Is susceptibility to chronic rheumatic heart disease determined in early infancy? An analysis of mortality in Britain during the 20th century


  • D I W Phillips MRC Lifecourse Epidemiology Unit, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD, UK
  • C Osmond MRC Lifecourse Epidemiology Unit, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD, UK


Background: The reason why some individuals but not others are susceptible to rheumatic fever and chronic rheumatic heart disease is not understood. Because of the substantial evidence that poverty is an important determinant of the disease and must operate in early life, we have investigated the role of the early environment in an ecological study using 20thcentury mortality as an index of disease prevalence. 

Methods: We analysed 37,321 deaths from rheumatic heart disease in England and Wales during 1968–78. We compared the geographical distribution of deaths with previous infant mortality records from 1911 onwards. These records included details of mortality at different ages and from different causes. They also included data on housing and population density. 

Results: Mortality from rheumatic heart disease showed a strong correlation with past infant mortality that was consistently stronger with postneonatal mortality (deaths from one month to one year) than with neonatal mortality (deaths during the first month of life). Areas with high infant mortality from diarrhoea or bronchitis had the highest subsequent mortality from rheumatic heart disease. Although rheumatic heart disease was linked with early overcrowding, regression analyses suggested that overcrowding could not per seexplain the infant mortality associations. 

Conclusions: Chronic rheumatic heart disease may have its origins in early infancy. Our findings raise the possibility that susceptibility to rheumatic fever and rheumatic heart disease may be linked with infection in the postneonatal period. Alternatively, they may be explained by the operation of environmental factors that both predispose to infection in infancy and the subsequent liability to heart disease.






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