More histological information in acute coronary death

with no demonstrable dose response it calls the reliability of this finding into question. Of most striking impact was a significantly lower all-cause mortality over the 14 day observation period after starting the treatment period in the four active groups compared to placebo (11·7% compared to 19·6%, P=0·031). Yet again no dose response was seen. There were borderline effects on symptomatic status and patient self-assessments. No consistent effect was seen for objective signs of worsening cardiac function, however. Perhaps the most convincing effect was a significant reduction in the need for additional heart failure therapy, as would be expected for an effective therapy for the acutely failing heart. Does this study alone require us to consider this a proven therapy for acute heart failure complicating myocardial infarction? The answer is definitely no. It does, however, give valuable information on the safety and tolerability of an effective positive inotropic therapy that appears at least unlikely in the short term to increase mortality. The benefits were seen with an increase in hypotension and ischaemia only in the highest dose group. Does this make us revisit the possibility of acute pharmacological inotropic support in acute transient heart failure with the calcium sensitizers? Here more of an argument can be made. Particularly in the modern era of beta-blockade in heart failure the risk/benefit ratio of positive inotropic agents may be different if the myocardium is protected by betablockers, a situation we are much more likely to see in the future. One must be careful, of course, given the evidence for selection bias in reporting positive as opposed to negative trials in heart failure that we do not exaggerate the significance of these findings. It does tell us, however, that more rather than fewer clinical trials of acute heart failure are needed, and that the positive inotropes may still earn their evidence-based credentials in certain circumstances. A. J. S. COATS National Heart and Lung Institute, Imperial College, at Royal Brompton Hospital, London, U.K.