In-vivo platelet activation and aggregation during and after acute atherothrombotic myocardial infarction in patients with and without Type-2 diabetes mellitus treated with ticagrelor.

INTRODUCTION: Patients with type-2 diabetes are twice as likely to suffer from acute myocardial infarction (AMI) and have a higher incidence of recurrent events than their non-diabetic counterparts. Ticagrelor is a platelet inhibitor known to reduce major adverse cardiovascular events (MACE) in AMI patients. This study measures the level and change in platelet activation and aggregation at the time of and following an AMI in patients with and without diabetes treated with ticagrelor. MATERIALS/METHODS: P2Y12 receptor inhibitor naïve patients presenting with AMI were prospectively enrolled. Blood collection occurred before coronary angiography (baseline: T0), 2, 4, 24, 48 h after baseline, and at a three-month follow-up. Ticagrelor was administered within five minutes of T0. We assessed platelet activation via measurements of surface P-selectin and platelet activated glycoprotein IIb/IIIa-1 (PAC-1) and assessed platelet aggregation via monocyte, lymphocyte, and granulocyte aggregates. We hypothesize that platelet activation and aggregation will be proportionally impacted to the same degree by ticagrelor, regardless of diabetes status. RESULTS: Ninety-seven patients were prospectively enrolled (diabetes, N = 33; no diabetes, N = 64). No difference was observed in the expression of P-selectin and PAC-1 at any given point between diabetes and non-diabetes groups (p > 0.05). No difference was observed in the percentage of platelet bound to leukocytes at any measured timepoint between patients with and without diabetes (p > 0.05). Platelet leukocyte aggregation was suppressed during the acute phase compared to quiescence equally among both groups. DISCUSSION: Ticagrelor demonstrated similar in-vivo effects on platelet activation and aggregation regardless of diabetes status in patients presenting with AMI.