Electrocardiographic changes in acute poliomyelitis in childhood.

The early pathological accounts of poliomyelitis were limited to descriptions of the changes in the neuraxis. Wickman (1907) in his classical monograph on the disease alluded to the common occurrence of lymphoid hyperplasia, as did Harbitz and Scheel (1907), and Peabody et al. (1912), but none of these writers mentioned myocardial lesions. Robertson and Chesley (1910) observed swelling of myocardial fibres accompanied by interstitial cedema in 4 of 6 patients dying from poliomyelitis: this appears to be the first mention of myocardial damage in poliomyelitis. In 1918, Abramson described perivascular collections of mononuclear cells in the connective tissue septa between normal muscle bundles. Further brief descriptions of myocardial lesions were given by Cowie et al. (1934) and Clark (1938). Saphir and Wile (1942) noted myocardial changes in 6 of 7 patients dying early in the disease; five of these patients were children between 4 and 14 years old; one was 23, and one 34. They described foci of infiltration with lymphocytes and polymorphonuclear leucocytes around vessels in the myocardium and, in some cases, monocytes and adventitial cells were also present; the muscle fibres showed only minimal degenerative changes. Further reports on the myocardial lesions have been made by Peale and Lucchesi (1943), Dublin and Larson (1943), Saphir (1945), Gefter et al. (1947), Dolgopol and Cragan (1948), Ludden and Edwards (1949), and Spain et al. (1950). Detailed reports on single cases have been given by Hassin (1943), Boucek et al. (1949), and Baskin et al. (1950). It is of interest that similar cardiac findings have been described in infective polyneuritis by Sabin and Aring (1941). The incidence of myocardial damage detected in poliomyelitis varies widely. This may be due to the thoroughness of examination for if the whole heart is examined microscopically more lesions will be revealed than when only a few sections are examined. It is also possible that the incidence of cardiac damage varies in different epidemics (Spain et al., 1950).