Glycoprotein IIb/IIIa inhibitors use in the setting of primary percutaneous coronary intervention for ST elevation myocardial infarction in patients pre-treated with newer P2Y12 inhibitors.

OBJECTIVES: We sought to investigate the safety and potential benefit of administrating glycoprotein IIb-IIIa inhibitors (GPIs) on top of more potent P2Y12 inhibitors. BACKGROUND: A number of clinical trials, performed at a time when pretreatment and potent platelet inhibition was not part of routine clinical practice, have documented clinical benefits of GPI in ST-segment elevation myocardial infarction (STEMI) patients at the cost of a higher risk of bleeding. METHODS: We used the data of a prospective, ongoing registry of patients admitted for STEMI in our center. For the purpose of this study only patients presenting for primary percutaneous coronary intervention and pretreated with new P2Y12 inhibitors (prasugrel or ticagrelor) were included. We compared patients who received GPI with those who did not. RESULTS: Eight hundred twenty-four STEMI patients were included in our registry; GPIs were used in 338 patients (41%). GPI patients presented more often with cardiogenic shock and Thrombolysis in myocardial infarction (TIMI) flow grade <3. GPI use was not associated with an increase in in-hospital or 3-month mortality. Bleeding endpoints were similar in both groups. CONCLUSIONS: Our study suggests that GPI may be used safely in combination with recent P2Y12 inhibitors in STEMI patients in association with modern primary percutaneous coronary intervention strategies (radial access and anticoagulation with enoxaparin) with similar bleeding and mortality rates at hospital discharge and 3-month follow-up.

Residual platelet reactivity after pre-treatment with ticagrelor prior to primary percutaneous coronary intervention is associated with suboptimal myocardial reperfusion.

BACKGROUND: The evidence of a clinical benefit of P2Y12 inhibitor pre-treatment in primary percutaneous coronary intervention (PCI) and the relation between the level of platelet inhibition and myocardial reperfusion with newer potent P2Y12 inhibitors remain unclear. We aimed to assess the relationship between platelet reactivity at the time of primary PCI after pre-treatment with aspirin and ticagrelor and the post-PCI myocardial blush grade (MBG). METHODS: We prospectively included 61 patients. Platelet reaction units for ticagrelor (PRU) and aspirin reaction units (ARU) were measured using the point-of-care test VerifyNow before PCI. The high on-ticagrelor (PRU >208) and on-aspirin (ARU ⩾ 550) platelet reactivity (HPR and HaPR) were assessed. Patients were divided into two groups according to MBG 3 or <3. RESULTS: MBG 3 was identified in 28 (46%) patients. Mean PRU was lower in such patients as compared with those with MBG <3 (155.82 ± 90.91 vs. 227.42 ± 65.18; p=0.001) while mean ARU was similar between groups. HPR and HaPR were observed in 30 (49.2%) and 11 patients (18%), respectively. HPR but not HaPR was more frequent in the group with impaired MBG (66.7 vs. 28.6%; p=0.003 and 21.2 vs. 14.3%; p=0.48 respectively). CONCLUSION: Our study shows that higher PRU and the subsequent HPR at the time of primary PCI, after pretreatment with ticagrelor, are the only correlates of post PCI MBG. These findings support the earliest possible loading with ticagrelor prior to primary PCI.

Residual platelet reactivity after pre-treatment with ticagrelor prior to primary percutaneous coronary intervention is associated with suboptimal myocardial reperfusion.

BACKGROUND: The evidence of a clinical benefit of P2Y12 inhibitor pre-treatment in primary percutaneous coronary intervention (PCI) and the relation between the level of platelet inhibition and myocardial reperfusion with newer potent P2Y12 inhibitors remain unclear. We aimed to assess the relationship between platelet reactivity at the time of primary PCI after pre-treatment with aspirin and ticagrelor and the post-PCI myocardial blush grade (MBG). METHODS: We prospectively included 61 patients. Platelet reaction units for ticagrelor (PRU) and aspirin reaction units (ARU) were measured using the point-of-care test VerifyNow before PCI. The high on-ticagrelor (PRU >208) and on-aspirin (ARU ⩾ 550) platelet reactivity (HPR and HaPR) were assessed. Patients were divided into two groups according to MBG 3 or <3. RESULTS: MBG 3 was identified in 28 (46%) patients. Mean PRU was lower in such patients as compared with those with MBG <3 (155.82 ± 90.91 vs. 227.42 ± 65.18; p=0.001) while mean ARU was similar between groups. HPR and HaPR were observed in 30 (49.2%) and 11 patients (18%), respectively. HPR but not HaPR was more frequent in the group with impaired MBG (66.7 vs. 28.6%; p=0.003 and 21.2 vs. 14.3%; p=0.48 respectively). CONCLUSION: Our study shows that higher PRU and the subsequent HPR at the time of primary PCI, after pretreatment with ticagrelor, are the only correlates of post PCI MBG. These findings support the earliest possible loading with ticagrelor prior to primary PCI.