805

It is best to express the single-dimensional measurements

obtained with the echocardiographic M-mode as such and not makeunnecessary, and often inaccurate, assumptions about the shape ofthe ventricle so as to express the results as volumes. Having donethis, however, they might as well have estimated the cardiac output.I calculate that after one month of acebutolol therapy the cardiacoutput fell from 8 - 46 to 6 - 86 1/min. It is unlikely that this apparentreduction in output is due entirely to any reduction in mitralregurgitation which might occur as a result of the lowering of thearterial pressure by the beta-blocker. The lower cardiac outputwould result in reduced exercise tolerance and also lower the mixedvenous PO2. As Ikram and Fitzpatrick note, this lowering of the P02would result in an increase in the oxygen pulse, which they havesuggested is due to maintenance of cardiac output and increase instroke volume.In conclusion I would suggest that decrease in cardiac output with

secondary congestion of the right side of the heart and decreasedexercise tolerance is a simpler and more plausible explanation of thedata. The conclusion that acebutolol does not improve the conditionof patients with congestive cardiomyopathy is the same.

Department of Pharmacology and Therapeutics,University of Dundee,Nmewells Hospital,Dundee DD1 9SY NEIL F. HOCKINGS

PROBUCOL AND ISCHAEMIC HEART DISEASE

SIR,-During an exchange of letters on high density lipoprotein(HDL) cholesterol and ischaemic heart disease, Professor Miettinenand colleagues (Aug. 29, p. 478) present a table from which theydeduce that, despite lowered HDL cholesterol, the five yearincidence of new cardiac events was lower than predicted in theprobucol group (n = 114) compared with the control group (n = 184).From the references quoted, it appears that this is the first time

that any clinical results have been published from their smallprobucol trial. The lack of detail is unacceptable. Even whenpresenting summary tables research-workers must providesufficiently complete data on the design and conduct of trials topermit readers to assess the validity and value of the results,especially in a "five year multifactorial primary prevention trial"where interventions other than probucol were, apparently, used.

It is also of interest, in view of the results of the W.H.O. PrimaryPrevention Trial,’ that there appears to be an excess of cases in theclofibrate treated group. But, again, it is impossible to appraise theimportance of this result.

Cardiovascular Research Unit,Department of Medicine,University of Edinburgh,Edinburgh EH8 9XF M. F. OLIVER

EVALUATING AUTOMATED BLOOD PRESSUREDEVICES

SiR,-Dr Nielsen and Dr Andersen’s letter (Aug. 22, p. 416),describing a new automated blood pressure measuring device andtheir attempts to evaluate its performance, illustrates an issue whichwill become increasingly important. In North America, there arealready dozens of automated or electronic sphygmomanometers("autosphygs") available for home and clinical use, and highlysophisticated microprocessor-based units are appearing for thehospital market. There is, however, no way as yet for the clinicaluser to readily determine whether or not these devices will functionproperly under normal and abnormal conditions.The Association for the Advancement of Medical Instrumen-

tation (in August, 1980) drafted standards for electronic and auto-mated and for non-automated sphygmomanometers which includeperformance criteria. Determinations must be within certain limitsof those obtained concurrently by the auscultatory method or viaindwelling arterial catheters, calculated on the basis of at least 15

1. Report of the Committee of Principal Investigators W.H.O. cooperative trial on

primary prevention of ischaemic heart disease using clofibrate to lower serumcholesterol: Mortality follow-up. Lancet 1980; ii 379-85.

comparisons with invasive blood pressure measurements or 50manual auscultatory determinations. Even if such a standard wereto be adopted and automated devices could be certified to complywith it when new, there would be no neans to verify performance inthe field or evaluate the relative performance of different unitswithout resorting to lengthy clinical trials. The algorithms on whichdeterminations are made are seldom, if ever, made available to theclinical user or biomedical engineer. On some units, such as the onedescribed in the letter, it is not even possible to perform a test forstatic pressure accuracy without blocking off a fixed bleed orificeand cutting through the cuff inflation line to insert a Y fitting.The development of a prototype autosphygmomanometer tester

(AST) was undertaken at the behest of the Canadian Bureau ofMedical Devices. Central to the AST is a controllable "artificalarm" which simulates the mechanical and acoustic behaviour of anormal human arm and emits realistic Korotkoff sounds betweenthe systolic and diastolic pressure limits selected by the operator.Sounds are generated in a water column to reproduce the prominentlow frequency components in Korotkoff sounds and match the bulkacoustic impedance of human flesh. The problems associated withgenerating reproducible sounds in water, however, are such that theprototype AST has limited usefulness outside the controlledenvironment of a laboratory.

Investigators have suggested that the frequency changes insounds which best correlate with systolic and diastolic blood

pressures are in the ranges above 60 Hz, 1-3 and thus an audiospeakerbased artifical arm might constitute an acceptable simulation if lowfrequency components can be neglected. Such an arm would still beunsuitable for evaluating the performance of the many deviceswhich employ oscillometric techniques,4 but would permit thetesting of Korotkoff sound detecting units and resolution of many ofthe questions surrounding autosphygmomanometer performance.Further development of an autosphyg testing system is required, asis a consensus on which elements of the-Korotkoff sounds producedby human arms are significant.Biomedical Engineering Department,Vancouver General Hospital,Vancouver, B.C., Canada;and Bureau of Medical Devices,

Health and Welfare Canada

CAROLYN F. SMALL

JAMES A. MCEWENNEIL B. COXDAVID L. JOHNSON

LICHEN PLANUS AND THE LIVER

SIR,-The letter from Dr Powell and Dr Rogers (Sept. 9, p. 525)on the coexistence of lichen planus and penicillamine-treatedprimary biliary cirrhosis prompts me to report on seven consecutivecases of erosive lichen planus from my files. Five of them had severeliver disease.A woman aged 68 with erosive oral lichen planus, jaundice, and

purpura had high transaminase levels, hyperbilirubinaemia, raisedalkaline phosphatase, reduced prothrombin activity, hyper-gammaglobulinaemia (IgG and IgM), and high titres of rheuma-toid factor and antinuclear antibodies (homogeneous pattern).Laparoscopy confirmed liver cirrhosis; liver biopsy was not done.A 72-year-old woman had erosive lichenoid glossitis, ascites, and

purpura. SGOT and alkaline phosphatase were moderatelyincreased. There was leucopenia and thrombocytopenia.Rheumatoid factor was present and C3 decreased. Microscopy ofascitic fluid did not show atypical cells. The patient’s age and poorgeneral health precluded liver biopsy.A man aged 64 with erosive oral lichen planus had raised

transaminase levels and reduced prothrombin activity. There wasthrombocytopenia, hypergammaglobulinaemia (IgG and IgM), andraised serum bilirubin and alkaline phosphatase. Laparoscopydisclosed liver cirrhosis. Biopsy was not done.

1. Ware RW, Anderson WL. Spectral analysis of Korotkoff sounds. IEEE Trans Bio MedEng 1966; 13: 170-74.

2. McCutcheon EP, Baker DW, Wiederhelm CA, Frequency Spectrum changes ofKorotkoff sounds with muffling. Med Res Eng 1969; 30

3. McCutcheon EP, Rushmer RF. Korotkoff sounds. an experimental critique. Circul Res1976; 20: 149-61.

4 Paulus DA. Noninvasive blood pressure measurement Med Instrumentation 1981; 15:91-94.