title: Influence of HbA1c levels on platelet function profiles associated with tight glycemic control in patients presenting with hyperglycemia and an acute coronary syndrome. A subanalysis of the CHIPS Study ("Control de HIperglucemia y Actividad Plaquetaria en Pacientes con Síndrome Coronario Agudo").
abstract: Patients with hyperglycemia, an acute coronary syndrome and poor glycemic control have increased platelet reactivity and poor prognosis. However, it is unclear the influence of a tight glycemic control on platelet reactivity in these patients. This is a subanalysis of the CHIPS study. This trial randomized patients with hyperglycemia to undergo an intensive glucose control (target blood glucose 80-120 mg/dL), or conventional glucose control (target blood glucose <180 mg/dL). We analyzed platelet function at discharge on the subgroup of patients with poor glycemic control, defined with admission levels of HbA1c higher than 6.5%. The primary endpoint was maximal platelet aggregation following stimuli with 20 μM ADP. We also measured aggregation following collagen, epinephrine, and thrombin receptor-activated peptide, as well as P2Y12 reactivity index and surface expression of glycoprotein IIb/IIIa and P-selectin. A total of 67 patients presented HbA1c ≥ 6.5% (37 intensive, 30 conventional), while 42 had HbA1c < 6.5% (20 intensive, 22 conventional). There were no differences in baseline characteristics between groups. At discharge, patients with HbA1c ≥6.5% had significantly reduced MPA with intensive glucose control compared with conventional control (46.1 ± 22.3 vs. 60.4 ± 20.0%; p = 0.004). Similar findings were shown with other measures of platelet function. However, glucose control strategy did not affect platelet function parameters in patients with HbA1c < 6.5%. Intensive glucose control in patients presenting with an acute coronary syndrome and hyperglycemia results in a reduction of platelet reactivity only in the presence of elevated HbA1c levels.
authors.affiliation: Cardiovascular Institute, San Carlos University Hospital, Profesor Martin Lagos s/n, 28040 Madrid, Spain. dvivas@secardiologia.es
authors.forename: David
authors.initials: D
authors.lastname: Vivas
authors.forename: Juan C
authors.initials: JC
authors.lastname: García-Rubira
authors.forename: Esther
authors.initials: E
authors.lastname: Bernardo
authors.forename: Dominick J
authors.initials: DJ
authors.lastname: Angiolillo
authors.forename: Patricia
authors.initials: P
authors.lastname: Martín
authors.forename: Alfonso
authors.initials: A
authors.lastname: Calle-Pascual
authors.forename: Iván
authors.initials: I
authors.lastname: Núñez-Gil
authors.forename: Carlos
authors.initials: C
authors.lastname: Macaya
authors.forename: Antonio
authors.initials: A
authors.lastname: Fernández-Ortiz
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology*; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D006442:Glycated Hemoglobin / Q000096:biosynthesis / Q000502:physiology*; D038321:Glycemic Index / Q000502:physiology*; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000175:diagnosis* / Q000453:epidemiology*; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000502:physiology; D010979:Platelet Function Tests / Q000379:methods; D011446:Prospective Studies
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D006442:Glycated Hemoglobin; C517652:hemoglobin A1c protein, human