A decision support system improves the interpretation of myocardial perfusion imaging

PURPOSE: The aim of this study was to investigate the influence of a computer-based decision support system (DSS) on performance and inter-observer variability of interpretations regarding ischaemia and infarction in myocardial perfusion scintigraphy (MPS). METHODS: Seven physicians independently interpreted 97 MPS studies, first without and then with the advice of a DSS. Four physicians had long experience and three had limited experience in the interpretation of MPS. Each study was interpreted regarding myocardial ischaemia and infarction in five myocardial regions. The patients had undergone a gated MPS using a 2-day stress/gated rest (99m)Tc sestamibi protocol. The gold standard used was the interpretations made by one experienced nuclear medicine specialist on the basis of all available clinical and image information. RESULTS: The sensitivity for ischaemia of the seven readers increased from 81% without the DSS to 86% with the DSS (p = 0.01). The increase in sensitivity was higher for the three inexperienced physicians (9%) than for the four experienced physicians (2%). There was no significant change in specificity between the interpretations. The interpretations of ischaemia made with the advice of the DSS showed less inter-observer variability than those made without advice. CONCLUSION: This study shows that a DSS can improve performance and reduces the inter-observer variability of interpretations in myocardial perfusion imaging. Both experienced and, especially, inexperienced physicians can improve their interpretation with the advice from such a system

Electroanatomic characterization of post-infarct scars comparison with 3-dimensional myocardial scar reconstruction based on magnetic resonance imaging.

International audienceOBJECTIVES: This study was designed to compare electroanatomic mapping (EAM) and magnetic resonance imaging (MRI) with delayed contrast enhancement (DCE) data for delineation of post-infarct scars. BACKGROUND: Electroanatomic substrate mapping is an important step in the post-infarct ventricular tachycardia (VT) ablation strategy, but this technique has not yet been compared with a gold-standard noninvasive tool informing on the topography and transmural extent of myocardial scars in humans. METHODS: Ten patients (9 men, age 71 +/- 10 years) admitted for post-infarct VT ablation underwent both a left ventricle DCE MRI and a sinus-rhythm 3-dimensional (3D) (CARTO) EAM (Biosense Webster, Johnson & Johnson, Diamond Bar, California). A 3D color-coded MRI-reconstructed left ventricular endocardial shell was generated to display scar data (intramural location and transmural extent). A matching process allocated any CARTO point to its corresponding position on the MRI map. Electrogram (EGM) characteristics were then evaluated in relation to scar data. RESULTS: A spiky EGM morphology, a reduced unipolar or bipolar EGM voltage amplitude (56 ms) independently correlated with the presence of scar whatever its intramural position. Endocardial scars had a larger degree of signal reduction than intramural or epicardial scars. None of the parameters was correlated with transmural scar depth. A clear mismatch in infarct surface between CARTO and MRI maps was observed in one-third of infarct zones. CONCLUSIONS: Sinus-rhythm EAM helps identify the limits of post-infarct scars. However, the accuracy of EAM for precise scar delineation is limited. This limit might be circumvented using anatomical information provided by 3D MRI data

Superoxide dismutase 1 (SOD1) is a target for a small molecule identified in a screen for inhibitors of the growth of lung adenocarcinoma cell lines

We previously described four small molecules that reduced the growth of lung adenocarcinoma cell lines with either epidermal growth factor receptor (EGFR) or KRAS mutations in a high-throughout chemical screen. By combining affinity proteomics and gene expression analysis, we now propose superoxide dismutase 1 (SOD1) as the most likely target of one of these small molecules, referred to as lung cancer screen 1 (LCS-1). siRNAs against SOD1 slowed the growth of LCS-1 sensitive cell lines; conversely, expression of a SOD1 cDNA increased proliferation of H358 cells and reduced sensitivity of these cells to LCS-1. In addition, SOD1 enzymatic activity was inhibited in vitro by LCS-1 and two closely related analogs. These results suggest that SOD1 is an LCS-1–binding protein that may act in concert with mutant proteins, such as EGFR and KRAS, to promote cell growth, providing a therapeutic target for compounds like LCS-1