Key result
High platelet reactivity (aspirin resistance) was found in 23% of stable T2DM patients and was strongly related to insulin resistance and CAD severity, but not to inflammatory markers.
Why the study?
Aspirin resistance in type 2 diabetes mellitus is related to accelerated platelet turnover with persistent high platelet reactivity (HPR) 24 hours after aspirin intake, but the underlying mechanisms remained unknown.
What are the clinical and biochemical determinants of aspirin resistance in patients with type 2 diabetes?
Cross-Sectional (n=116)
No
What are the clinical and biochemical determinants of aspirin resistance in patients with type 2 diabetes?
Aspirin resistance is common in type 2 diabetes (23%) and is driven by insulin resistance and associated with CAD severity, suggesting these patients may need alternative antiplatelet strategies.
May warrant testing twice-daily aspirin dosing in T2DM with HPR; leaves open whether this reduces events in RCTs.
Cardiovascular disease is a leading cause of mortality among patients with type 2 diabetes mellitus (T2DM). Numerous patients with T2DM show resistance to aspirin treatment, which may explain the higher rate of major adverse cardiovascular events observed compared with non-diabetes patients, and it has recently been shown that aspirin resistance is mainly related to accelerated platelet turnover with persistent high platelet reactivity (HPR) 24 h after last aspirin intake. The mechanism behind HPR is unknown. The aim of this study was to investigate the precise rate and mechanisms associated with HPR in a population of T2DM patients treated with aspirin. Included were 116 consecutive stable T2DM patients who had attended our hospital for their yearly check-up. HPR was assessed 24 h after aspirin intake using light transmission aggregometry (LTA) with arachidonic acid (AA) and serum thromboxane B2 (TXB2) measurement. Its relationship with diabetes status, insulin resistance, inflammatory markers and coronary artery disease (CAD) severity, using calcium scores, were investigated. Using LTA, HPR was found in 27 (23%) patients. There was no significant difference in mean age, gender ratio or cardiovascular risk factors in patients with or without HPR. HPR was significantly related to duration of diabetes and higher fasting glucose levels (but not consistently with HbA1c), and strongly related to all markers of insulin resistance, especially waist circumference, HOMA-IR, QUICKI and leptin. There was no association between HPR and thrombopoietin or inflammatory markers (IL-6, IL-10, indoleamine 2,3-dioxygenase activity, TNF-α, C-reactive protein), whereas HPR was associated with more severe CAD. Similar results were found with TXB2. Our results reveal that ‘aspirin resistance’ is frequently found in T2DM, and is strongly related to insulin resistance and severity of CAD, but weakly related to HbA1c and not at all to inflammatory parameters. This may help to identify those T2DM patients who might benefit from alternative antiplatelet treatments such as twice-daily aspirin and thienopyridines.
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Paven et al. (2019) conducted a cross-sectional in Type 2 diabetes mellitus (n=116). High platelet reactivity (HPR) vs. Patients without HPR was evaluated on High platelet reactivity (HPR) assessed 24 h after aspirin intake using light transmission aggregometry. High platelet reactivity (aspirin resistance) was found in 23% of stable T2DM patients and was strongly related to insulin resistance and CAD severity, but not to inflammatory markers.
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