title: Thrombocytopenia in patients with an acute coronary syndrome (from the Global Registry of Acute Coronary Events [GRACE]).
abstract: The incidence of thrombocytopenia after hospital admission, patient and treatment characteristics, and outcomes in patients enrolled in the prospective multinational GRACE were examined. Heparin (unfractionated or low molecular weight) and glycoprotein IIb/IIIa-inhibition can be associated with immune-mediated thrombocytopenia of clinical importance. The prevalence of thrombocytopenia in patients with acute coronary syndromes (ACSs) in general and specifically related to these therapies and associated outcomes have been studied little outside of clinical trials. Patients with an ACS were stratified into 4 groups of those with heparin-induced thrombocytopenia (HIT), those with glycoprotein IIb/IIIa-associated thrombocytopenia (GAT), those with other thrombocytopenia (not diagnosed as HIT or associated with glycoprotein inhibitors), and those with no thrombocytopenia. From June 2000 to September 2007, a total of 52,647 patients with an ACS and information for platelet count were enrolled in GRACE. Of these, 152 (0.3%) were reported to develop HIT, 324 (0.6%) developed GAT, and 368 (0.7%) developed other thrombocytopenia. Patients with HIT, GAT, or other thrombocytopenia were significantly more likely to die in the hospital versus those without these diseases (adjusted odds ratio [OR] 1.94, 95% confidence interval [CI] 1.07 to 3.53; adjusted OR 3.45, 95% CI 2.35 to 5.05; and adjusted OR 2.83, 95% CI 1.97 to 4.06, respectively). They were also more likely to experience major bleeding, (re)infarction, or stroke. In conclusion, in this large multinational registry, 1.6% of patients with ACS were reported to develop thrombocytopenia, with only 0.3% being HIT. Regardless of whether patients had clinically recognized HIT, GAT, or other thrombocytopenia, all 3 groups had significantly higher rates of major bleeding, recurrent infarction, stroke, and death.
authors.affiliation: University of Massachusetts Medical School, Worcester, Massachusetts, USA. gorej@ummhc.org
authors.forename: Joel M
authors.initials: JM
authors.lastname: Gore
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Spencer
authors.forename: Enrique P
authors.initials: EP
authors.lastname: Gurfinkel
authors.forename: José
authors.initials: J
authors.lastname: López-Sendón
authors.forename: Ph Gabriel
authors.initials: PG
authors.lastname: Steg
authors.forename: Christopher B
authors.initials: CB
authors.lastname: Granger
authors.forename: Gordon
authors.initials: G
authors.lastname: FitzGerald
authors.forename: Giancarlo
authors.initials: G
authors.lastname: Agnelli
mesh_terms: D054058:Acute Coronary Syndrome / Q000150:complications* / Q000188:drug therapy* / Q000401:mortality; D000368:Aged; D000369:Aged, 80 and over; D000925:Anticoagulants / Q000009:adverse effects*; D005260:Female; D006470:Hemorrhage / Q000209:etiology / Q000401:mortality; D006493:Heparin / Q000009:adverse effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D011446:Prospective Studies; D012008:Recurrence; D012042:Registries; D012306:Risk; D020521:Stroke / Q000209:etiology / Q000401:mortality; D013921:Thrombocytopenia / Q000139:chemically induced* / Q000401:mortality
chemical_list: D000925:Anticoagulants; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D006493:Heparin