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MITRAL STENOSIS
83 MITRAL STENOSIS
MEDICAL knowledge has been built up largely by clinicopathological correlations based on necropsy studies. But this method, however well it -served our ancestors, had many disadvantages. It only revealed the state of affairs at the time of death, and the accompanying physiological conditions had to be reconstructed by simple clinical observation supplemented by shrewd guess-work. The advent of cardiac surgery in mitral stenosis has persuaded many physicians to adopt the bolder method of cardiac catheterisation in order to assess the physiological effects of valve disease likely to be amenable to surgical treatment. In Stockholm 49 cases of mitral stenosis have been carefully investigated in this way.1 The patients were subdivided according to degrees of breathlessness on effort into four functional grades. By passing a catheter down the branches of the pulmonary artery to a point at which it occludes one of the subdivisions, a pressure record can be obtained which is probably the pressure in the pulmonary capillaries and which also reflects to some extent the pressure changes in the pulmonary veins. This information, together with pressure records taken from the pulmonary artery and right ventricle, and also the cardiac output, gives a remarkably complete picture of the dynamics of the circulation. In groups 1 and 2, with little limitation of physical activity, cardiac output was normal and there was only slight abnormality in pulmonary arterial and pulmonary capillary pressures. In groups 3 and 4, with incapacitating dyspnoea, cardiac output was reduced and pulmonary arterial pressure was raised ; while in group 4 pulmonary capillary pressure averaged 29 mm. Hg (close to the osmotic pressure of the plasma-proteins). In these two groups exercise increased the pulmonary capillary pressure to a level above the protein osmotic pressure at which oedema of the lungs could readily occur. In each functional group auricular fibrillation was associated with a lower average cardiac output than in the patients with sinus rhythm. A diffuse " cardiac impulse was taken to indicate right ventricular hypertrophy, and in patients with this clinical manifestation the mean pulmonary arterial pressure was nearly always above 30 mm. Hg (normal 13 mm.). Other clinical signs said to indicate pulmonary hypertension (accentuated pulmonary second sound, pulmonary systolic murmur 2) were found to be unreliable. The electrocardiogram was unreliable as evidence of absent right ventricular enlargement. Bifid p waves suggested hypertrophy of the left auricle, since they were associated with a high presystolic pressure wave in the pulmonary capillary pressure tracing. A loud apical systolic murmur was evidence of mitral incompetence, as indicated by a high systolic wave in the record of pulmonary capillary pressure, though sometimes pulmonary capillary tracings showed a high systolic wave in the absence of such a murmur. Gorlin and Gorlin 3 have suggested a hydraulic formula for calculating the area of the mitral valve orifice ; but the Swedish workers point out certain fallacies in this, particularly when the mitral valve is incompetent. In this connection it is interesting that Brock4 holds that in mitral stenosis the mitral valve is nearly always ovalshaped and measures about 1 by 0-5 cm. This nearly standard size is encountered whether the symptoms are mild or severe ; he holds that the fusion of the valves always takes place at the critical areas of insertion of the chordae tendineoe, which are at the junction of the middle and outer thirds of the valve edges. If this is true, then we cannot picture the course of mitral stenosis as related to progressive narrowing of the valve ; the "
1. 2. 3. 4.
Wade, G., Werkö, L., Eliasch, H., Gidlund, A., Lagerlöf, H. Quart. J. Med. 1952, 21, 361. Bedford, D. E. Proc. R. Soc. Med. 1951, 44, 597. Gorlin, R., Gorlin, S. G. Amer. Heart J. 1951, 41, 1. Brock, R. C. Brit. Heart J. 1952, 14, 489.
clinical course in different types would depend various physiological adaptations, perhaps determined by different effects of the rheumatic process on other valves and on different parts of the myocardium. Another interesting point brought out by the Swedish investigators is the relatively slight increase in bloodcontent of the lungs even in the presence of high pulmonary vascular pressures. This agrees with the findings of Kopelman and his associates in this country 56 and is possibly7 related to reactive narrowing of the pulmonary vessels. While the Swedish work lays an excellentpractical foundation for further studies of mitral stenosis, it leaves many questions unanswered. Why do some patients develop such an extremely pulmonary arterial pressure, which may reach or even exceed that in the systemic arteriest Why do those patients who develop massive left auricles or tricuspid insufficiency have such a relatively benign course ? 8 If the stenosed valve orifice is of Brock’s standard size, why are there such varied courses of different clinical severity ? Closer study of the various subvarieties of mitral valve disease will be necessary, and each individual patient will be found to vary in some respect from his neighbour.
varying
on
high
A NEW ANTIPRURITIC
THE best treatment of an itching dermatosis is to the cause ; and to do so an accurate diagnosis and the choice of an appropriate remedy are essential. Unfortunately, there is as yet no specific treatment for a large number of pruritic conditions, which must be dealt with empirically and largely symptomatically. Of the older local antipruritics, many are messy or relatively ineffective, or they smell disagreeably. Local-anesthetic ointments of the benzocaine class often sensitise the skin, and the contact dermatitis so provoked may become very severe before the doctor or the patient realises that it is being caused by the supposed remedy for the itching. Such a patient may be sensitised to related chemicals such as the sulphonamides, p-aminosalicylic acid, and hair dyes. In the absence of a really effective antipruritic which can be given by mouth, we need good local applications of low sensitising power. 1T-ethyl-o-crotonotoluide, which is on the market in a vanishing-cream base, seems to be highly effective and relatively harmless. This compound was developed after the discovery that certain substituted crotonamides increased the "knock-down and kill " power of insecticides. It was found to have a potent action in vitro on rabbit itch-mites,9and extensive trials in human scabies gave excellent results.10-12 During these trials, the application was shown to have a considerable antipruritic action, and this observation led to its use in non-parasitic itchy dermatoses. Hitch,13 who usedEurax,’ a preparation of N-ethylo-crotonotoluide, on 200 patients suffering from a variety of skin disorders, said that over 75% found greater relief from this preparation than from any of the others previously used. The improvement in the itching was described as excellent or good in 65%. He had 4 patients who were sensitised by the application, but only one of them was affected by the active principle itself. Similarly, Peck.and Michelfelder,14 reported 1 case of sensitisation to 1‘T-ethyl-o-crotonotoluide in a series of 400 patients. A further case has been seen by Bereston,15 in which remove
5. Kopelman, H., Lee, G. de J. Clin. Sci. 1951. 10, 383. 6. Ball, J. D , Kopelman, H., Witham, A. C. Brit. Heart J. 1952, 14,
363. 7. Goodwin, J. F., Steiner, R. E., Lowe, K. G. J. Fac. Radiol., Lond. 1952, 4, 2. 8. McMichael, J. Brit. med. J. 1952, ii. 525, 578. 9. Domenjoz, R. Schweiz. med. Wschr. 1946, 76, 1210. 10. Burckhardt, W., Rymarowics, R. Ibid, p. 1213. 11. Couperus, M. J. invest. Derm. 1949, 13, 35. New Engl. J. Med. 1950, 243, 74. 12. Appel, B. Brit. J. Derm. 1952, 64, 408. 13. Hitch, J. M. N. Y. St. J. Med. 1950, 50, 1934. 14. Peck, S. M., Michelfelder, T. J. Arch. Derm. Syph., Chicago, 1952, 65, 100. 15. Bereston, E. S.
MEDICAL knowledge has been built up largely by clinicopathological correlations based on necropsy studies. But this method, however well it -served our ancestors, had many disadvantages. It only revealed the state of affairs at the time of death, and the accompanying physiological conditions had to be reconstructed by simple clinical observation supplemented by shrewd guess-work. The advent of cardiac surgery in mitral stenosis has persuaded many physicians to adopt the bolder method of cardiac catheterisation in order to assess the physiological effects of valve disease likely to be amenable to surgical treatment. In Stockholm 49 cases of mitral stenosis have been carefully investigated in this way.1 The patients were subdivided according to degrees of breathlessness on effort into four functional grades. By passing a catheter down the branches of the pulmonary artery to a point at which it occludes one of the subdivisions, a pressure record can be obtained which is probably the pressure in the pulmonary capillaries and which also reflects to some extent the pressure changes in the pulmonary veins. This information, together with pressure records taken from the pulmonary artery and right ventricle, and also the cardiac output, gives a remarkably complete picture of the dynamics of the circulation. In groups 1 and 2, with little limitation of physical activity, cardiac output was normal and there was only slight abnormality in pulmonary arterial and pulmonary capillary pressures. In groups 3 and 4, with incapacitating dyspnoea, cardiac output was reduced and pulmonary arterial pressure was raised ; while in group 4 pulmonary capillary pressure averaged 29 mm. Hg (close to the osmotic pressure of the plasma-proteins). In these two groups exercise increased the pulmonary capillary pressure to a level above the protein osmotic pressure at which oedema of the lungs could readily occur. In each functional group auricular fibrillation was associated with a lower average cardiac output than in the patients with sinus rhythm. A diffuse " cardiac impulse was taken to indicate right ventricular hypertrophy, and in patients with this clinical manifestation the mean pulmonary arterial pressure was nearly always above 30 mm. Hg (normal 13 mm.). Other clinical signs said to indicate pulmonary hypertension (accentuated pulmonary second sound, pulmonary systolic murmur 2) were found to be unreliable. The electrocardiogram was unreliable as evidence of absent right ventricular enlargement. Bifid p waves suggested hypertrophy of the left auricle, since they were associated with a high presystolic pressure wave in the pulmonary capillary pressure tracing. A loud apical systolic murmur was evidence of mitral incompetence, as indicated by a high systolic wave in the record of pulmonary capillary pressure, though sometimes pulmonary capillary tracings showed a high systolic wave in the absence of such a murmur. Gorlin and Gorlin 3 have suggested a hydraulic formula for calculating the area of the mitral valve orifice ; but the Swedish workers point out certain fallacies in this, particularly when the mitral valve is incompetent. In this connection it is interesting that Brock4 holds that in mitral stenosis the mitral valve is nearly always ovalshaped and measures about 1 by 0-5 cm. This nearly standard size is encountered whether the symptoms are mild or severe ; he holds that the fusion of the valves always takes place at the critical areas of insertion of the chordae tendineoe, which are at the junction of the middle and outer thirds of the valve edges. If this is true, then we cannot picture the course of mitral stenosis as related to progressive narrowing of the valve ; the "
1. 2. 3. 4.
Wade, G., Werkö, L., Eliasch, H., Gidlund, A., Lagerlöf, H. Quart. J. Med. 1952, 21, 361. Bedford, D. E. Proc. R. Soc. Med. 1951, 44, 597. Gorlin, R., Gorlin, S. G. Amer. Heart J. 1951, 41, 1. Brock, R. C. Brit. Heart J. 1952, 14, 489.
clinical course in different types would depend various physiological adaptations, perhaps determined by different effects of the rheumatic process on other valves and on different parts of the myocardium. Another interesting point brought out by the Swedish investigators is the relatively slight increase in bloodcontent of the lungs even in the presence of high pulmonary vascular pressures. This agrees with the findings of Kopelman and his associates in this country 56 and is possibly7 related to reactive narrowing of the pulmonary vessels. While the Swedish work lays an excellentpractical foundation for further studies of mitral stenosis, it leaves many questions unanswered. Why do some patients develop such an extremely pulmonary arterial pressure, which may reach or even exceed that in the systemic arteriest Why do those patients who develop massive left auricles or tricuspid insufficiency have such a relatively benign course ? 8 If the stenosed valve orifice is of Brock’s standard size, why are there such varied courses of different clinical severity ? Closer study of the various subvarieties of mitral valve disease will be necessary, and each individual patient will be found to vary in some respect from his neighbour.
varying
on
high
A NEW ANTIPRURITIC
THE best treatment of an itching dermatosis is to the cause ; and to do so an accurate diagnosis and the choice of an appropriate remedy are essential. Unfortunately, there is as yet no specific treatment for a large number of pruritic conditions, which must be dealt with empirically and largely symptomatically. Of the older local antipruritics, many are messy or relatively ineffective, or they smell disagreeably. Local-anesthetic ointments of the benzocaine class often sensitise the skin, and the contact dermatitis so provoked may become very severe before the doctor or the patient realises that it is being caused by the supposed remedy for the itching. Such a patient may be sensitised to related chemicals such as the sulphonamides, p-aminosalicylic acid, and hair dyes. In the absence of a really effective antipruritic which can be given by mouth, we need good local applications of low sensitising power. 1T-ethyl-o-crotonotoluide, which is on the market in a vanishing-cream base, seems to be highly effective and relatively harmless. This compound was developed after the discovery that certain substituted crotonamides increased the "knock-down and kill " power of insecticides. It was found to have a potent action in vitro on rabbit itch-mites,9and extensive trials in human scabies gave excellent results.10-12 During these trials, the application was shown to have a considerable antipruritic action, and this observation led to its use in non-parasitic itchy dermatoses. Hitch,13 who usedEurax,’ a preparation of N-ethylo-crotonotoluide, on 200 patients suffering from a variety of skin disorders, said that over 75% found greater relief from this preparation than from any of the others previously used. The improvement in the itching was described as excellent or good in 65%. He had 4 patients who were sensitised by the application, but only one of them was affected by the active principle itself. Similarly, Peck.and Michelfelder,14 reported 1 case of sensitisation to 1‘T-ethyl-o-crotonotoluide in a series of 400 patients. A further case has been seen by Bereston,15 in which remove
5. Kopelman, H., Lee, G. de J. Clin. Sci. 1951. 10, 383. 6. Ball, J. D , Kopelman, H., Witham, A. C. Brit. Heart J. 1952, 14,
363. 7. Goodwin, J. F., Steiner, R. E., Lowe, K. G. J. Fac. Radiol., Lond. 1952, 4, 2. 8. McMichael, J. Brit. med. J. 1952, ii. 525, 578. 9. Domenjoz, R. Schweiz. med. Wschr. 1946, 76, 1210. 10. Burckhardt, W., Rymarowics, R. Ibid, p. 1213. 11. Couperus, M. J. invest. Derm. 1949, 13, 35. New Engl. J. Med. 1950, 243, 74. 12. Appel, B. Brit. J. Derm. 1952, 64, 408. 13. Hitch, J. M. N. Y. St. J. Med. 1950, 50, 1934. 14. Peck, S. M., Michelfelder, T. J. Arch. Derm. Syph., Chicago, 1952, 65, 100. 15. Bereston, E. S.