Usually the success of reperfusion after primary PCI is easily visualized on coronary angiography. However, a substantial proportion of patients deemed to have successful reperfusion have persistent compromise of myocardial blood flow owing to microvascular obstruction (15,16). Several methods may be used for identification of microvascular obstruction, including myocardial contrast echocardiography, ST-segment resolution, magnetic resonance tomography (MRT), intracoronary Doppler flow measurement, and coronary angiography using the myocardial blush grade. The utilization of cardiac markers for this purpose is relatively novel and the rationale for their use is largely based on findings from fibrinolytic trials.
Successful reperfusion of the IRA is associated with a rise in blood concentrations ("washout") that is more brisk after mechanical reperfusion than after fibrinolytic therapy (17). Because this washout phenomenon reflects both reperfusion at the myocardial tissue level and epicardial blood flow, it is tempting to speculate that marker kinetics might be helpful for assessment of microvascular reperfusion.
Accordingly, Frostfeldt et al. (18) found a significantly higher relative increase in myoglobin concentration and a trend toward higher rates of complete resolution (>70%) of ST-segments in patients who tested negative for cardiac troponin T (cTnT) on admission, suggesting normal microvascular reperfusion. Lehrke et al. (19) demonstrated that abcixi-mab administered during primary PCI improved the early washout of cTnT in patients who tested positive for troponin on admission, in patients with diabetes, and in older patients, suggesting a higher propensity for impaired microvascular perfusion in some subsets of patients. A close association between baseline elevation in troponin and abnormal tissue-level reperfusion was also shown in patients with an acute coronary syndrome (ACS) without ST-elevation (20). Thus, there is increasing evidence that elevations in troponin resulting from embolization of platelet microaggregates may not only be a surrogate for the presence of unstable plaque but also for microvascular obstruction independent of recanal-ization of the occluded IRA.
Kurowski et al. (21) reported higher mortality rates for patients with elevated cTnT levels on admission, despite restoration of TIMI 3 grade flow (Fig. 1). Troponin T remained independently predictive even after adjustment for longer time delays from the onset of symptoms to admission and for infarct location. These findings may relate to the adverse
Time after AMI (Days)
Fig. 1. Survival plot showing higher short- and long-term mortality (log rankp = 0.0022) associated with elevated troponin T on admission despite subsequent successful primary PCI. (Adapted from ref. 21.)
prognostic impact that has been attributed to microvascular dysfunction (15,16). It follows that less efficient marker washout may identify those likely to benefit from glycopro-tein (Gp) IIb/IIIa inhibition. In randomized trials, however, GpIIb/IIIa inhibitors did not improve prognosis, suggesting a need for individualized therapy (22). Selected clinical variables, including measurement of cardiac troponins on admission or infarct scores, may prove more useful for identification of patients who will benefit from adjunctive administration of GpIIb/IIIa inhibitors during direct PCI. Further studies are necessary to prove whether troponin testing could also be helpful to monitor the effects of GpIIb/IIIa inhibitors or other drugs on microvascular reperfusion.
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