Aspirin’s cardioprotective benefits stem from its soothing effect, which calms arterial inflammation. The drug also has antiplatelet properties, making platelets (tiny blood-cell fragments with no nuclei) less sticky and less likely to form clots.
Although aspirin can reduce the risk of secondary events (repeat heart attacks or strokes) by about one-quarter in those with established cardiovascular disease, recent studies expose a worrying aspect of the drug: it doesn’t work for everyone. While its pain-relieving potential is universally accepted, its antiplatelet properties are more hit-and-miss - indeed, missing a substantial number of exactly those people who take it religiously in hopes that it will save their lives.
This phenomenon - the occurrence of blood clots that can cause heart attack or stroke despite regular aspirin therapy - is referred to by the medical profession as ‘aspirin resistance’ (Am Heart J, 2005; 149: 675-80). Given this definition, however, it’s no surprise that researchers are now asking whether ‘aspirin failure’ might not be a more accurate term.
Aspirin resistance appears to be dose-related in some patients and so may be overcome with higher doses. But those are the dosages associated with an increased risk of gastrointestinal bleeding and other established uncomfortable or just plain dangerous side-effects. Yet, for some people, aspirin initially works to thin the blood, but the effect lessens over time.
In other words, they slowly develop a tolerance for aspirin.
A brief history
In the late 1980s, a series of trials showed that the regular use of aspirin reduced the risk of non-fatal stroke and heart attack in cardiovascular patients, as well as lowered the risk of heart attack in men without cardiovascular disease (BMJ, 1988; 296: 320-31; Am J Cardiol 1988; 61: 637-40). This led to the 1989 US Preventive Services Task Force’s general recommendation that, from the age of 40 onwards, men who had a propensity for heart disease consider routinely taking low doses of aspirin as a preventative measure.
And more major support of aspirin was yet to come. The 1994 meta-analysis by the Antiplatelet Trialists’ Collaboration (ATC) further recommended aspirin use as treatment against stroke, claiming that a few weeks of antiplatelet therapy could halve the risk of deadly blood clots in high-risk patients (BMJ, 1994; 308: 235-46).
However, a critical look at the ATC analysis later that same year exposed major flaws in the studies it covered. In fact, only one of the 16 studies was properly conducted and error-free. Appalling mistakes were rife among the rest of them, including mathematical mistakes and the avoidance of safety issues. In short, there was no evidence to support the widespread use of aspirin to prevent stroke (BMJ, 1994; 309: 1213-5).
Nevertheless, initial enthusiasms die hard. Today, the UK’s National Health Service still recommends a daily 75-mg aspirin for secondary prevention of stroke and arterial disease, and a daily 150-mg dose in the event of an acute heart attack (providing there are no contraindications to aspirin such as a history of stomach ulcers or kidney disease).
As for the use of aspirin as primary prevention (reducing the possibility of a first heart attack), the Aspirin Foundation admits that “this has yet to be adequately tested” before ignoring said uncertainties and suggesting that aspirin reduces the risk of non-fatal heart attack by about a third, with a minor (10 per cent) reduction of risk for other cardiovascular problems.