What is the clinical evidence from this study?

Study design: Other. Population: Coronary artery disease (CAD) (n=120). Intervention: Aspirin vs. Nondiabetic patients. Primary outcome: Aspirin resistance at 81-mg dose using collagen-induced LTA (p=0.001).

What does this research mean for the field?

Diabetic patients with coronary artery disease exhibit a higher prevalence of aspirin resistance at the 81 mg dose compared to nondiabetic patients, a high platelet reactivity phenotype that can be partially overcome by higher aspirin doses. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

September 12, 2007Open Access

The Effect of Aspirin Dosing on Platelet Function in Diabetic and Nondiabetic Patients

Key Result

Diabetic patients with CAD treated with 81 mg aspirin exhibited higher aspirin resistance than nondiabetic patients (27% vs 4%, P=0.001), which was partially overcome by higher aspirin doses.

Structured PICO

Does escalating aspirin dosing improve platelet aspirin responsiveness in diabetic compared to nondiabetic patients with CAD?

Population

120 stable outpatients with coronary artery disease (CAD), consisting of 30 diabetic patients and 90 nondiabetic patients

Intervention

Aspirin at escalating doses (81, 162, and 325 mg/day for 4 weeks each)

Comparator

Nondiabetic patients receiving the same aspirin doses, and within-subject comparison of lower versus higher aspirin doses

Outcome

Platelet aspirin responsiveness and resistance measured by light transmittance aggregometry (LTA), VerifyNow, platelet function analyzer (PFA)-100, and levels of urinary 11-dehydro-thromboxane B(2) (11-dh-TxB(2))surrogate

Diabetic patients with CAD exhibit a high platelet reactivity phenotype and higher aspirin resistance on 81 mg/day compared to nondiabetics, which can be partially overcome by higher aspirin doses.

Main Result

Absolute Event Rate: 27% vs 4%

p-value: p=0.001

Abstract

OBJECTIVE: Diabetic patients may have a higher prevalence of platelet aspirin resistance than nondiabetic patients. Our goal was to analyze platelet aspirin responsiveness to various aspirin doses in diabetic and nondiabetic patients. RESEARCH DESIGN AND METHODS: We examined the effect of aspirin (81, 162, and 325 mg/day for 4 weeks each) on platelet aspirin responsiveness in 120 stable outpatients (30 diabetic patients and 90 nondiabetic patients) with coronary artery disease (CAD) using light transmittance aggregometry (LTA), VerifyNow, platelet function analyzer (PFA)-100, and levels of urinary 11-dehydro-thromboxane B(2) (11-dh-TxB(2)). RESULTS: In the total group, a low prevalence (0-2%) of aspirin resistance was observed with all aspirin doses as determined by arachidonic acid-induced LTA. Aspirin resistance was higher at the 81-mg dose in diabetic versus nondiabetic patients using collagen-induced LTA (27 vs. 4%, P = 0.001), VerifyNow (13 vs. 3%, P = 0.05), and urinary 11-dh-TxB(2) (37 vs. 17%, P = 0.03). Diabetic patients treated with 81 mg exhibited higher platelet function measured by VerifyNow, collagen- and ADP-induced LTA, and 11-dh-TxB(2) levels (P <or= 0.02 for all comparisons). Higher aspirin doses significantly inhibited platelet function and decreased aspirin resistance in diabetic patients (P < 0.05). CONCLUSIONS: Diabetic patients with CAD treated with 81 mg aspirin exhibit a higher prevalence of aspirin resistance and have significantly higher ADP- and collagen-induced platelet aggregation, 11-dh-TxB(2) levels, and aspirin reaction units measured by VerifyNow than nondiabetic patients. Increased aspirin dosing resulted in similar rates of resistance and platelet function levels between groups. These findings indicate that diabetic patients exhibit a global high platelet reactivity phenotype that may be partially overcome by higher aspirin doses.

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