1340

plasma (P.R.P.) anticoagulated by ethylenediamine tetraacetic acid (E.D.T.A.). With Giemsa staining, azure granules appeared in the pale-violet cytoplasm of the small bodies. Phase microscopy showed that the bodies were spherical or spheroid in shape with an irregular and pitted surface, and sometimes having small projections (dendritic shape). Most of the platelets in blood and those added to urine were spheres or spheroids with projections. On scanning electron microscopy, the small bodies were discshaped with an irregular and pitted surface (average diameter of 3-8 ), spherical with a smooth surface (average diameter of 2-7 .), or dendritic (as in the accompanying figure). Most of the platelets added to urine were spherical with a smooth surface or dendritic with a distorted surface, although some remained as discs, as described by Larrimer et al.1 Samples of P.R.p.-urine were left at room-temperature and at 4°C, respectively. On Giemsa staining, the platelets in urine after one week did not stain so well as those in the fresh preparation; but the number of platelets in urine stored for one week did not decrease. Further investigation is required, but we suggest that these small bodies in urine are platelets. We thank Mr T. Fujiwara, Keio University, and Mr T. Mizokami, Nishinippori Clinic, for help.

Tokyo Electric Power Hospital, Shinanomachi, Shinjuku-ku, Tokyo. Nishinippori Clinic, 5-24-7, Nishinippori, Arakawa-ku, Tokyo, Japan.

N. KÕNO S. UEHARA.

N. SASAKI.

EASIER CHEST ASPIRATION

SiR,—Surgical textbooks 2-4 recommend the use of metal cannulse, three-way stopcocks, and 20-50 ml. syringes for aspiration of pleural effusion. A number of unnecessary problems arise when these implements are employed, including pneumothorax and jamming of the stopcock. The procedure is exhausting not only to the already dyspnoeic patient but also to the doctor. The patient has to restrict respiratory effort for fear of trauma to the lung or diaphragm with the sharp needle. All these disadvantages and complications are lessened, if not eliminated, by a simple method whereby a plastic intravenous cannula (e.g., Braunula size 1) is connected to an intravenous giving-set, for drainage by a one-way system controlled by the plastic valve supplied with the giving-set. The cannula is inserted through a small nick in the locally anaesthetised area selected to drain the maximum amount of pleural effusion. The patient holds his breath for only a second or two while the metal introducer is removed and the giving-set connected. The connection between the giving-set and the cannula is certainly more secure than in the previous method. The patient can lie back comfortably at 45 degrees, breathe, and even cough without fear of injury. The pleural effusion drains freely into a receiver on the floor; its rate of flow is easily controlled and any air that may enter the tubing is prevented from reaching the pleural cavity by simply closing the valve. At the end of the procedure the plastic tubing is cut short for injection of any chemotherapeutic agent, still leaving the valve in position to stop any possible air entry. In a series of over sixty aspirations of malignant pleural effusion with the above technique the drainage was more complete, simple, comfortable than with the standard method and not a single case of pneumothorax or any other 1.

2. 3. 4.

Larrimer, N. R., Balcerzak, S. P., Metz, E. N., Lee, R. E. Am. J. med. Sci. 1970, 259, 242. Kyle, J. Pye’s Surgical Handicraft; p. 307. Bristol, 1969. Sabiston, D. C. Jr., Davis-Christopher Textbook of Surgery; p. 1815. Philadelphia, 1972. Kyle, D. Minor Surgery; p. 129. London, 1968.

serious rays

noted. In all the taken after each procedure.

complication

were

57 Cromwell Road, London SW7 2ED.

was

cases

ADEL A. M.

chest X-

AULAQI.

ROLE OF CATECHOLAMINES IN ARRHYTHMIAS AFTER ACUTE MYOCARDIAL INFARCTION

SiR,-Dr Gupta (March 15, p. 641) discounts completely the arrhythmogenic role of the sympathetic nervous system (s.N.s.) and questions the relevance of the proven of catecholamines in the blood and urine after myocardial infarction (A.M.I.) to production of arrhythmias in man. This requires comment. Lown’s group1 showed that sympathetic stimulation lowers ventricular fibrillation threshold (v.F.T.)-i.e., it increases cardiac vulnerability to fibrillation-and they suggested that inappropriate sympathetic discharge may induce ventricular fibrillation (v.F.) and, therefore, sudden death. Dr Gupta considers these conclusions unwarranted because the study was made in dogs and because electrical stimulation was used to provide sympathetic discharge. Lown’s group showed also that V.F.T. is reduced by hypothalamic stimulation and that this effect is suppressed by beta-blockers 2; in addition, they showed that cardiac vulnerability to v.F. is increased when dogs are placed in a stressful environment3 and conclude: " Thus, intense activity of the central nervous system, whether induced by direct electrical stimulation or by psychological means, can profoundly affect the susceptibility of the heart to fatal arrhythmias" .2 Bilateral stellectomy increases V.F.T.4 Striking changes in v.F.T. have also been obtained by unilateral stellate-ganglion ablation or blockade: removal of the right stellate ganglion lowers V.F.T. (48%), whereas removal of the left increases v.F.T. (72%).5 These profound changes in cardiac vulnerability to v.F. are the result of unilateral withdrawal of spontaneous cardiac sympathetic activity and do not depend on electrical stimulation. Similarly, blockade of the right stellate ganglion increases the arrhythmias associated with coronary-6 artery occlusion, while blockade of the left reduces them. Dr Gupta reports a study where adrenaline infusion was used to produce lung oedema and where cardiac arrhythmias were not mentioned; since that paper deals with lung cedema, the lack of description of arrhythmias does not rule out that they occurred. He reports also an anecdotal suicidal attempt with adrenaline which did not produce arrhythmias (continuous E.c.G. monitoring ?). He uses these data against the role of catecholamines in arrhythmia production, but he does not quote papers reporting arrhythmias produced by catecholamine infusion.7.8 The major point, however, is that Dr Gupta seems to be unaware of the fact that stimulation of cardiac sympathetic nerves increases the temporal dispersion of excitability recovery in ventricular muscle (a factor known to favour arrhythmias 9), and that administration of catecholamines decreases it.lo In fact, stimulation of cardiac nerves increases cardiac vulnerability to v.F., whereas catecholamine infusion decreases it (after about 3 minutes of infusion, when the substance

excess

acute

1.

Verrier, R. L., Thompson, P. L., Lown, B. Cardiovasc. Res. 1974, 8, 602.

Verrier, R. L., Calvert, A., Lown, B. Am. J. Physiol. 1975, 228, 923. Lown, B., Verrier, R., Corbalan, R. Science, 1973, 182, 834. Kliks, B. R., Burgess, M. J., Abildskov, J. A. Circulation, 1972, 46, 115. 5. Schwartz, P. J., Snebold, N. G., Brown, A. M. Am. J. Cardiol. 1975, 35, 169. 6. Schwartz, P. J., Stone, H. L., Brown, A. M. Circulation, 1974, 50, 204. 7. Lepeschkin, E. Cardiologia, 1950, 16, 278. 8. Szakacs, J. E., Mehlman, B. Am. J. Cardiol. 1960, 5, 619.

2. 3. 4.

9. Han, J., Goel, B. G. Archs intern. Med. 1972, 129, 749. 10. Han, J., Moe, G. K. Circulation Res. 1964, 14, 44.

1341 becomes uniformly distributed).11 Therefore, the possible lack of arrhythmias after catecholamine infusion is not surprising and does not imply at all that noradrenaline released at the adrenergic terminals by a sympathetic discharge will not produce or facilitate arrhythmias. The " most important objection to the arrhythmogenic role of the s.i.r.s. ", in Dr Gupta’s opinion, is a paper in which cardiac arrhythmias produced in dogs (no criticism of animal experiments this time) by electrical stimulation of the left ventrolateral cardiac sympathetic nerve were not abolished by pharmacological blockade of adrenergic (beta Unand alpha) and cholinergic cardiac receptors.12 fortunately for Dr Gupta, the conclusions of this work have been completely discounted by the finding 13 that with the technique used in those experiments the electrical stimulation was applied, not only to the nerve, but also to a ligament containing atrial muscle fibres1 Caution is always necessary in transposing experimental animal data into the clinic, but to discount them is a mistake. The recognition of a human disease in which arrhythmias depend upon the s.N.s. is therefore relevant. The long Q-T syndrome, which is characterised by electrocardiographic abnormalities and by syncopal attacks due to ventricular fibrillation, follows emotional or physical stress.14 These episodes are the effect of sudden sympathetic discharges, and the underlying mechanism is an imbalance in the cardiac sympathetic innervation, likely to be a congenital decrease in right cardiac sympathetic activity.14 The mortality of untreated patients is very high, and the most effective treatments are beta-blockers and/or ablation of the left stellate ganglion. The latter resulted in the complete suppression of syncopal attacks in all 4 patients so treated.14 The role of cardiac sympathetic innervation in the production of arrhythmias is, in this case, evident. As to A.M.I., a few considerations are worth while. There is electrophysiological evidence that coronary-artery occlusion excites cardiac sympathetic afferent fibres, 16 leading to an excitatory cardio-cardiac sympathetic reflex.16 Harris et al. showed that bilateral stellectomy in dogs almost completely suppresses the arrhythmias associated with coronary-artery occlusion 17; these arrhythmias are also reduced by sectioning the dorsal roots (from c8 to T5) which represent the afferent limb of the cardio-cardiac sympathetic reflex.18 In man, signs of increased sympathetic activity are especially common in anterior A.M.I.,19 and it is well known that the early phase of A.M.I. is very often accompanied by arrhythmias. To assume that at least part of them depend upon the interaction between the local effects of myocardial ischaemia and sympathetic activity does not seem illogical. The arrhythmogenic role of the s.N.s. should not, therefore, be overlooked. Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston, Texas 77550, and Istituto Ricerche Cardiovascolari, Universitá di Milano, Via F. Sforza 35, 20122 Milano, Italy.

PETER

J. SCHWARTZ.

11. Han, J., Garcia de Jalon, P., Moe, G. K. ibid. p. 516. 12. Gillis, R. A., Pearle, D. L., Hoekman, T. Science, 1974, 195, 70. 13. Euler, D. E., Jacobs, H. K., Hageman, G. R., Randall, W. C. Fedn Proc. 1975, 34, 375. 14. Schwartz, P. J., Periti, M., Malliani, A. Am. Heart J. 1975, 89, 378. 15. Malliani, A., Recordati, G., Schwartz, P. J. J. Physiol., Lond.

1973, 229, 457. 16.

Malliani, A., Schwartz, P. J., Zanchetti, A. Am. J. Physiol. 1969, 217, 703. 17. Harris, A. S., Estandia, A., Tillotson, R. F. ibid. 1951, 165, 505. 18. Schwartz, P. J., Foreman, R. D., Stone, H. L., Brown, A. M. Fedn Proc. 1975, 34, 421. 19. Webb, S. W., Adgey, A. A. J., Pantridge, J. F. Br. med. J. 1972, iii, 89.

THE CUMULATIVE COST OF DEATH

SIR,-Mr Longmore and Miss Rehahn (May 3,

p. 1023) justification whatever for the established view that sophisticated medical treatment is too costly for the community to bear ". They attempt to

argue that " there is

no

show that the lost economic output as a result of illness is so great that government is implicitly " underinvesting in health ". The extent to which considerations of lost output should determine the size and allocation of the health services budget is, of course, a matter on which opinions can differ radically. Even within the terms of their own argument, however, the examples given ’by Mr Longmore and Miss Rehahn, when properly analysed, can be shown not to make the case claimed for them. They suggest that for chronic renal failure the long-term loss of output attributable to the 628 males of working age who die each year more than offsets the cost of treating all patients with renal failure. But, even if this were true, this only makes a case for treating the 628 working males. The cost of treating non-workers, whatever it may be, still exceeds the loss of economic output (which is zero). Even relaxing their extreme assumption that no woman carries out paid work it would still be the case that, for at least 65% of those dying of nephritis and nephrosis, the cost of their treatment would be greater than their lost economic output. The criterion of " economic efficiency ", even using the incorrect (see below) figures in the article, would only justify at most a programme for about onethird of all patients or under one-half of all those regarded as treatable by these workers. In their cost calculations they assumed that half of the patients have transplants. This would require about 1000 cadaver kidneys a year compared with the present supply of about 500. Dialysis is an even more expensive A detailed study put the cost of hospital treatment. in the U.K. at E5600 a year.1 Home dialysis was dialysis estimated to have a running cost of S3390 per year and an initial capital cost of S1300 (all in 1973 prices). These costs are substantially more than the E1000 allowed by Mr Longmore and Miss Rehahn. Although the " cost of death " may be cumulative, so also is the cost of dialysis and retransplant. Furthermore, Mr Longmore and Miss Rehahn assume all patients return to work immediately. This is certainly not true for dialysis patients. Buxton and West found return-to-work rates (for dialysis patients) of much less than 100%. Even in the case of the more successful home-dialysis group return-to-work rates had only reached 75% by the end of the third year and were as low as 30% for hospital patients at the end of the first year. If patient five-year survival-rates of 80% for home dialysis, 60% for hospital dialysis, and 50% for transplantation are incorporated into the analysis the savings in lost output are further reduced. Mr Longmore and Miss Rehahn do not take account of the fact that for a given cohort the costs of transplant and the capital costs of home dialysis are incurred now, while the savings in lost output occur later and therefore should be appropriately discounted. While they incorporate the costs of the terminal hospital episode of non-treated patients they seem to assume that treated patients never die and hence never incur terminal costs. Treated patients also seem not to receive sickness benefits. The use of gross national product (G.N.P.) as a measure of benefit entails certain problems. Firstly, sickness benefits do not reduce G.N.p.-they simply transfer the existing G.N.P. from the well to the sick. To add them to lost output, therefore, constitutes a form of doublecounting and is incorrect. Secondly, if a working person 1. Buxton, M. J., West, R. R. Br. med. Glass, N. Hlth Trends, 1973, 3, 51.

2.

J. 1975, ii,

376.

Letter: Role of catecholamines in arrhythmias after acute myocardial infarction.

1340 plasma (P.R.P.) anticoagulated by ethylenediamine tetraacetic acid (E.D.T.A.). With Giemsa staining, azure granules appeared in the pale-violet...
341KB Sizes 0 Downloads 0 Views