Comparison of Platelet Inhibition in Patients with ST-Elevation Myocardial Infarction vs. non-ST Elevation Myocardial Infarction after a Loading Dose of Swallowed vs. Chewed Ticagrelor

Background: The pathogenesis of both ST-elevation (STEMI) and non-ST-elevation Myocardial Infarction (NSTEMI) involves coronary thrombosis over a ruptured atherosclerotic plaque, yet the reason for the different extent of coronary thrombosis in the two syndromes is largely unknown. Furthermore, recent studies showed that STEMI is associated with delayed and reduced platelet response to a novel P2Y12 antagonists loading dose (LD). It was suggested that delayed gastric absorption accounts for the delayed response in STEMI.

Methods: In this study we prospectively compared platelet inhibition in response to a Ticagrelor LD in consecutive STEMI (N=73) vs. NSTEMI (N=41) patients, when a ticagrelor LD (180 mg) was swallowed (TS) or chewed (TC) in order to "bypass" any potential effect of delayed in gastric absorption on platelet response. Platelet reactivity was determined in response to ADP by VerifyNow and expressed as PRU at admission, (before ticagrelor LD) and 1 hour later.

Results: There were no differences in baseline characteristics between STEMI and NSTEMI patients. Platelet reactivity was higher at 1 hour in STEMI vs. NSTEMI regardless of whether Ticagrelor was swallowed (175±93 vs. 115±85, p = 0.03) or chewed (126±93 vs. 46±54, p=0.001). Among STEMI patients with a chewing vs. swallowing a Ticagrelor LD, it accelerated the inhibition of platelet aggregation (IPA) over the first hour (42% vs. 14%, p < 0.05), probably by bypassing the delayed GI absorption. Yet, only among patients who chewed the LD, the IPA at 1 hour was significantly higher in NSTEMI vs. STEMI (83% vs. 52%, p = 0.001), figure.

Conclusions: Our findings suggest that beyond the delayed gastric absorption of Ticagrelor, which contributes to delayed response to P2Y12 antagonists in STEMI, STEMI as compared with NSTEMI is also associated with intrinsic platelet hypo-responsiveness that might be related to the extent of thrombous formation between theese two syndromes.