Hemosiderin deposits confounds tracking of iron-oxide-labeled stem cells: an experimental study.

BACKGROUND: The aim of the present research was to study the possible interference of hemosiderin deposits with the histological detection of dextran-coated, iron-labeled, mesenchymal stem cells after intracoronary administration in a porcine model of myocardial infarction. MATERIALS AND METHODS: A myocardial infarction was induced in six animals that received intracoronary iron-labeled autologous mesenchymal stem cells (group 1; n = 2) or placebo (group 2; n = 4). Six control animals without myocardial infarction underwent direct intramyocardial injections of iron-labeled autologous mesenchymal stem cells (group 3; n = 2) or placebo (group 4; n = 4). Histological sections from explanted hearts were stained with Prussian blue to identify dextran-coated, iron-labeled, mesenchymal stem cells. RESULTS: After Prussian blue staining, granular blue labeling in the tissue was observed in both groups of animals with infarcts. Similar granular blue labeling was detected in hearts from control animals without infarction that had received iron-labeled mesenchymal stem cells. However, hearts from control animals without infarction that received placebo did not have any granular blue labeling in the tissue. CONCLUSIONS: Hemosiderin from infarction hemorrhage interferes with detection of dextran-coated iron-labeled mesenchymal stem cells after intracoronary administration, suggesting that this marker is not useful to detect mesenchymal stem cells in a porcine model of myocardial infarction.

Combination of clinical risk profile, early exercise testing and circulating biomarkers for evaluation of patients with acute chest pain without ST-segment deviation or troponin elevation.

OBJECTIVE: To investigate the combination of clinical data, exercise testing and biomarkers for the evaluation of patients with chest pain without ST-segment deviation or troponin elevation. DESIGN: Prospective cohort design. SETTTING: Two teaching hospitals in Spain. PATIENTS: 422 patients presenting to the emergency department were studied. Leukocyte count, C-reactive protein (CRP), pregnancy-associated plasma protein A (PAPP-A) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were determined. A validated clinical risk score (number of points according to pain characteristics and risk factors) was used for clinical evaluation and early exercise testing was performed. MAIN OUTCOME MEASURES: Adverse events (death, myocardial infarction or revascularisation) during a median 60 weeks follow-up. RESULTS: By receiver operating characteristic curve analysis, the association between death or myocardial infarction and adverse events was not significant with leukocyte count (p = 0.3, p = 0.3) or CRP (p = 0.5, p = 0.8), was borderline significant with PAPP-A (p = 0.07, p = 0.04) and strongly significant with NT-pro-BNP (p = 0.0001, p = 0.0001). By Cox regression including clinical risk score, exercise testing result and biomarkers, exercise testing was the independent predictor of revascularisation (p = 0.0001), whereas risk score (p = 0.03) and NT-proBNP (p = 0.0004) predicted death or myocardial infarction. The inclusion of NT-proBNP improved the accuracy of the model for death or myocardial infarction (C-statistic 0.84 versus 0.76, p = 0.01). The combination of clinical score and NT-proBNP afforded the stratification in high (17.2%, p = 0.0001), intermediate (5.3%) and low (1.1%) risk categories of death or myocardial infarction. CONCLUSIONS: NT-proBNP provides incremental prognostic information above that given by clinical history and exercise testing in patients with chest pain without ST-segment deviation and negative troponin.