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Published on: November 8, 2024
Impact of residual platelet reactivity on reperfusion in patients with ST-segment elevation myocardial infarction
Piera Capranzano1, Davide Capodanno2, Chiara Bucciarelli-Ducci3
1Cardiovascular Department, Ferrarotto Hospital, University of Catania, Catania, Italy.
Insights
High platelet reactivity (HPR) in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI) is linked to poorer coronary reperfusion. This indicates HPR negatively impacts outcomes after PPCI.
Area of Science:
- Cardiology
- Interventional Cardiology
- Platelet Physiology
Background:
- High platelet reactivity (HPR) is a concern in ST-segment elevation myocardial infarction (STEMI) patients.
- The impact of HPR on coronary reperfusion after primary percutaneous coronary intervention (PPCI) is not fully understood.
Purpose of the Study:
- To investigate the association between P2Y12-mediated HPR and angiographic outcomes in STEMI patients undergoing PPCI.
- To assess the effect of HPR on coronary patency and reperfusion before and after PPCI.
Main Methods:
- 164 STEMI patients pretreated with P2Y12 inhibitors underwent platelet function testing (VerifyNow™ assay, LTA subgroup).
- HPR was defined by expert consensus.
- Pre-PCI coronary patency, thrombotic burden (Thrombus Score), and post-PCI reperfusion (corrected TIMI frame count) were compared between HPR and non-HPR groups.
Main Results:
- 71.3% of patients exhibited HPR.
- HPR patients showed significantly lower pre-PCI TIMI flow grades 2/3 (32.5% vs 51.1%) and higher thrombus scores (TS grade 3/4: 52.1% vs 29.8%).
- HPR was associated with a worse corrected TIMI frame count (cTFC), indicating impaired reperfusion.
Conclusions:
- Pre-PPCI HPR in STEMI patients treated with P2Y12 inhibitors is associated with reduced coronary patency.
- HPR correlates with increased thrombotic burden and poorer coronary reperfusion post-PPCI.
- These findings highlight HPR as a significant factor influencing angiographic outcomes in STEMI management.
Aim:
Whether high platelet reactivity (HPR) immediately after diagnostic angiography is associated with worse coronary reperfusion prior to and after primary percutaneous coronary intervention (PPCI) for ST-segment elevation myocardial infarction (STEMI) is unknown. This study aimed to assess the impact of P2Y12-mediated HPR on angiographic outcomes in patients with STEMI undergoing PPCI.
Methods:
STEMI patients undergoing PPCI and pretreated with a P2Y12 receptor antagonist underwent platelet function testing with the VerifyNow™ assay at the time of angiography. Light transmission aggregometry (LTA) was performed in a subgroup. HPR was defined according to expert consensus definitions. Pre-PCI coronary patency, thrombotic burden and indices of impaired post-PCI reperfusion were compared between HPR and non-HPR patients.
Results:
Among 164 patients, the prevalence of VerifyNow™-derived HPR was 71.3% at a median (interquartile range (IQR)) of 55 (40-75) minutes after a P2Y12 inhibitor loading dose. Compared with non-HPR patients, those with HPR had significantly lower rates of pre-PCI Thrombolysis in Myocardial Infarction (TIMI) flow grades 2 or 3 (51.1% vs. 32.5%, p = 0.04), higher rates of thrombus score (TS) grade 3/4 (29.8% vs. 52.1%, p = 0.015) and 4 (14.9% vs. 32.5%, p = 0.037) and lower median (IQR) corrected TIMI frame count (cTFC; 23.2 (15.8-32.5) vs. 26.0 (21.0-35.0), p = 0.02), respectively. These findings were consistent using LTA-based data. HPR and TS grade 4 were predictors of higher cTFC.
Conclusions:
In patients with STEMI undergoing PPCI pretreated with P2Y12 receptor inhibitors, pre-PPCI HPR was found to be associated with lower pre-PCI coronary patency, higher thrombotic burden and a worse index of post-PCI coronary reperfusion.
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