Figure 1: Day 2 MPO Inhibition With PF-1355

(A) Mice with permanent coronary ligation were administered with oral 50 mg/kg PF-1355 (2-[6-(2,5-dimethoxyphenyl)-4-oxo-2-thioxo-3,4-dihydropyrimidin-1(2H)-yl]acetamide) twice daily and compared with vehicle-treated control animals (n = 4 to 7 per group). On day 2 post–myocardial infarction (MI), hearts were processed for extracellular protein fractions (ECF), intracellular protein fractions (ICF), and myeloperoxidase (MPO) activity was performed with antibody capture assay with 10-acetyl-3,7-dihydroxyphenoxazine, reported as relative fluorescence units (RFU)/s/μg of protein. (B to D) In vivo MPO inhibition as measured by bis-5-hydroxytryptamide-diethylenetriaminepentaacetate-gadolinium imaging. (B) Representative T1-weighted midventricular slices showing pre-contrast, early (15 min), and delayed (60 min) contrast-enhanced images; dotted areas represent the infarct areas. (C) Lesion activation ratio (LAR) of untreated (n = 4) and PF-1355–treated groups (n = 15); bar graphs represent 60-min CNR values. (D) CNR values plotted as a function of time show a decrease in enhancement over time compared with untreated control subjects. (E) There is no significant difference in infarct area between groups at day 2 post-MI. Data plotted as mean ± SEM; *p < 0.05; **p < 0.01; ∗∗∗p < 0.001.