The present large pooled analysis of randomized trials suggests that thrombectomy (in particular manual thrombectomy) significantly improves the clinical outcome in patients with STEMI undergoing mechanical reperfusion and that its effect may be additional to that of IIb/IIIa-inhibitors.

Background/Objectives. A rapid diagnosis of STsegment elevation myocardial infarction (STEMI)is mandatory for optimal treatment. However, a small proportion of patients with suspected STEMI suffer from other conditions. Although case reports have described these conditions, a contemporary systematic analysis is lacking. We report the incidence, clinical characteristics and outcome of patients with suspected STEMI referred for primary percutaneous coronary intervention (PCI) with a final diagnosis other than STEMI.

We thank Niccoli et al for their letter, which interestingly suggested that intracoronary administration of abciximab may exert its action in patients with ST-segment elevation myocardial infarction through facilitation of reversible no reflow. Our study was designed to detect a difference in electrocardiographic and angiographic measures of immediate myocardial reperfusion after primary percutaneous coronary intervention, markers that are frequently used in medium-sized randomized studies and show strong correlation with clinical outcome. 1,2 In this regard, we did not include recovery of myocardial perfusion at a later time point as a prespecified end point. It is not our center's routine clinical practice to reevaluate the initial angiographic result and recovery of myocardial perfusion in the infarct-related artery before discharge, either by repeat angiography or by cardiac magnetic resonance imaging. Because the infarct-related artery may have been filmed in additional revascularization procedures only in highly selected cases, we believe that analysis of this small, nonprespecified subset of patients would not produce meaningful results. In fact, an early study has indicated that intracoronary administration of abciximab significantly reduced the primary end point of microvascular obstruction on cardiac magnetic resonance 2 days after primary percutaneous coronary intervention compared with intravenous administration. 3 Therefore, we agree with Niccoli et al that facilitation of reversible no reflow is one of the plausible mechanisms of action of intracoronary abciximab, a hypothesis that may be further tested in ongoing randomized studies on intracoronary versus intravenous abciximab administration that include cardiac magnetic resonance end points. 4 Rationale and design of the INFUSE-AMI study: a 2ϫ2 factorial, randomized, multicenter, single-blind evaluation of intracoronary abciximab infusion and aspiration thrombectomy in patients undergoing percutaneous coronary intervention for anterior ST-segment elevation myocardial infarction.

BackgroundEarly detection of acute myocardial infarction (AMI) using cardiac biomarkers of myocardial necrosis remains limited since these biomarkers do not rise within the first hours from onset of AMI. We aimed to compare the temporal release pattern of the C-terminal portion of provasopressin (copeptin) with conventional cardiac biomarkers, including creatine kinase isoenzyme (CK-MB), cardiac troponin T (cTnT), and high-sensitivity cTnT (hs-cTnT), in patients with ST-elevation AMI.MethodsWe included 145 patients undergoing successful primary percutaneous coronary intervention (PCI) for a first ST-elevation AMI presenting within 12 h of symptom onset. Blood samples were taken on admission and at four time points within the first 24 h after PCI.ResultsIn contrast to all other markers, copeptin levels were already elevated on admission and were higher with a shorter time from symptom onset to reperfusion and lower systolic blood pressure. Copeptin levels peaked immediately after symptom onset at a maximum of 249 pmol/L and normalized within 10 h. In contrast, CK-MB, cTnT, and hs-cTnT peaked after 14 h from symptom onset at a maximum of 275 U/L, 5.75 μg/L, and 4.16 μg/L, respectively, and decreased more gradually.ConclusionsCopeptin has a distinct release pattern in patients with ST-elevation AMI, peaking within the first hour after symptom onset before conventional cardiac biomarkers and falling to normal ranges within the first day. Further studies are required to determine the exact role of copeptin in AMI suspects presenting within the first hours after symptom onset.