TY - JOUR
T1 - Importance of reperfusion on thromboxane A2 metabolite excretion after thrombolysis
AU - Rebuzzi, Antonio Giuseppe
AU - Natale, Andrea
AU - Bianchi, Claudio
AU - Albanese, Santino
AU - Lanza, Gaetano Antonio
AU - Coppola, Elda
AU - Ciabattoni, Giovanni
PY - 1992
Y1 - 1992
N2 - Fibrinolytic therapy is a major advance in the treatment of coronary artery disease. A marked elevation in plasma and urinary metabolites of thromboxane A2 (TXA2) after administration of thrombolytic therapy has been observed and has been related to a direct effect of thrombolytic drugs on platelets. To test this hypothesis we evaluated the 11-dehydrothromboxane B2 (11-d-TXB2) level, as an index of platelet activation, in 20 healthy subjects and in 30 patients with acute myocardial infarction (AMI). Patients with infarction received streptokinase (n = 8), recombinant tissue-type plasminogen activator (rt-PA) (n = 8), or thrombolytic therapy preceded by acetylsalicylic acid (n = 7) or were treated without thrombolytic therapy (n = 7). The urinary 11-d-TXB2 level in healthy control subjects was 327 ± 126 pg/mg creatinine. A significant increase was observed in patients with AMI with no difference between those who received no thrombolytic therapy (673 ± 283 pg/mg creatinine in the first 12 hours) and those who received streptokinase (833 ± 613 pg/mg creatinine) or rt-PA (836 ± 653 pg/mg creatinine). Patients pretreated with acetylsalicylic acid had urinary 11-d-TXB2 values ranging between 361 and 155 pg/mg creatinine. A significant difference in 11-d-TXB2 values was observed only when patients who were reperfused were separated from those who remained occluded according to angiographic criteria (1085 ± 498 vs 391 ± 227 pg/mg creatinine in the first 12 hours, p <0.001). We conclude that reperfusion and not thrombolytic agents per se appears to be the factor that induces platelet activation and consequently facilitates reocclusion.
AB - Fibrinolytic therapy is a major advance in the treatment of coronary artery disease. A marked elevation in plasma and urinary metabolites of thromboxane A2 (TXA2) after administration of thrombolytic therapy has been observed and has been related to a direct effect of thrombolytic drugs on platelets. To test this hypothesis we evaluated the 11-dehydrothromboxane B2 (11-d-TXB2) level, as an index of platelet activation, in 20 healthy subjects and in 30 patients with acute myocardial infarction (AMI). Patients with infarction received streptokinase (n = 8), recombinant tissue-type plasminogen activator (rt-PA) (n = 8), or thrombolytic therapy preceded by acetylsalicylic acid (n = 7) or were treated without thrombolytic therapy (n = 7). The urinary 11-d-TXB2 level in healthy control subjects was 327 ± 126 pg/mg creatinine. A significant increase was observed in patients with AMI with no difference between those who received no thrombolytic therapy (673 ± 283 pg/mg creatinine in the first 12 hours) and those who received streptokinase (833 ± 613 pg/mg creatinine) or rt-PA (836 ± 653 pg/mg creatinine). Patients pretreated with acetylsalicylic acid had urinary 11-d-TXB2 values ranging between 361 and 155 pg/mg creatinine. A significant difference in 11-d-TXB2 values was observed only when patients who were reperfused were separated from those who remained occluded according to angiographic criteria (1085 ± 498 vs 391 ± 227 pg/mg creatinine in the first 12 hours, p <0.001). We conclude that reperfusion and not thrombolytic agents per se appears to be the factor that induces platelet activation and consequently facilitates reocclusion.
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U2 - 10.1016/0002-8703(92)90491-D
DO - 10.1016/0002-8703(92)90491-D
M3 - Article
C2 - 1539506
AN - SCOPUS:0026553533
VL - 123
SP - 560
EP - 566
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
IS - 3
ER -