Aspirin resistance emerges as potential CV risk. (Bedside Device can Assess Clotting Effect).

Aspirin may be the first-line agent for patients at risk of cardiovascular disease, but what about the small fraction of patients whose platelets don't respond to aspirin?

After years of relative obscurity, aspirin resistance has begun to edge into the collective consciousness. Last year, Cleveland Clinic researchers reported a 5.5% prevalence of aspirin resistance among 325 patients with stable cardiovascular disease (Am. J. Cardiol. 88[3]:230-35, 2001). Their definition of aspirin resistance was that platelets taken from aspirin-treated patients clotted almost as readily in vitro as platelets from people who got no aspirin.

In March of this year, the same team reported at the American College of Cardiology's annual meeting that these aspirin-resistant patients had a fourfold increased risk of death, myocardial infarction, or cerebrovascular accident in a prospective study during nearly 2 years of follow-up, compared with similar patients whose platelets were fully sensitive to aspirin.

More evidence of aspirin resistance came last spring from a retrospective, case-control analysis of urine specimens from 976 Canadian patients who had participated in the Heart Outcomes Prevention Evaluation (HOPE) study a trial that was designed to assess the efficacy of enalapril and vitamin E for preventing cardiovascular disease events. The analysis involved 488 patients who had a myocardial infarction, stroke, or cardiovascular death, compared with an equal number of patients who had no events during the same 5 years of follow-up. All 976 patients received a daily dosage of aspirin throughout the study.

Aspirin resistance was assessed by measuring the level of thromboxane in the urine specimens. Aspirin cuts thromboxane production in sensitive people, so higher urinary thromboxane levels signal greater aspirin resistance.

The patients who fell into the highest quartile for urinary thromboxane level had 80% more events than the people in the lowest quartile for urinary thromboxane (Circulation 105[14]: 1650-55, 2002).

The urine test that was used in this study is not considered ideal for clinical screening since it gauges aspirin's long-term effects rather than providing a snapshot measure. Also, it's a surrogate marker rather than a direct measure of aspirin's effect on clotting.