Vol 60, No 5 (2004)
Other
Published online: 2005-12-12
Submitted: 2012-12-28
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Platelet inhibition by increased tirofiban dosing during primary coronary angioplasty for ST elevation myocardial infarction

Paweł Kralisz, Sławomir Dobrzycki, Konrad Nowak, Wacław Kochman, Hanna Gajewska-Bachórzewska, Kamil Gugała, Grzegorz Mężyński, Przemysław Prokopczuk, Jerzy Żuk, Janusz Korecki, Bogusław Poniatowski, Włodzimierz Musiał
Kardiol Pol 2004;60(5):464-467.
Vol 60, No 5 (2004)
Other
Published online: 2005-12-12
Submitted: 2012-12-28

Abstract

Background: Platelet receptor IIb/IIIa inhibition during percutaneous coronary interventions (PCI) decreases incidence of major adverse cardiac events (MACE). These effects directly result from the level of platelet inhibition. Due to existing data indicating that standard dosing of tirofiban is insufficient for optimal platelet inhibition, we proposed a novel, experimental dosing.
Aim: In this study we assessed, with the use of Ultegra Rapid Platelet Function Assay (RFPA), the level of platelet inhibition with increased tirofiban dosing during primary PCI for ST elevation myocardial infarction (STEMI).
Methods: Twenty eight patients (22 males, 6 females, mean age 63 years, range 32-78 years) with STEMI were included into the study. All patients received 300 mg of aspirin, iv. heparin in a dose of 10 000 IU, which was followed by platelet receptor GP IIb/IIIa inhibitor tirofiban - 10 µg/kg iv bolus, 0.4 µg/kg/min for 30 min and infusion 0.1 µg/kg/min continued for 12-24 h. Platelet function was assessed with RFPA before tirofiban administration and after 10, 30, 90 minutes as well as 8 hours from the initial dose of tirofiban. Baseline fibrinogen binding to platelet receptor IIb/IIIa was defined as PAU (platelet aggregation unit) and the effects of tirofiban on platelets were expressed as a percentage of platelet inhibition.
Results: During in-hospital stay, no deaths, re-infarction nor recurrences of ischaemia requiring intervention were noted. The mean total duration of tirofiban administration was 21 hours. Thrombocytopenia was not observed in any patient. Bleeding complications occurred in 5 (17.9%) patients. Blood transfusion was required in three patients. The percentages of platelet inhibition measured at the pre-specified time-points were 95%, 94%, 91% and 87%, respectively. In 32% of patients an inhibition of platelet exceeding 95%, measured 10 minutes from the onset of tirofiban infusion, was not achieved. At the same time, platelet inhibition

Abstract

Background: Platelet receptor IIb/IIIa inhibition during percutaneous coronary interventions (PCI) decreases incidence of major adverse cardiac events (MACE). These effects directly result from the level of platelet inhibition. Due to existing data indicating that standard dosing of tirofiban is insufficient for optimal platelet inhibition, we proposed a novel, experimental dosing.
Aim: In this study we assessed, with the use of Ultegra Rapid Platelet Function Assay (RFPA), the level of platelet inhibition with increased tirofiban dosing during primary PCI for ST elevation myocardial infarction (STEMI).
Methods: Twenty eight patients (22 males, 6 females, mean age 63 years, range 32-78 years) with STEMI were included into the study. All patients received 300 mg of aspirin, iv. heparin in a dose of 10 000 IU, which was followed by platelet receptor GP IIb/IIIa inhibitor tirofiban - 10 µg/kg iv bolus, 0.4 µg/kg/min for 30 min and infusion 0.1 µg/kg/min continued for 12-24 h. Platelet function was assessed with RFPA before tirofiban administration and after 10, 30, 90 minutes as well as 8 hours from the initial dose of tirofiban. Baseline fibrinogen binding to platelet receptor IIb/IIIa was defined as PAU (platelet aggregation unit) and the effects of tirofiban on platelets were expressed as a percentage of platelet inhibition.
Results: During in-hospital stay, no deaths, re-infarction nor recurrences of ischaemia requiring intervention were noted. The mean total duration of tirofiban administration was 21 hours. Thrombocytopenia was not observed in any patient. Bleeding complications occurred in 5 (17.9%) patients. Blood transfusion was required in three patients. The percentages of platelet inhibition measured at the pre-specified time-points were 95%, 94%, 91% and 87%, respectively. In 32% of patients an inhibition of platelet exceeding 95%, measured 10 minutes from the onset of tirofiban infusion, was not achieved. At the same time, platelet inhibition
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Keywords

tirofiban - platelet inhibition - primary angioplasty - acute myocardial infarction

About this article
Title

Platelet inhibition by increased tirofiban dosing during primary coronary angioplasty for ST elevation myocardial infarction

Journal

Kardiologia Polska (Polish Heart Journal)

Issue

Vol 60, No 5 (2004)

Pages

464-467

Published online

2005-12-12

Bibliographic record

Kardiol Pol 2004;60(5):464-467.

Keywords

tirofiban - platelet inhibition - primary angioplasty - acute myocardial infarction

Authors

Paweł Kralisz
Sławomir Dobrzycki
Konrad Nowak
Wacław Kochman
Hanna Gajewska-Bachórzewska
Kamil Gugała
Grzegorz Mężyński
Przemysław Prokopczuk
Jerzy Żuk
Janusz Korecki
Bogusław Poniatowski
Włodzimierz Musiał

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