ABSTRACT
Treatment for ST- elevation acute coronary syndromes (acute myocardial infarction: AMI) has advanced rapidly in the last decade with major improvements in early fibrinolytic therapy (FT), primary percutaneous interventions (PCI) with the aid of platelet glycoprotein IIb/IIIa inhibitors. Recent interest has shifted from infarct related artery (IRA) patency to microvascular perfusion in the evaluation of patients with AMI. It is well known that establishing epicardial patency after AMI (TIMI 3 E) is not synonymous with tissue-level perfusion (TIMI 4M). Microvascular dysfunction due to the roles of platelet and inflammatory mediators in the no-reflow phenomenon occurs in a substantial proportion of patients despite thrombolytic therapy or PCI procedures. Techniques are now available that measure real tissue-level perfusion and also therapy is directed to optimize myocardial perfusion in patients with AMI. Despite advances, contemporary FT strategies with the combination of platelet glycoprotein IIb/IIIa inhibitors restore normal coronary flow (TIMI 3) in the IRA in only 50-75% and PCI achieves TIMI 3 flow rates in 90-95%, but only with modest reductions in mortality, but with significant reductions in rethrombosis of the IRA or stents, reinfarctions and in some patients with benefits in ventricular dysfunction. Therefore moving beyond the importance of TIMI 3 flow, the TIMI 4 flow, or improving tissue-level perfusion in the setting of AMI seems to be the paradigm for the treatment of ST-elevation acute coronary syndromes.
Subject(s)
Myocardial Ischemia/physiopathology , Myocardial Ischemia/surgery , Myocardial Reperfusion , Acute Disease , Electrocardiography , Humans , Myocardial Infarction/diagnosis , Myocardial Infarction/immunology , Myocardial Infarction/physiopathology , Myocardial Infarction/surgery , Myocardial Infarction/therapy , Myocardial Ischemia/classification , Myocardial Ischemia/complications , Myocardial Ischemia/diagnosis , Myocardial Ischemia/immunology , Myocardial Ischemia/therapy , SyndromeABSTRACT
En el tratamiento de los Síndromes Coronarios Agudos con elevación del segmento ST se ha avanzado en la última década de manera favorable en relación a la terapia fibrinolítica (TF), en los procedimientos coronarios intervencionistas (PCI) y con la utilización concomitante de los inhibidores de los receptores plaquetarios IIb/IIIa (IRP). El interés actual en relación al objetivo ha alcanzar en la reperfusión del infarto agudo del miocardio (IAM) ha girado de la arteria responsable del infarto (ARI) a obtener perfusión microvascular-tisular óptima. Se ha puntualizado que el establecer la mejor permeabilidad de la ARI (TIMI 3E) no es sinónimo de que también se ha obtenido en el tejido miocárdico (TIMI 4 M). Sabemos que puede existir disfunción microvascular producto de la microembolización plaquetaria o la ocasionada por la propia reperfusión, misma que esta ligada a los mediadores inflamatorios lo que da origen al "fenómeno de no- flujo", anomalía todas que ocurren en un número no despreciable de enfermos a pesar de haberse obtenido TIMI 3E. Hoy día hay técnicas y tratamientos que van encaminados a identificar y resolver estas anomalías con el fin de mejorar la perfusión microvascular en el IAM. A pesar de existir progresos en las estrategias de reperfusión en el IAM particularmente con el empleo adjunto de IRP y con la TF y que se obtienen en la ARI flujos TIMI 3E en el 50-75% de las veces y con los PCI en el 90-95%, no se han alcanzado reducciones significativas en la mortalidad, mas sí en la frecuencia de la retrombosis de la ARI, de los stents, de reinfartos y en algunos sujetos se observa mejoría de la función ventricular. Por lo tanto, hoy día estamos conscientes de lo que representa obtener perfusión óptima microvascular en el escenario del IAM. El gran paradigma es saber por lo tanto que hay más allá del TIMI 3E y si se alcanzo o no flujo TIMI 4 o miocárdico.
Treatment for ST- elevation acute coronary syndromes (acute myocardial infarction: AMI) has advanced rapidly in the last decade with major improvements in early fibrinolytic therapy (FT), primary percutaneous interventions (PCI) with the aid of platelet glycoprotein IIb/IIIa inhibitors. Recent interest has shifted from infarct related artery (IRA) patency to microvascular perfusion in the evaluation of patients with AMI. It is well known that establishing epicardial patency after AMI (TIMI 3 E) is not synonymus with tissue-level perfusion (TIMI 4M). Microvascular dysfunction due to the roles of platelet and inflammatory mediators in the no-reflow phenomenon occurs in a substancial proportion of patients despite thrombolytic therapy or PCI procedures. Techniques are now available that measure real tissue-level perfusion and also therapy is directed to optimize myocardial perfusion in patients with AMI. Despite advances, contemporary FT strategies with the combination of platelet glycoprotein IIb/IIIa inhibitors restore normal coronary flow (TIMI 3) in the IRA in only 50-75% and PCI achieves TIMI 3 flow rates in 90-95%, but only with modest reductions in mortality, but with significant reductions in rethrombosis of the IRA or stents, reinfarctions and in some patients with benefits in ventricular dysfunction. Therefore moving beyond the importance of TIMI 3 flow, the TIMI 4 flow, or improving tissue-level perfusion in the setting of AMI seems to be the paradigm for the treatment of ST-elevation acute coronary syndromes.