ENDOMYOCARDIAL FIBROSIS

ENDOMYOCARDIAL FIBROSIS

552 ENDOMYOCARDIAL FIBROSIS SiR,-The letter from Dr. McLaren in your issue of Aug. 7 has interested us greatly. It is the first report from -India of ...

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552 ENDOMYOCARDIAL FIBROSIS SiR,-The letter from Dr. McLaren in your issue of Aug. 7 has interested us greatly. It is the first report from -India of which we have knowledge, suggesting that endomyocardial fibrosis may occur there. We look forward with interest to reading his detailed observations, and particularly to hearing more of the obliterative lesion in the right ventricle. Clinical diagnosis of this lesion is difficult because constrictive pericarditis can resemble it so exactly. The possible relationship of endomyocardial fibrosis to malnutrition and to hepatic disease has been considered here. The reportsof Gillanders and his colleagues from Johannesburg, as well as some early observations2 here, have made us consider this question closely. We have little doubt that congestive heart-failure is not infrequently seen in Africans with liver disease. The connection between the two is obscure. However, although hepatic lesions in this area are very frequent in Africans generally, in our cases of endomyocardial fibrosis which came to necropsy we have not been impressed with the evidence or importance of changes in the liver ; frank cirrhosis was seen in only one case in this series. While endomyocardial fibrosis may eventually prove to be a disease of malnutrition, we have as yet no direct evidence of this, nor of any constant association with hepatic lesions other than those of congestive heart-failure. We hope that Dr. McLaren’s letter will stimulate comment from other parts of the world, as fuller knowledge of its geographical distribution may shed much-needed light upon the aetiology of this disorder. J. D. BALL J. N. P. DAVIES Mulago Hospital, A. W. WILLIAMS. Kampala, Uganda. very interested in the paper by Dr. Ball colleagues in your issue of May 22. They have put on a scientific basis the clinical impressions which many physicians in Africa and probably elsewhere have formed about the important group of heart-failures where a primary myocardial fault is responsible. Their correlation of clinical features with morbid anatomical findings is particularly admirable. It is to be hoped that their paper will give sufficiently solid facts to enable authors of textbooks on tropical medicine to break with their traditional silence on this

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important matter. I suggest that research-workers on this subject should not limit their work to cases manifesting fibrosis of the myocardium. My impression is that there are probably other pathological groups of cardiac disease, probably of similar geographical distribution, often clinically indistinguishable from myocardial fibrosis, but which do not show any appreciable fibrosis of the myocardium at the time congestive failure sets in. Some of these mav or may not be aetiologically related to endomyocardial fibrosis. If the net is cast wide enough, the elusive pathological states preceding fibrosis of the myocardium are almost certain to be found. In the past thirteen months, in the eastern region of Nigeria, I have seen over a dozen cases of cardiac failure in relatively young patients in which other accepted causes of cardiac disease had been excluded and in which a primary myocardial disorder appeared to be the main fault. A typical case was that of a nightwatchman, aged about 30, who was admitted in September, 1953, with congestive heartfailure. The heart was moderately enlarged and a grade-2 systolic murmur was audible in the mitral area. His bloodGillanders, A. D. Brit. Heart J. 1951, 13, 177. Higginson, J., Gillanders, A. D., Murray, J. F. Ibid, 1952, 14, 213. 2. Davies, J. N. P. Transactions of Ninth Conference on Liver Injury, 1950. New York; p. 151.

pressure was 130/82 mm. Hg and the rhythm was regular. He responded clinically to digitalis, mersalyl, and salt restriction, and was discharged at his own request after a few weeks in hospital. He was readmittod, however, two months later with engorged neck veins, tender liver, and triple rhythm. No murmurs were audible at this stage and he died within 24 hours of admission. At necropsy the left ventricle was hypertrophied and the right ventricle was dilated. The myocardium showed no macroscopic abnormality, and the valves and coronary vessels were normal. The histological report stated : The sections show a fairly diffuse myocarditis intensified in some areas, sometimes near blood-vessels, but never reproducing the appearance of Aschoff nodes. The predominant cells are eosinophils but polymorphs, lymphocytes, and monocytes are also present. The muscle tissue is rather cedematous but no necrosis or fibrosis is observed." "

It should be added that Chagas’s disease and trichiniasis have not been reported in Eastern Nigeria. This case is reported to emphasise the importance of keeping an open mind in the investigation of the group of myocardial diseases of obscure aetiology which have been encountered in various parts of Africa. CHUKUEDU NWOKOLO. BLOOD-TRANSFUSION WITH PLATELET PRESERVATION

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SjR,—Dr. Johnston, in his report (Aug. 14) of a case aplastic anaemia, referred to the question of the

of the platelets in blood-transfusion. The work of Stefanini and Gardner and their associates has shown that it is possible to transfer blood from a donor to a recipient with the loss of only about 25% of the platelets. The most important precautions that they advocate are :

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(1) The blood should not come into contact with a waterwettable surface. (2) The minimum of time should elapse between taking and giving the blood. (3) ’Sequestrene (’ Versene ’) should be used in preference to citrate as anticoagulant. that they found to be the most efficient transfusion by multiple siliconed syringes and transfusion with a plastic taking set, storage bag, and giving set, using siliconed needles.’2 Using sequestrene, siliconed needles and bottles, and plastic tubing and giving sets, we have now given 7 transfusions to 4 thrombocytopenic patients. We would like to acknowledge our indebtedness to Dr. P. L. Mollison, of the M.R.C. Blood Transfusion Research Unit at Hammersmith, under whose guidance the first of these transfusions was performed. After 5 of the 7 transfusions a significant rise in the platelet-count was demonstrated, in 2 of the patients dangerous vaginal bleeding was arrested, and in another curative splenectomy with lienorenal anastomosis was performed without excessive bleeding (Prof. R. S. Pilcher). In the only 1 of our patients requiring repeated transfusions these became less and less effective, a recognised drawback of the procedure, which is due to the development of platelet antibodies in the recipient. As would be expected, we found that the best results were obtained when the donor’s blood was rich in platelets. We have not yet had an opportunity to perform a transfusion using siliconed 100 ml. syringes, but we believe that this method may prove to be the more useful one in this country until plastic transfusion equipment becomes generally available. The short survival of the transfused platelets and the development of platelet antibodies limit the usefulness of the procedure. We believe that it is indicated when The

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is occurring in a thrombocytopenic in whom the patient underlying condition is potentially reversible, or to reduce the bleeding during splenectomy

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1. Stefanini, M., Dameshek, W. New Engl. J. Med. 1953, 248, 797. 2. Gardner, F. H., Howell, D., Hirsch, E. O. J. Lab. clin. Med. 1954, 43, 196.