The contrast-devoid core of revascularized STEMI contains extensive erythrocyte extravasation with microvascular damage. Attenuating the reperfusion-induced haemorrhage may be a novel target in future adjunctive STEMI treatment.

This study shows an association between a proinflammatory monocyte response, characterized by high levels of classical monocytes, and severe myocardial injury and poor functional outcome after STEMI. Future studies are required to investigate the biologic nature of this association and therapeutic implications.

LV thrombus still occurs in a substantial amount of patients after PCI-treated MI, especially in larger infarct sizes. Routine TTE had a low sensitivity for the detection of LV thrombi and the interobserver variation of TTE was large.

Background-A total of40% to 50% of patients with ST-segment-elevation myocardial infarction develop microvascular injury (MVI) despite angiographically successful primary percutaneous coronary intervention (PCI). We investigated whether hyperemic microvascular resistance (HMR) immediately after angiographically successful PCI predicts MVI at cardiovascular magnetic resonance and reduced myocardial blood flow at positron emission tomography (PET). Methods and Results-Sixty patients with ST-segment-elevation myocardial infarction were included in this prospective study. Immediately after successful PCI, intracoronary pressure-flow measurements were performed and analyzed off-line to calculate HMR and indices derived from the pressure-velocity loops, including pressure at zero flow. Cardiovascular magnetic resonance and H 2 15O PET imaging were performed 4 to 6 days after PCI. Using cardiovascular magnetic resonance, MVI was defined as a subendocardial recess of myocardium with low signal intensity within a gadoliniumenhanced area. Myocardial perfusion was quantified using H 2 15 O PET. Reference HMR values were obtained in 16 stable patients undergoing coronary angiography. Complete data sets were available in 48 patients of which 24 developed MVI. Adequate pressure-velocity loops were obtained in 29 patients. HMR in the culprit artery in patients with MVI was significantly higher than in patients without MVI (MVI, 3.33±1.50 mm Hg/cm per second versus no MVI, 2.41±1.26 mm Hg/cm per second; P=0.03). MVI was associated with higher pressure at zero flow (45.68±13.16 versus 32.01±14.98 mm Hg; P=0.015). Multivariable analysis showed HMR to independently predict MVI (P=0.04). The optimal cutoff value for HMR was 2.5 mm Hg/cm per second. High HMR was associated with decreased myocardial blood flow on PET (myocardial perfusion reserve <2.0, 3.18±1.42 mm Hg/cm per second versus myocardial perfusion reserve ≥2.0, 2.24±1.19 mm Hg/cm per second; P=0.04). 1 CMRdefined MVI is assessed by T2-weighted imaging and late gadolinium enhancement. MVI refers to the areas within the infarcted myocardium where wash-in of contrast medium is severely impaired, as opposed to the wash-in (and delayed wash-out) of the contrast medium in the remaining areas of the infarct. It has been postulated that within these areas devoid of contrast, the microvasculature is obstructed, hence the term microvascular obstruction. Recently, however, it was shown that CMR-defined microvascular obstruction actually contains intramyocardial hemorrhage and complete microvascular destruction. Conclusions-Doppler2 Therefore, the term MVI seems to be more appropriate.The occurrence of MVI is linked to negative remodeling and left ventricular dysfunction, leading to decreased longterm survival, increased morbidity, and reduced quality of life as compared with patients with ST-segment-elevation myocardial infarction (STEMI) without MVI.3 MVI is related to ischemia-reperfusion damage and can potentially be reversed by pharmacological treatment in addition to the stand...