title: Increased morning ADP-dependent platelet aggregation persists despite dual antiplatelet therapy in patients with first ST-segment elevation myocardial infarction: Preliminary report.
abstract: BACKGROUND
  Numerous trials have reported on the morning increase in the occurrence of myocardial infarction, stroke and sudden cardiac death. Similarly, enhanced morning platelet aggregation has been observed in healthy individuals and in subjects with coronary artery disease without adequate antiplatelet treatment. The purpose of the study was to assess circadian variation in platelet aggregation in patients with first ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary interventions (pPCI) and dual antiplatelet therapy.
  
  
  METHODS
  Fifteen consecutive patients (12 men and 3 women) were prospectively recruited into the study. Blood samples were collected at 6.00 a.m., 10.00 a.m., 2.00 p.m. and 7.00 p.m. on the third day of hospitalization. Aggregation in response to arachidonic acid and adenosine diphosphate (ADP) was assessed in the whole blood on a new generation impedance aggregometer.
  
  
  RESULTS
  A morning increase of 75% in ADP-dependent platelet aggregation was noted in the study population (p < 0.04). In contrast, we failed to show any significant diurnal variation in arachidonic acid-mediated platelet aggregation. The magnitude of the morning surge in platelet aggregation after ADP stimulation did not correlate with its baseline level.
  
  
  CONCLUSIONS
  Increased morning ADP-dependent platelet aggregation persists despite dual antiplatelet therapy in patients with first STEMI undergoing pPCI. The clinical significance of this finding remains to be demonstrated.
authors.affiliation: Department of Cardiology and Internal Medicine, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, Poland. marekkozinski@wp.pl
authors.forename: Marek
authors.initials: M
authors.lastname: Koziński
authors.forename: Liliana
authors.initials: L
authors.lastname: Bielis
authors.forename: Joanna
authors.initials: J
authors.lastname: Wiśniewska-Szmyt
authors.forename: Adam
authors.initials: A
authors.lastname: Sukiennik
authors.forename: Zofia
authors.initials: Z
authors.lastname: Grabczewska
authors.forename: Iwona
authors.initials: I
authors.lastname: Swiatkiewicz
authors.forename: Michał
authors.initials: M
authors.lastname: Ziołkowski
authors.forename: Danuta
authors.initials: D
authors.lastname: Rość
authors.forename: Jacek
authors.initials: J
authors.lastname: Kubica
mesh_terms: D000077284:Abciximab; D000368:Aged; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000627:therapeutic use; D000925:Anticoagulants / Q000008:administration & dosage / Q000627:therapeutic use; D002940:Circadian Rhythm / Q000502:physiology*; D000077144:Clopidogrel; D004305:Dose-Response Relationship, Drug; D004333:Drug Administration Routes; D004359:Drug Therapy, Combination; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006493:Heparin / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000008:administration & dosage / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D006493:Heparin; D000077144:Clopidogrel; D013988:Ticlopidine; D000077284:Abciximab