Electron-microscope studies of experimental models of myocardial ischaemia have provided basic information on the pathogenesis of hypoxic heart injury. Correlation of ultrastructural changes with biochemical data confirms the importance of catecholamine release and ionic shifts in the early evolution of ischaemic injury. An altered cellular metabolism induced by ischaemia causes rapid depletion of glycogen and is followed quickly by alterations in the nucleus, the mitochondria and the sarcotubular system; the myofibril is the organelle most resistant to hypoxia.Postmortem autolysis mimics early ischaemic change very closely and it probably has an initial hypoxic basis. Significant hypoxic-autolytic changes may begin during the agonal state. The time elapsing and the techniques of tissue preservation are critical in determining the amount of artefact. At present it is unrealistic to expect to obtain acutely ischaemic human myocardium soon enough after death to be of value in the estimation of the degree or duration of ischaemia by electron-microscope techniques. Rapidly progressive autolytic changes preclude the meaningful morphological assessment of hypoxic change at the ultrastructural level.