Potential mechanism of acute stent thrombosis with bivalirudin following percutaneous coronary intervention in acute coronary syndromes
Randomized controlled trial published in International journal of cardiology (2016)
Abstract
BACKGROUND: Clinical trials have demonstrated an excess of acute stent thrombosis (AST) in acute coronary syndromes patients (ACS) undergoing percutaneous coronary intervention (PCI) with bivalirudin compared to heparin. We aimed to investigate the potential mechanisms responsible for thrombus formation under bivalirudin. METHODS: We compared heparin and bivalirudin during PCI for ACS in a prospective monocentre randomized study. Twenty patients were included after coronary angiography and received a loading dose (LD) of 180mg of ticagrelor at the time of PCI. They were randomly assigned to heparin (70UI/kg) intra-venous (IV) bolus or bivalirudin IV bolus of 0.75mg/kg followed by an infusion of 1.75mg/kg/h until the end of the PCI. The VASP index and thrombin generation test were used to assess the course of platelet reactivity (PR) and thrombin generation. RESULTS: Thrombin generation and PR were identical in both groups at baseline. There was no difference in the course of PR following the LD over time. An optimal PR inhibition was reached 4h after the LD of ticagrelor. Heparin and bivalirudin infusion effectively inhibited thrombin generation during PCI. However, 4h after the end of bivalirudin infusion, thrombin generation had returned to its baseline value whereas in the heparin group it remained significantly inhibited compared to baseline and to the bivalirudin group 4h after the end of the infusion (p<0.01 and p<0.02 respectively). CONCLUSIONS: The present study suggests that the short half-life of bivalirudin and the quick restoration of thrombin activity at a time when optimal PR is not reached may be responsible for acute stent thrombosis. Clinicaltrial.gov: NCT02428725.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Resumen
Clinical trials have demonstrated an excess of acute stent thrombosis (AST) in acute coronary syndromes patients (ACS) undergoing percutaneous coronary intervention (PCI) with bivalirudin compared to heparin.
Por qué esto importa para la hirudoterapia
Este pequeño estudio prospectivo aleatorio (20 pacientes con ACS sometidos a PCI sobre ticagrelor) comparó la bivalirudina con la heparina para investigar por qué la bivalirudina se ha vinculado a una trombosis de stent aguda excesiva; el resumen indica que ambos fármacos suprimieron efectivamente la generación de trombina durante la PCI, pero cuatro horas después del final de la infusión de bivalirudina la generación de trombina había regresado al valor basal mientras que permanecía significativamente inhibida en el grupo de heparina, lo que sugiere que la vida media corta de la bivalirudina restaura la actividad de la trombina antes de alcanzar la inhibición óptima de la plaqueta. Esto es relevante para la ASH porque la bivalirudina es un análogo sintético de la hirudina, el inhibidor directo de la trombina prototípico aislado de la medusa medicinal, por lo que su farmacodinámica en la práctica clínica forma parte de la historia de la evidencia clínica de la línea DTI derivada de la medusa. Nota: este es un ensayo aleatorio único y mecanicista con solo 20 pacientes que examina un sustituto (generación de trombina) en lugar de resultados clínicos, por lo que el mecanismo propuesto es preliminar y generador de hipótesis, no una explicación definitiva.
Citación
Potential mechanism of acute stent thrombosis with bivalirudin following percutaneous coronary intervention in acute coronary syndromes
Laine M et al. · International journal of cardiology, 2016
Contexto clínico relacionado
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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: June 18, 2026