Key result
Novel TEG parameter nMAadp identifies post-PCI high on-treatment platelet reactivity with ~0.85 AUC.
Why the study?
Current indicators for HTPR may lack specificity, contributing to the failure of tailored antiplatelet therapy in post-PCI patients, necessitating more specific indicators.
Does the novel TEGpm variable nMAadp improve the specific identification of high on-treatment platelet reactivity in post-PCI patients compared to standard TEGpm variables?
Observational (n=110)
No
Does the novel TEGpm variable nMAadp improve the specific identification of high on-treatment platelet reactivity in post-PCI patients compared to standard TEGpm variables?
The novel TEGpm parameter nMAadp isolates platelet-specific clot strength, offering enhanced diagnostic accuracy for identifying high on-treatment platelet reactivity in post-PCI patients.
Answers are grounded in this paper and cite their sources.
nMAadp may aid HTPR identification post-PCI on DAPT; hypothesis-generating and requires prospective validation before practice change.
High-on treatment platelet reactivity (HTPR) leads to more prevalence of thrombotic event in patients undergoing percutaneous coronary interventions (PCI). Dual antiplatelet therapy with aspirin in addition to one P2Y12 inhibitor is commonly administrated to reduce HTPR. However, 'one size fits all' antiplatelet strategy is widely implemented due to lacking benefits with tailored strategy. One reason for the failure of tailored treatment might be less specificity of the current indicators for HTPR. Therefore, searching for specific indicators for HTPR is critical. Thromboelastograph with platelet mapping (TEGpm) assay has been explored for identifying HTRP. Variables of TEGpm assay, including maximum amplitude (MA) induced by thrombin (MAthrombin), R time, platelet aggregation rate induced by ADP (TEGaradp) and MA induced by ADP (MAadp) have been demonstrated to be able to identify HTPR in post-PCI patients. However, these variables for HTPR might be less specific. Thus, in the present study, a novel variable nMAadp was derived by removing fibrin contribution from MAadp and analyzed for its usefulness in determining HTPR. In addition, MAthrombin, R time, MAadp and TEGaradp were also examined for determining HTPR. In conclusion, nMAadp and TEGaradp were demonstrated to be independent indicators for HTPR; nMAadp had the strongest power to identify HTPR with cutoff value of 26.3 mm; MAthrombin and R time were not significantly different between patients with and without HTPR; combination of TEGaradp and nMAadp further improved the ability to identify HTPR with an AUC of 0.893.
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Cheng et al. (2020) conducted an observational in post-PCI patients with unstable angina or AMI on DAPT (n=110). nMAadp (net MAadp) derived from TEGpm vs. Standard TEGpm parameters was evaluated on Identification of High On-treatment Platelet Reactivity (HTPR) defined by LTAaradp > 46% (AUC 0.849, 95% CI 0.768-0.910). The novel TEGpm variable nMAadp independently identified high on-treatment platelet reactivity with an AUC of 0.849 and a cutoff of >26.3 mm in post-PCI patients on dual antiplatelet therapy.
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