In reply: Aroney's letter raises a number of important issues. The first of these is the question of whether a scientific fact requires the blessing of peer review to become established as such. The corollary of this is whether or not all peer-reviewed facts are necessarily true. The answer to both questions is probably no.

The second issue is how to control a media report, irrespective of whether it is based on a peer-reviewed study. The issue which concerns Aroney is an abstract presentation of the association of gastrointestinal bleeding with aspirin, non-steroidal anti-inflammatory drugs (NSAIDs) and cyclo-oxygenase II (COX-II) inhibitors, the conclusion of which was that, while the last two might be important in their own right, concurrent use of aspirin, even in a small dose, was more closely associated with bleeding risk, particularly if there was a past history of peptic ulceration.1

A "meta-analysis" of the media reports, which included both television and radio in addition to the quoted report in the Sydney Morning Herald,2 would have made it clear that the theme of the interviews reaffirmed the relative safety of aspirin in the vast majority of individuals, and highlighted the risk of aspirin use concurrently with NSAIDs and COX-II inhibitors, particularly when there is a history of past ulceration. The fact that the SMH report focused on one aspect of the study was counterbalanced by the others. We do not know how journalistic reporting is controlled.

A primary question is whether or not aspirin is an effective agent for the prevention of cardiovascular disease beyond the management of acute myocardial infarction. More recent literature than that quoted by Aroney is now questioning the overall cardioprotective value of aspirin.3 This showed that aspirin given as prophylaxis against cardiovascular disease increased the risk of sudden death in every secondary prevention study and left the overall rate of myocardial infarction unchanged.4 Aspirin consistently failed to reduce overall mortality in every study of long-term prophylaxis after myocardial infarction, and in all but one after stroke.3 Furthermore, Cleland and colleagues have argued that a series of meta-analyses, which most people have accepted as proof of the efficacy of aspirin, are of doubtful validity.4 They questioned whether it is appropriate for the medical community to invest so much time and effort in prescribing aspirin and dealing with the adverse consequences of its long-term ingestion to the neglect of other, better proven and apparently more effective therapies such as angiotensin-converting enzyme inhibitors, β-blockers, and statins. At the very least, it can be said that there is controversy in the cardiovascular literature about the benefits of aspirin.

Just as important is the issue of the safety of long-term aspirin use for cardioprotection. A recent multidisciplinary expert statement on NSAIDs concluded that, on current evidence, prophylactic use of aspirin should be reserved for patients with established vascular disease, because in other patients bleeding risks may outweigh cardiovascular benefit.5 A Danish study showed that 100–150 mg of aspirin daily increased the risk of haematemesis by a factor of 2.6, with no difference in the risk between enteric and non-coated product; when combined with an NSAID the risk was increased by a factor of 5.6.6 The authors concluded that the bleeding risk may offset some of the benefits of aspirin.

It is no longer appropriate to simply "bury" the adverse gastrointestinal effects of low-dose aspirin in the NSAID side-effect "basket".7 It is apparent to us that dogma should not be so enshrined that it prevents the discussion of issues that might helpfully modify that dogma.