Related Experiment Video
Updated: Dec 26, 2025

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Platelet-Derived Thrombogenicity Measured by Total Thrombus-Formation Analysis System in Patients With ST-Segment
Shinnosuke Kikuchi1, Kengo Tsukahara1, Shinya Ichikawa1
1Division of Cardiology, Yokohama City University Medical Center.
Insights
High platelet-derived thrombogenicity during primary percutaneous coronary intervention (PPCI) in ST-elevation myocardial infarction (STEMI) patients is linked to larger enzymatic infarct size. This finding highlights the importance of assessing platelet activity during PPCI for STEMI management.
Area of Science:
- Cardiology
- Thrombosis Research
- Interventional Cardiology
Background:
- Effective antiplatelet therapy is crucial for ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI).
- Platelet-derived thrombogenicity during PPCI can influence patient outcomes.
- Assessing thrombogenicity is key to optimizing STEMI management.
Purpose of the Study:
- To evaluate the association between platelet-derived thrombogenicity during PPCI and enzymatic infarct size in STEMI patients.
- To identify determinants of enzymatic infarct size in STEMI patients undergoing PPCI.
Main Methods:
- Platelet-derived thrombogenicity assessed using the total thrombus-formation analysis system (T-TAS) PL-chip (PL18-AUC10) and VerifyNow P2Y12 reaction units (PRU).
- 127 STEMI patients undergoing PPCI were categorized into High and Low PL18-AUC10 groups based on median values.
- Enzymatic infarct size measured by the area under the curve for creatine kinase (AUC_CK).
Main Results:
- High PL18-AUC10 during PPCI was associated with a significantly greater enzymatic infarct size (AUC_CK).
- The High PL18-AUC10 group showed a lower percentage of final Thrombolysis in Myocardial Infarction (TIMI) 3 flow and a higher incidence of slow-flow/no-reflow.
- Multivariate analysis identified high PL18-AUC10 and poor initial TIMI flow as independent determinants of AUC_CK.
Conclusions:
- High platelet-derived thrombogenicity, as measured by T-TAS, during PPCI is significantly associated with larger enzymatic infarct size in STEMI patients.
- These findings underscore the clinical relevance of T-TAS in assessing thrombotic risk and guiding treatment in STEMI.
- Optimizing antiplatelet therapy based on thrombogenicity assessment may reduce infarct size and improve outcomes in STEMI.
Background:
Prompt and potent antiplatelet effects are important aspects of management of ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI). We evaluated the association between platelet-derived thrombogenicity during PPCI and enzymatic infarct size in STEMI patients.
Methods And Results:
Platelet-derived thrombogenicity was assessed in 127 STEMI patients undergoing PPCI by: (1) the area under the flow-pressure curve for the PL-chip (PL18-AUC10) using the total thrombus-formation analysis system (T-TAS); and (2) P2Y12reaction units (PRU) using the VerifyNow system. Patients were divided into 2 groups (High and Low) based on median PL18-AUC10during PPCI. PRU levels during PPCI were suboptimal in both the High and Low PL18-AUC10groups (median [interquartile range] 266 [231-311] vs. 272 [217-317], respectively; P=0.95). The percentage of final Thrombolysis in Myocardial Infarction (TIMI) 3 flow was lower in the High PL18-AUC10group (75% vs. 90%; P=0.021), whereas corrected TIMI frame count (31.3±2.5 vs. 21.0±2.6; P=0.005) and the incidence of slow-flow/no-reflow phenomenon (31% vs. 11%, P=0.0055) were higher. The area under the curve for creatine kinase (AUCCK) was greater in the High PL18-AUC10group (95,231±7,275 IU/L h vs. 62,239±7,333 IU/L h; P=0.0018). Multivariate regression analysis identified high PL18-AUC10during PPCI (β=0.29, P=0.0006) and poor initial TIMI flow (β=0.37, P<0.0001) as independent determinants of AUCCK.
Conclusions:
T-TAS-based high platelet-derived thrombogenicity during PPCI was associated with enzymatic infarct size in patients with STEMI.
Related Concept Videos
Acute Coronary Syndrome I: Introduction
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...

