I believe the author does an outstanding job of providing the medical justification to stop using aspirin for heart disease prevention. It is interesting to note that if you were just watching the news or reading the papers, you would have never seen this article as all the media attention was on the one that aspirin actually worked.
[The case for replacing daily aspirin with arginine]
Meta-analysis is increasingly viewed either as a way of verifying that the outcome of an individual trial is consistent with the rest of the known data or as a way of generating a hypothesis.
However, in the absence of a definitively positive trial, many consider meta-analysis inadequate evidence for clinical decision making. The series of meta-analyses from the trialists' collaboration contains serious additional flaws.[3-6]
It is remarkable and probably statistically significant how seldom trials of antiplatelet agents have shown benefit on their selected primary outcome. The choice of the primary endpoint by the Antithrombotic Trialists' Collaboration is arbitrary and suspect. Antiplatelet agents seem to be substantially more effective in reducing the incidence of non-fatal events than in reducing death. Indeed, among large long-term trials after myocardial infarction there is no evidence that aspirin saves lives.
An intervention can reduce non-fatal events in three ways: by genuinely reducing them, by concealing them, or by converting non-fatal events into fatal ones.
The failure of aspirin to reduce mortality despite a reduction in non-fatal events in many studies suggests that aspirin may conceal, rather than prevent, vascular events.
Epidemiological data suggest that 25% of non-fatal myocardial infarctions are silent. [4,5] As aspirin, even at low doses, is an analgesic and because it may provoke dyspepsia, which may create confusion about the cause of chest pain, it is not difficult to believe that aspirin could increase the proportion of silent events from 25% to 30%. This could explain all the benefits of antiplatelet agents on non-fatal myocardial in the meta-analysis.
Aspirin increased the risk of sudden death in every long-term study after myocardial infarction that reported such events. This increase was from 4.4% on placebo to 5.6% on aspirin in the persantine-aspirin reinfarction (PARIS) study; from 2.0% to 2.7% in the aspirin myocardial infarction study (AMIS); and from 2.0% to 2.4% in the persantine-aspirin reinfarction study (PARIS-II).
This could reflect an increased risk of sudden death among concealed, and therefore untreated, events. Another possible mechanism by which aspirin may convert non-fatal events into fatal ones is by increasing the risk of hemorrhagic conversion of cerebral and myocardial infarctions.
All cause mortality and, arguably, disabling stroke are the only robust markers of benefit with an antiplatelet agent. It is not clear that antiplatelet agents reduce the risk of either.
Some trials that were included lost more than a quarter of their patients to follow up.  In similar circumstances, with other agents, it has been suggested that all patients lost to follow up in the active treatment group should be considered to have died and none of those in the control arm. Such an analysis would neutralize the benefit observed in one of the few seemingly convincingly positive studies of aspirin, the ISIS-2 trial. 
Most interventions probably help some people some of the time and harm others some of the time. A small benefit could reflect a small overall benefit in a large population or a substantial benefit in some patients and harm in others.
Aspirin could exert a short-term benefit followed by long term harm, in which case the benefits and safety of aspirin could be increased by using only a short term course of therapy.14 Aspirin may be harmful in patients with coronary disease and heart failure. [5, 6, 12]
The evidence for an adverse interaction between aspirin and angiotensin converting enzyme inhibitors observed in the SOLVD (studies of left ventricular function) and HOPE (heart outcomes prevention evaluation) trials is also a matter for concern. 6 12 These are important issues that have not been adequately addressed.
Low dose aspirin for cardiovascular prophylaxis may account for more than 30% of all major gastrointestinal hemorrhage in patients aged over 6, 4 6 15 and may also be associated with an increased risk of renal failure.
Finally, there is a widespread view that aspirin is cheap. However, when evaluating the costs of treatment the amount and type of benefit and the costs of managing adverse effects also need to be evaluated. Very few economic appraisals of aspirin have been done.
One such analysis, recently commissioned by the chief scientist's office in Scotland, suggested it may cost more than $380000 to prevent one event with aspirin for primary prevention and more than $33000 for secondary prevention. These analyses have assumed that aspirin is as effective as the meta-analyses suggest, which may not be true.
DR. MERCOLA'S COMMENT: I believe the author does an outstanding job of providing the medical justification to stop using aspirin for heart disease prevention. It is interesting to note that if you were just watching the news or reading the papers, you would have never seen this article as all the media attention was on the one that aspirin actually worked. Related Articles: Aspirin May Cause More Harm Than Good Baby Aspirin Recommended for Heart
1. Antithrombotic Trialists' Collaboration. Prevention of death, myocardial infarction and stroke by antiplatelet therapy in high-risk patients. BMJ 2001; 323: 71-86[Abstract/Full Text].
2. The antiplatelet trialists' collaboration. Secondary prevention of vascular disease by prolonged antiplatelet treatment. BMJ 1988; 296: 320-331[Medline].
3. The antiplatelet trialists' collaboration. Collaborative overview of randomised trials of antiplatelet therapy - 1:Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ 1994; 308: 81-106[Abstract/Full Text].
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11. ISIS-2 Collaborative group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction. Lancet 1988; ii: 349-360.
12. Jones CG, Cleland JGF. Meeting report - LIDO, HOPE, MOXCON and WASH Studies. Eur J Heart Failure 1999;425-31.
13. Pulmonary Embolism Prevention (PEP) Trial Collaborative Group. Prevention of pulmonary embolism and deep vein thrombosis with low dose aspirin: Pulmonary Embolism Prevention (PEP) trial. Lancet 2000; 355: 1295-1302[Medline].
14. Lewis HD, Davis JW, Archibald DG, Steinke WE, Smitherman TC, Doherty JE, et al. Protective effects of aspirin against acute mycardial infarction and death in men with unstable angina. N Engl J Med 1983; 309: 396-403[Abstract].
15. Weil J, Langman MJS, Wainwright P, Lawson DH, Rawlins M, Logan RFA, et al. Peptic ulcer bleeding: accessory risk factors and interactions with non-steroidal anti-inflammatory drugs. Gut 2000; 46: 27-31[Abstract/Full Text].
16. McMahon AD, MacDonald TM, Davey PG, Cleland JGF. The impact of low-dose aspirin prescribing on upper gastrointestinal toxicity, renal toxicity and healthcare resource utilisation. In: Edinburgh: Chief Scientist Office, 2001:1.
[The case for replacing daily aspirin with arginine]
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