be used by many physicians in this way, though many patients with identical symptoms do not have the endocardial reaction of EFE. In the latter decades of the twentieth century, new discoveries and new thinking about heart muscle disease gave rise to the term "cardiomyopathy". Many of the cases of infantile cardiac failure were accordingly called "primary cardiomyopathy" as well as "primary EFE", while those with identifiable congenital anomalies stressing the heart were called "secondary EFE". In 1957 Black-Schaffer proposed a unitary explanation that stress on the ventricle, of any kind, may trigger the endocardial reaction, so that all EFE could be thought of as secondary. Evidence gradually accumulated as to the role of infection as one such type of stress. The studies of Fruhling and colleagues in 1962 were critical. They followed a series of epidemics of Coxsackie virus infection in their part of France. After each epidemic there were increased numbers of cases with EFE coming to autopsy. On closer study there were cases of pure acute myocarditis, cases of mixed myocarditis and EFE, and cases where myocarditis had healed, leaving just EFE. They were able to culture Coxsackie virus from the tissues of many of the cases at all stages of this apparent progression. A similar progression from myocarditis to EFE was later observed at Johns Hopkins but no virology was done. Noren and colleagues at the University of Minnesota, acting on an idea floated at a pediatric meeting, were able to show a relation between exposure to maternal mumps in fetal life, EFE, and a positive skin test for mumps in infants. This brought on a large ongoing controversy and finally prompted a virologist colleague of theirs to inject embryonated eggs with mumps virus. The chicks at first showed the changes of myocarditis, about a year later, typical EFE, and transitional changes in between. Despite this, the controversy about the role of mumps continued as the actual incidence of EFE plummeted. The proponents of mumps as a cause pointed to this as the effect of the recent implementation of widespread mumps immunization. Evidence that viral infection may play a role as a cause or trigger of EFE was greatly reinforced by the study directed by Towbin in the virus laboratory of Texas Children's Hospital. They applied the methods of today's genetics to old preserved specimens from autopsies of patients with EFE done well before mumps immunization