Heart failure in the setting of acute cardiogenic shock secondary to an extensive myocardial infarction is an example where a relatively well defined single mechanism is operative ie insufficient numbers of viable myocytes remain to sustain effective contraction'31. Under these conditions a fairly close relationship exists between myocyte loss and functional impairment'4'. Myocyte loss is also prominent in more chronic forms of heart failure secondary to both ischaemia'51 and dilated cardiomyopathy* 61, but here there is a weaker correlation between histological abnormalities and the severity of longstanding heart failure171. This implies that functional abnormalities among the remaining viable myocytes and in the interstitium are also important in the development of chronic myocardial failure.