title: Platelet reactivity and endothelial function in children of patients with early acute myocardial infarction.
abstract: OBJECTIVE
  To assess whether platelet reactivity is increased in offspring of patients with early acute myocardial infarction (AMI) and its possible relation with endothelial dysfunction.
  
  
  RESULTS
  We studied 23 healthy children (15±3 years, 13 males) of patients with early AMI (≤50 years old; Group 1) and 21 healthy children of healthy subjects without any history of cardiovascular disease (14±3 years, 10 males; Group 2). Platelet reactivity was assessed by flow cytometry as the increase in monocyte-platelet aggregates (MPA) and CD41 and PAC-1 platelet expression in response to exercise stress test (EST), adenosine diphosphate (ADP) stimulation (10(-7) M), or both. Endothelial function was assessed by measuring brachial artery dilation during post-ischaemic forearm hyperaemia [flow-mediated dilation (FMD)]. Both EST and ADP induced a higher percentage increase in platelet receptor expression in Group 1, compared with Group 2, with the most significant difference being shown for the response to the combined stimuli (e.g. MPA, 23.1±12 vs. 5.63±8%, P<0.001; platelet PAC-1, 57.7±47 vs. 13.2±7%, P<0.001). Compared with Group 2, Group 1 children showed lower FMD (10.7±3.1 vs. 8.0±2.9%, respectively; P=0.007). However, no significant association was found between FMD and platelet reactivity.
  
  
  CONCLUSIONS
  Our results show increased platelet reactivity in children of patients with early AMI; the finding was not significantly correlated with endothelial dysfunction, suggesting that other mechanisms are mainly involved in the enhanced platelet response to agonistic stimuli.
authors.affiliation: Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Largo A. Gemelli, 8, 00168 Roma, Italy. g.a.lanza@inwind.it
authors.forename: Gaetano A
authors.initials: GA
authors.lastname: Lanza
authors.forename: Giancarla
authors.initials: G
authors.lastname: Scalone
authors.forename: Lucy
authors.initials: L
authors.lastname: Barone
authors.forename: Fabio
authors.initials: F
authors.lastname: Infusino
authors.forename: Ilaria
authors.initials: I
authors.lastname: Coviello
authors.forename: Antonio
authors.initials: A
authors.lastname: Di Monaco
authors.forename: Angelica
authors.initials: A
authors.lastname: Delogu
authors.forename: Irma
authors.initials: I
authors.lastname: Battipaglia
authors.forename: Alessia
authors.initials: A
authors.lastname: De Nisco
authors.forename: Alfonso
authors.initials: A
authors.lastname: Sestito
authors.forename: Costantino
authors.initials: C
authors.lastname: Romagnoli
authors.forename: Filippo
authors.initials: F
authors.lastname: Crea
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000293:Adolescent; D000328:Adult; D000704:Analysis of Variance; D058846:Antibodies, Monoclonal, Murine-Derived / Q000378:metabolism; D002648:Child; D004730:Endothelium, Vascular / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000502:physiology; D009203:Myocardial Infarction / Q000097:blood* / Q000235:genetics; D010375:Pedigree; D010974:Platelet Aggregation / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000378:metabolism; D040201:Platelet Membrane Glycoprotein IIb / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D014664:Vasodilation / Q000502:physiology
chemical_list: D058846:Antibodies, Monoclonal, Murine-Derived; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D040201:Platelet Membrane Glycoprotein IIb; D019010:Vascular Cell Adhesion Molecule-1; D000244:Adenosine Diphosphate