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Thrombogenicity and endothelial progenitor cells function during Acute myocardial infarction - comparison of
Maya Wiessman1,2, Mark Kheifets3,4, Nili Schamroth Pravda3,4
1Department of Cardiology, Rabin Medical Center, Beilinson Campus, 39 Ze'ev Jabotinsky St, 4941492, Petach Tikva, Israel. mparyente@gmail.com.
Insights
Prasugrel demonstrated superior thrombin generation inhibition and enhanced endothelial progenitor cell (EPC) function compared to ticagrelor in ST-segment elevation myocardial infarction (STEMI) patients. This study highlights prasugrel
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hematology
Background:
- Thrombin generation (TG), platelet function, and circulating endothelial progenitor cells (EPCs) are crucial in coronary artery disease (CAD) pathophysiology.
- Previous studies on P2Y12 inhibitors' effects primarily focused on the sub-acute phase post-myocardial infarction.
Purpose of the Study:
- To compare the efficacy of prasugrel and ticagrelor in modulating TG and EPCs during the acute phase of ST-segment elevation myocardial infarction (STEMI).
Main Methods:
- STEMI patients were randomized to receive either ticagrelor or prasugrel.
- Thrombin generation, platelet reactivity, and EPCs were assessed before (T0) and one day after (T1) the P2Y12 inhibitor loading dose.
Main Results:
- While P2Y12 reactivity units (PRU) did not differ between groups at T1, prasugrel showed significantly more potent TG inhibition.
- Prasugrel treatment resulted in a longer lag time to TG initiation, longer time to peak, and lower endogenous thrombin potential (AUC).
- EPCs, including CD34+, CD133+ cells, and colony-forming units (CFUs), were significantly higher in the prasugrel group.
Conclusions:
- In STEMI patients, prasugrel exhibits more potent TG inhibition compared to ticagrelor.
- Prasugrel treatment is associated with improved EPC count and function in the acute phase of STEMI.
Background:
Thrombin generation (TG), platelet function and circulating endothelial progenitor cells (EPCs) have an important role in the pathophysiology of coronary artery disease (CAD). To date, the effect of novel P2Y12 inhibitors on these aspects has mostly been studied in the sub-acute phase following myocardial infarction.
Objectives:
Comparing the effects of prasugrel and ticagrelor on TG and EPCs in the acute phase of ST-segment elevation myocardial infarction (STEMI).
Methods:
STEMI patients were randomized to either ticagrelor or prasugrel treatment. TG, platelet reactivity and EPCs were evaluated prior to P2Y12 inhibitor loading dose (T0), and one day following (T1).
Results:
Between December 2018 - July 2021, 83 consecutive STEMI patients were randomized to ticagrelor (N = 42) or prasugrel (N = 41) treatment. No differences were observed at T0 for all measurements. P2Y12 reactivity units (PRU) at T1 did not differ as well (prasugrel 13.2 [5.5-20.8] vs. ticagrelor 15.8 [4.0-26.3], p = 0.40). At T1, prasugrel was a significantly more potent TG inhibitor, with longer lag time to TG initiation (7.7 ± 7.5 vs. 3.9 ± 2.1 min, p < 0.01), longer time to peak (14.1 ± 12.6 vs. 8.3 ± 9.7 min, p = 0.03) and a lower endogenous thrombin potential (AUC 2186.1 ± 1123.1 vs. 3362.5 ± 2108.5 nM, p < 0.01). Furthermore, EPCs measured by percentage of cells expressing CD34 (2.6 ± 4.1 vs. 1.1 ± 1.1, p = 0.01) and CD133 (2.3 ± 1.8 vs. 1.4 ± 1.5, p = 0.01) and number of colony forming units (CFU, 2.1 ± 1.5 vs. 1.1 ± 1.0, p < 0.01) were significantly higher in the prasugrel group.
Conclusion:
Among STEMI patients, prasugrel as compared to ticagrelor was associated with more potent TG inhibition and improved EPCs count and function.
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