That haemolytic streptococci of human origin produce a substance capable of liquefying human fibrin was first demonstrated by Tillet and Garner in 1933. The fibrin from patients recently recovered from haemolytic streptococcal infection was in many cases found to be resistant to the action of this fibrinolysin.Further work (Tillett, Edwards and Garner, 1934 ;Tillet, 1935) Tillett found that in some cases it was present at the time of recovery, but that in others its appearance was delayed for two to four weeks after the acute infection. There was a suggestion that it developed earlier in cases of erysipelas than in those with an acute streptococcal pharyngitis. These observations were confirmed by Myers, Keefer and Holmes (1935), who also showed that the resistance of the plasma to fibrinolysin, once developed, persisted for a varying time, and Spink and Keefer (1936) found that in erysipelas antifibrinolysin can be demonstrated from eight to a hundred and fifty days after the attack. Waaler (1936) found that patients with scarlatina did not all develop antifibrinolysin, and that in those who did, it might first appear from one to five weeks after the infection, similar observations being made by Stuart-Harris (1935, a and b). From this work it is now clear that it is rare for antifibrinolysin to be present in the blood unless the patient has comparatively recently experienced a streptococcal infection. The occasional cases to the contrary can be explained by assuming that the antifibrinolysin has persisted long after the infection to which it is due has been forgotten. Antifibrinolysin ranks with antistreptolysin as one of the antibodies produced as part of the immunity mechanism following infections with haemolytic streptococci. The presence of these antibodies in the blood does not necessarily run parallel, and Stuart- Harris (1935b) has shown that there is no correlation between antistreptolysin and antifibrinolysin except that when the fibrin is completely resistant to fibrinolysin there is usually some rise in the antistreptolysin titre.Shortly after Tillett and Garner's original reports, Hadfield, Magee and Perry (1934) found that the fibrin of many patients in the active stage of acute rheumatism was partially or completely resistant to fibrinolysin. This was regarded as further evidence of the frequent occurrence of a haemolytic 32 on 13 May 2018 by guest. Protected by copyright.
It has long been recognized that acute rheumatism and rheumatic heart disease occur more frequently in some families than in others. It is, however, far from clear whether this increased incidence is due to genetic factors or to exposure to the same environment.
This investigation was undertaken to serve as a control to electrocardiographic observations on children of school age suffering from heart disease.We were particularly concerned to note the incidence of low voltage, bizarre and splintered Q.R.S. complexes, and of inversion of the T-waves.In 1913 HechtL studied the electrocardiogram of children and concluded that all the deflections were smaller in childhood, and the transmission time shorter, than in adult life. Krumbhaar and Jenks2 in 1916 studied the changes occurring in the electro cardiogram in normal infants, but their investigations did not extend far into school years. Seham3 in 1921 studied the tracings of 101 children, aged from one hour to 13 years, these included 26 subjects aged 6 to 13 years. In 1928 Lincoln and Nicholson4 reported their findings in 222 normal children aged from 3 to 12 years in a very detailed paper.Technique.-The method of investigation adopted in the present series of children was as follows. Children selected by the school doctor as having normal hearts were picked out for examination. These were examined clinically for any evidence of disease. All those showing any abnormal physical signs, abnormal blood-pressure readings, or giving a history of rheumatism or chorea were excluded from the series. One hundred children, fifty boys and fifty girls, were examined. These were cardiographed in the sitting position, with non-polarizable immersion electrodes, and the galvanometer standardized so that one millevolt gave a deflection of 10 mm.Rate.-The average rate for the whole group was 92-6 beats per minute. For girls the average was 98-5 per minute, and for boys 86-8 beats per minute. Figure 1 shows the rate at different ages for the two sexes. There is a slight tendency for the rate to fall with increasing age, but this is not very marked. Girls have a slightly higher rate than boys. These figures are probably high on account of the nervous factor, through being examined with a strange apparatus. They are a little higher than Seham's. Lincoln and Nicholson found a more definite decrease in the rate with increase in age, and their girls up to the age of seven years had a higher rate than boys, but from that age to iwelve the boys had the more rapid rate, and over twelve years of age the girls again showed the higher rate.Rhythm.-Sinus arrhythmia, following Krumbhaar and Jenks' standard, was considered present when the difference in the longest and shortest pulse periods was 041 seconds or over. This occurred in 72 per cent. of the cases and,
Whether diphtheria commonly causes any permanent cardiac damage has long been the subject of discussion; but it is generally accepted that the persistence of electrocardiographic changes of any serious significance is extremely rare (
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