title: Effects of platelet and inflammatory system activation on outcomes in diabetic patients with ST segment elevation myocardial infarction treated with primary percutaneous coronary intervention.
abstract: BACKGROUND
  Recurrent myocardial ischaemia and restenosis are more common in diabetic patients treated with primary percutaneous coronary intervention (PCI) due to an acute coronary syndrome (ACS) compared to patients without diabetes. Diabetes is also associated with increased residual platelet activity during dual antiplatelet treatment. In recent reports, platelet reactivity has been linked to outcomes after ACS. Appropriate platelet inhibition might lead to improved outcomes in this patient population. To this end, newest methods to evaluate platelet function may prove helpful.
  
  
  OBJECTIVE
  To evaluate 6-month outcomes in diabetic patients treated with primary PCI due to ST segment elevation myocardial infarction (STEMI) in relation to platelet reactivity evaluated at discharge.
  
  
  METHODS
  The study included 120 diabetic patients treated with primary PCI due to STEMI. Patients received loading doses of acetylsalicylic acid (ASA, 300 mg) and clopidogrel (600 mg) on admission, and later were treated with maintenance doses of 75 mg of ASA and clopidogrel. Blood for platelet aggregation testing was collected at discharge. We used whole blood impedance aggregometry using the Multiplate aggregometer with arachidonic acid (AA), adenosine diphosphate (ADP), collagen, and thrombin receptor peptide agonist (TRAP) as agonists. Six-month follow-up was based on telephone contact and hospital discharge summaries if hospitalisation occurred. The primary combined endpoint included recurrent ACS and restenosis.
  
  
  RESULTS
  The primary combined endpoint occurred in 28 (23%) patients. Among patients with the primary endpoint, we found significantly higher platelet reactivity as evaluated by aggregation testing using AA and TRAP at discharge following the initial infarction compared to patients without the primary endpoint (area under aggregation curve 1137.4 ± 198.5 vs 833.5 ± 253.4; p = 0.013 for TRAP-induced aggregation, and 333.0 ± 263.8 vs 186.9 ± 105.4; p = 0.019 for AA-induced aggregation). We found no relationship between ADP- and collagen-induced aggregation at discharge and the occurrence of the primary endpoint.
  
  
  CONCLUSIONS
  Increased platelet reactivity evaluated by TRAP-induced aggregation is related to a higher rate of restenosis and recurrent ACS during a 6-month follow-up of diabetic STEMI patients treated with PCI.
authors.affiliation: Silesian Centre for Heart Diseases, Zabrze, Poland. wkuliczkowski@wp.pl
authors.forename: Wiktor
authors.initials: W
authors.lastname: Kuliczkowski
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Greif
authors.forename: Mariusz
authors.initials: M
authors.lastname: Gąsior
authors.forename: Jacek
authors.initials: J
authors.lastname: Kaczmarski
authors.forename: Damian
authors.initials: D
authors.lastname: Pres
authors.forename: Lech
authors.initials: L
authors.lastname: Poloński
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D001241:Aspirin / Q000494:pharmacology; D000077144:Clopidogrel; D023903:Coronary Restenosis / Q000188:drug therapy; D048909:Diabetes Complications / Q000628:therapy*; D004562:Electrocardiography; D005260:Female; D006801:Humans; D007249:Inflammation / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000628:therapy*; D015539:Platelet Activation / Q000187:drug effects* / Q000502:physiology; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000494:pharmacology; D016896:Treatment Outcome
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin