and other agents. Proc Soc Exp Biol Med 1975, 149: 193-98

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Despite the attractions of the idea, there is no evidence thatcirculating catecholamines are excessively high in congestivecardiomyopathy. We do know that myocardial damage canoccur in man if the catecholamine levels are very high; forexample, adrenaline-secreting phaeochromocytomas are

associated with a congestive type of cardiomyopathy and nor-adrenaline-secreting phaeochromocytomas with hyper-trophic cardiomyopathy." 6There are other possible explanations. Renin and angio-

tensin levels are high in congestive cardiac failure if diureticshave been used, and captopril (an angiotensin convertingenzyme inhibitor which has proved useful in heart failure 7 ,8)lessens the high peripheral resistance which is produced bythese hormones. Beta blockers likewise reduce the raisedrenin levels in hypertensives. It is a pity that Swedberg et al.did not measure renin and angiotensin since 1 of the 4 patientsthey studied invasively had a distinct reduction in systemicvascular resistance and a large increase in cardiac output.Further, there is evidence that vasodilator prostaglandinsmay be stimulated by chronic beta receptor blockade;indomethacin, an inhibitor of prostaglandin synthesis, canattenuate the hypotensive effect of propranolol in man.IO,11 Itmay be that, in patients with congestive cardiomyopathy, thebeneficial afterload reduction by beta blockers just outweighsthe harmful negative inotropic action. These drugs are alsoantiarrhythmic agents; ventricular and atrial arrhythmias arecommon in congestive cardiomyopathy and their

suppression may help to maintain cardiac output and reducemortality. 12The dangers of this type of treatment need to be

emphasised; beta blockers commonly precipitate heart

failure. The cautionary tale related by Hoffbrand’3 is

salutary: taking the advice of the Swedish workers, he gave 10mg ofpropranolol by mouth to a woman of 68 with congestivecardiomyopathy and four hours later she was in cardiogenicshock with severe pulmonary oedema. A controlled trial isneeded before beta blockade can be recommended for thetreatment of congestive cardiomyopathy.

QUALITY OF PERFORMANCE IN PATHOLOGYLABORATORIES

AW.H.O. report, produced by a working group which met inDecember, 1979, and entitled External Quality Assessmentof Health Laboratories,14 is a welcome contribution to thepresent discussion of medical audit.l5 It illustrates how a self-

6 Darsee JR, Nutter DO. Two distinct catecholamine cardiomyopathies from

norepinephrine and epinephrine secreting phaeochromocytomas. Circulation 1980;62: suppl III, 317

7 Nicholls MG, Espiner EA, Donald RA, Hughes H. Aldosterone and its regulation dur-ing diuresis in patients with gross congestive heart failure. Clin Sci Mol Med 1974;47: 301-05

8 Maslowski AH, Ikram H, Nicholls MG, Espiner EA. Haemodynamic, hormonal andelectrolyte responses to captopril in resistant heart failure. Lancet 1981; i: 71-74.

9 Michelakis AM, McAllister RG. The effect of chronic adrenergic blockade on plasmarenin activity in man. J Clin Endocrinol Metab 1972; 34: 386-94.

10 Durao V, Martins-Prata M, Pires Goncalves LM Modification of antihypertensive ef-fect of beta adrenoreceptor blocking agents by inhibition of endogenous prosta-glandm synthesis. Lancet 1977; ii: 1005-07

11 Watkins J, Abbott EC, Hensby CN, Webster J, Dollery CT. Attenuation of thehypotensive effect of propanolol and thiazide diuretics by indomethacin. Br Med J1980; 281: 702-05

12 Goodwin IF. Cardiomyopathy: an interface between fundamental and clinicalcardiology Proceedings of VIII World Congress of Cardiology, Tokyo, 1978Amsterdam. Excerpta Medica: 103-16.

13 Hoffbrand BI. Beta adrenergic blockade in congestive cardiomyopathy. Lancet 1980, i:1031

14 World Health Organisation. External Quality Assessment of Health Laboratories:Report on a WHO working group (Euro Reports and Studies 38) CopenhagenWHO Regional Office for Europe, 1981. Sw fr 4.

15 Anon Medical audit Lancet 1981, i: 286.

monitoring system, devised with the object of improvingnationwide comparability of results, has in the course of littlemore than a decade yielded rich dividends in improvement oftechnical performance and has been largely accepted bypathologists as a valuable aid to self-improvement and con-tinuing education.

Accepted, that is to say, to a greater extent in Britain and theU.S.A. than in other countries, even in Western Europe.That the more numerical and mechanised areas of clinical

chemistry and haematology, especially haemocytometry,have led the way is not surprising-since it is easier and lesspainful to ascribe discrepancies amongst laboratories to

mechanical failings than to professional shortcomings. Buttoo much has been made of the blame-attributing andpunitive potential of external assessment, and the W.H.O.report wisely emphasises that the main object of such assess-ment schemes is educational. In few highly skilled jobs,surely, can the opportunity exist for a fortnightly glimpse, inprivate, of how one is doing in comparison either withnationally acknowledged experts or with the generality of col-leagues ; and few who have this opportunity can fail to be af-fected by it.

In calling the working group together, W.H.O.’s RegionalOffice for Europe sought to crystallise the accumulatedwisdom of experienced organisers of external quality assess-ment schemes. Schemes have been successfully established inBritain through professional leadership, discreetly aided bythe D.H.S.S.; Belgium, France, and West Germany areamong the countries which oblige laboratories to participate;and countries in the Eastern European bloc have imposedcompulsory external assessment on State-controlled clinicallaboratories.

Members of the working group, who came from countrieshaving State, private, and mixed types of health service, wereunanimous in thinking that governments have a primeresponsibility for establishing and supporting external quali-ty assessment of "health laboratories" (clinical, public health,epidemiological, and medical research laboratories), not onlyas one part of their responsibility for clinical care of thepopulation but also because policy decisions related to healthcare-in screening programmes, for example-rest on thepremise that different types of laboratory obtain results thatare strictly comparable. They also felt, however, that thisprime governmental responsibility needs to be entrusted toprofessional medical scientists who can design schemes thatwill be scientifically and professionally acceptable.

All this might have gone under the familiar heading "quali-ty control". In fact, the W.H.O. working group would like tosee this term restricted to circumstances susceptible to actualcontrol-specifically, when a laboratory director decideswhether particular results should be released either for use inpatient management or for the record. Under these cir-

cumstances the analogy with manufacturers’ process controlis exact, whereas "external quality control" is an inapposite(though long employed) term for the retrospective evaluationof interlaboratory comparability, with no actual control ap-plied or indeed intended by the external assessing agency.Terminological modifications usually seem monumentallydull to everyone other than their proponents and opponents,but in this case the modification seems not only well-foundedbut potentially extremely important, because it diminishesthe threatening aspects of peer review that are conjured up bythe juxtaposition of the words external and control