2003, Número 1
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Arch Cardiol Mex 2003; 73 (1)
Estrategias para mejorar la reperfusión con terapia fibrinolítica en infarto con elevación del ST-T
Jerjes-Sánchez C, Sosa del Angel E, García SA, Reyes CE, Garza RA
Idioma: Español
Referencias bibliográficas: 80
Paginas: 46-58
Archivo PDF: 126.88 Kb.
RESUMEN
Las estrategias de reperfusión en la fase temprana del infarto con elevación
del ST-T tienen como principal objetivo restituir y mantener la perfusión tisular.
La terapia fibrinolítica puede considerarse como el tratamiento estándar por su
accesibilidad y efectividad para disminuir daño miocárdico y mortalidad. La
principal imperfección de esta estrategia de reperfusión radica en el porcentaje
no despreciable de fracaso terapéutico y reoclusión por fenómenos de resistencia
y retrombosis. La terapia fibrinolítica asociada al ácido acetilsalicílico,
puede considerarse como el avance más importante en el tratamiento del infarto
con elevación del ST-T. En el sitio del daño vascular, la trombosis inducida por
trombina y agregación plaquetaria son los factores más importantes en la
fisiopatología de los SCA y el principal mecanismo que puede limitar la
efectividad de la terapia fibrinolítica. El conocimiento actual de la
fisiopatología subyacente a la trombosis coronaria sugiere que la terapia
fibrinolítica puede fracasar para inducir lisis óptima del trombo y refuerza
el raciocinio para la combinación de estrategias antitrombóticas y de reperfusión.
Podría mejorar su efectividad, un tratamiento adjunto antiplaquetario y
antitrombínico intenso y moderno, que a través de diferentes mecanismos
modificaría los principales componentes del trombo coronario. El propósito
de este artículo es revisar y discutir los mecanismos de resistencia a la
terapia fibrinolítica, las estrategias modernas para mejorar la perfusión que
incluyen dosis aceleradas de fibrinolíticos, fibrinólisis facilitada,
experiencia con heparina de bajo peso molecular y el posible papel
de los nuevos antitrombóticos que han demostrado efectividad en el tratamiento
de los síndromes coronarios agudos sin elevación del ST-T.
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