205 may have been that hypotensive treatment started too late. As an alternative explanation, may I suggest that, in recent years, pressure reduction has often been pushed too far and that this has precipitated infarction during phases of excess hypotension. Indeed, I believe that the success of the Goteborg group may be largely explained because they avoided this error. They had no rigid treatment policy apart from starting with a beta-blocker, to which they added other hypotensive agents if the blood-pressure did not fall below 160 mm Hg systolic and 95 mm Hg diastolic, levels still considerably above 82 mm Hg diastolic, the approximate average (so-called normal) in this country for men of the same age.’ They do not tell us the extent of their induced pressure-falls nor the final diastolic pressures that were recorded before infarction or its avoidance. These omissions, by clinicians who have brought such meticulous care to their observations on hypertension and its treatment, lead me to hazard a guess that they feel no great enthusiasm for the popular "restore to normality" doctrine of pressure reduction. I have recently completed a study of first myocardial infarction in severe essential uncomplicated hypertensives under treatment over a mean period of six years. A third of these infarctions had occurred shortly after the pre-infarction diastolic pressures had been recorded at normal levels, the percentage of patients with infarctions in this group being about four times that of those without. Moreover, two-thirds of those with infarctions had diastolic pre-infarction pressures from 80-100 mm Hg, twice the proportion of those without infarctions who had final pressures in that range. About half the remaining patients with infarctions had pressures which had escaped far upward out of control after failures of compliance. Those with infarctions who had final reduced diastolic pressures were then matched in pairs, for established untreated diastolic pressure, age, sex, and form of treatment, against controls who had not had infarctions. Below 106 mm Hg the extent of the pressurefalls in those with infarctions was greater than in the corresponding patients without infarction, whereas above this level there was little difference. My feeling, therefore, is that the failure of antihypertensive treatment to cut the infarction-rate in severe hypertensives stems from general acceptance of the precept that the aim should be to restore normality, a policy which may have precipitated just about as many infarctions as it has prevented. I take it that Berglund and his colleagues have preferred their reductions to be less vigorous and I feel that their encouraging findings owe much to this restraint. All the same, I would not be surprised to hear that a substantial proportion of the infarctions which were not prevented occurred at times of particularly "good" control.

against infarction

was

Department of Medicine, Victoria Hospital, Blackpool FY3 8NR

I. MCD. G. STEWART

PRENATAL DIAGNOSIS OF DUCHENNE MUSCULAR DYSTROPHY test for X-linked Duchenne muscular dysis urgently required, but since the basic biochemical defect is unknown, indirect tests, such as fetal serum-creatinekinase (S.C.K.) activity, are being considered. Professor Dubowitz and his colleagues (Jan. 14, p. 90) report a normal fetal S.C.K. (semiquantitative micromethod) in blood obtained by fetoscopy at 17-19 weeks’ gestation and the subsequent birth of a normal child. Taken in conjunction with the findings of others 2-4- it would seem that a normal fetal s.c.K. may well

SIR,-A prenatal

trophy

normal fetus and a raised S.c.K. an affected fetus. this can be accepted as a reliable test it would before However, seem wiser to continue to offer abortion of any at-risk male fetuses, irrespective of the fetal S.C.K. until, with further experience, it has been clearly established that abnormalities in muscle histology are present only when the fetal S.C.K. level is significantly increased and, conversely, that an apparently normal s.c.K. is always associated with a normal muscle histology. We have only recently been able to study blood-samples obtained by placental aspiration and so far S.C.K. levels at termination in two at risk fetuses have been normal, as has the muscle histology. Previously we have measured S.C.K. in cardiac blood obtained post mortem where values are exceptionally high even in apparently normal fetuses, probably due in part to autolysis.1 In an assumed affected fetus Mahoney et at. found significantly raised S.C.K. levels in blood obtained not only by placental aspiration but also by cardiac puncture, and we have observed a very high level in cardiac blood in an at-risk fetus in which the muscle histology was clearly abnorma1.1 Perhaps in affected fetuses the greater post-mortem efflux of creatine kinase from muscle tissue is a reflection of the defective muscle membrane. indicate

a

University Department of Human Genetics, Western General Hospital, Edinburgh

LONG-TERM PERITONEAL DIALYSIS

SIR,-Your Parliamentary commentary on dialysis machines5 stresses the dilemma that nephrologists and society face-the need to provide dialysis for all who need it and the need for financial restraint. Despite this dilemma, which is an international one, nephrologists are still reluctant to make more use of peritoneal dialysis even though it may be a better choice for some of the new groups of patients who may benefit from dialysis, such as those older than 60 and diabetics. With commercially available dialysate solutions and a small cycler, peritoneal dialysis is so simple that almost any patient6 can be trained to do it at home safely and over long periods. The reverse-osmosis peritoneal dialysis machines7 are slightly more complex than the cycler but are still simpler than hxmodialysis machines; they are very safe and can reduce the cost of peritoneal dialysis to levels well below that of hxmodialysis. With increasing experience and research further improvements in peritoneal dialysis may be achieved. One improvement is continuous ambulatory peritoneal dialysisIt uses no machines but only 8-10 litres of dialysate a day. During the past 4 months we have converted to continuous peritoneal dialysis twenty patients who previously had been maintained on the conventional intermittent peritoneal dialysis for an average of 19 months. The results have been dramatic, in terms of biochemistry and the patients’ acceptance, all enjoying their new life "without machine" and without dietary restrictions. Whether continuous ambulatory peritoneal dialysis will be the dialysis treatment of the future for a large percentage of patients with chronic renal failure remains to be proven. The

important point is that nephrologists should forget the problems that they encountered with peritoneal dialysis in the past, and instead incorporate peritoneal dialysis in their armamentarium for the treatment of chronic renal failure. In expert hands, peritoneal dialysis ’can become a significant life-saver for many patients, and a money-saver for the community at large. Toronto Western

1. Hamilton, M., Pickering, G. W., Roberts, J. A. F., Sowry, G. S. C., Clin. Sci. 1946, 13, 273. 2. Emery, A. E. H. Nature, 1977, 266, 472. 3. Stengel-Rutkowski, L., Scheuerbrandt, G., Beckmann, R., Pongratz, D. Lancet, 1977, i, 1359. 4. Mahoney, M. J., Haseltine, F. P., Hobbins, J. C., Banker, B. Q., Caskey, C. T., Golbus, M. S. New Engl. J. Med. 1977, 297, 968.

ALAN E. H. EMERY

Hospital,

Toronto, Ontario M5T 2S8, Canada.

D. G. OREOPOULOS

5. Lancet, 1977, ii, 938. 6. Oreopoulos D. G. Can. med. Ass. J. 1977, 116, 232. 7. Friedman, E. (editor). Strategies in Renal Failure; p. 393. New York, 1977. 8. Popovich R. P., Moncrief J. W., Nolph K. D. Am. Soc. Nephrol. 1977, abstr.

p. 35A.