Beyond TIMI III flow.

Abstract

The Western Washington Intracoronary Streptokinase randomized trial1 first demonstrated that intracoronary thrombolytic therapy improved survival for patients presenting within 12 hours of symptom onset of acute myocardial infarction (MI). Perhaps equally important, this invasive study demonstrated that in-hospital and long-term survival was greatly improved in patients with patent infarct-related arteries.2 These observations ushered in the modern era of reperfusion therapy, and they also firmly established the concept that achieving arterial patency was the predominant mechanism for the prognostic benefit of thrombolytic agents. Numerous trials since then have validated this open-artery hypothesis.3 4 5 In the early 1990s, Ross et al6 definitively established the relationship between prompt reinstitution of flow, improved myocardial salvage, and survival. Anderson et al7 clearly demonstrated that antegrade flow, as defined by the Thrombolysis in Myocardial Infarction (TIMI) criteria, can differentiate different levels of antegrade flow, with different prognostic implications. Although TIMI flow grades seem to segregate effective from ineffective flow, this analysis is only a qualitative measure that can be subject to bias and interlaboratory variability. Gibson et al8 further refined angiographic flow quantitation using corrected TIMI frame counts. This method of analysis quantitates angiographic contrast velocity measures and decreases variability. Currently, arterial patency is the gold standard for assessing the efficacy of different reperfusion protocols. Refinements in the quantitation of degrees of arterial patency have led to improvements in the prognostic value of this measure. It has, however, become increasingly apparent that contrast velocity alone does not adequately define the level of microvascular perfusion or predict the extent of return of myocardial function after successful reperfusion therapy. Coronary angiography remains a crude means to assess myocardial perfusion after infarction, and it is clear that infarct artery patency is not equivalent to the reestablishment of myocardial tissue perfusion. With the …