Study protocol All patients underwent cardiac biomarkers (creatine kinase-MB, troponin I) determinations and 12-lead ECG examinations at initial presentation to the emergency department and then followed-up at 6 and 24 hours LDN-193189 in vivo afterward. The serum level of troponin I was measured by the chemiluminescent assay (CLIA assay), and a value of troponin I >1.5 ng/mL was considered abnormal. The presence of significant ECG change was defined as an ST-segment depression >0.05 mV. After the initial clinical evaluation, MCE was performed and 740 MBq of technetium-99m sestamibi was administered intravenously in the emergency room within 6 hours of

presentation. As described previously,11) single-photon emission computed Inhibitors,research,lifescience,medical tomographic (SPECT) MPI acquisition occurred within 6 hours of tracer injection. The MCE and MPI results were not reported to the attending physicians, who made disposition decisions based on routine Inhibitors,research,lifescience,medical assessment. A diagnosis of acute myocardial infarction (AMI) was confirmed by the presence of more than two of the following criteria: chest

pain consistent with myocardial ischemia, Inhibitors,research,lifescience,medical development of Q wave and an increase of serum cardiac biomarkers (creatine kinase-MB >10 IU/L, 2 times the upper limit of the normal value).12),13) The definition of acute coronary syndrome was based on the development of AMI or documentation of significant coronary artery stenosis that required urgent revascularization Myocardial contrast echocardiography To evaluate Inhibitors,research,lifescience,medical regional wall motion abnormalities and myocardial perfusion, intravenous MCE was performed in apical 4-, 3-, and 2-chamber views with triggered replenishment imaging using Sonos 5500 instrument (Philips Medical Imaging, Andover, Massachusetts, USA). Intermittent harmonic power Doppler imaging was performed with a broadband harmonic transducer that transmitted and received at mean frequencies

of 1.8 and 3.6 MHz, respectively. Emission power was set at the highest level (mechanical index 1.3 to 1.6). Images were obtained by triggering at end-systole. In an attempt to differentiate true perfusion from motion artifact, a dual-frame imaging technique was Inhibitors,research,lifescience,medical used. The 2 frames were displayed side by side. One represented the perfusion frame and the other represented the post-destruction frame which was obtained approximately PD184352 (CI-1040) 50 milliseconds later. In the cases of tissue motion artifact, the post-destruction frame showed nearly the same signal intensity as the actual perfusion frame and the motion artifact could easily be recognized. The contrast agent, perfluorocarbon-exposed sonicated dextrose albumin (PESDA),14) was intravenously administered as a continuous infusion of 0.05 mL/kg in 30 mL of normal saline at a rate of 0.8 to 3 mL/min. The Doppler gain setting and infusion rate of a contrast agent were adjusted to maximize the left ventricular cavity signal without causing attenuation artifacts in the destruction-phase image.