Stress cardiomyopathy (SCM) is a unique cardiac disorder that more often occurs in women. SCM presents in a similar fashion as acute myocardial infarction (AMI), with chest pain, ECG changes, and congestive heart failure. The primary distinguishing feature is the absence of thrombotic coronary occlusion in SCM. How this reduction in cardiac function occurs in the absence of coronary occlusion remains unknown. Therefore, we tested the hypothesis that a targeted proteomic comparison of patients with acute SCM and AMI might identify relevant mechanistic differences. Blood was drawn in normal controls (n = 6), women with AMI (n = 12), or women with acute SCM (n = 15). Two-week follow-up samples were available in AMI (n = 4) and SCM patients (n = 11). Relative concentrations of 1,310 serum proteins were measured in each of the 48 samples using the SOMAscan assay. Women with AMI had greater myocyte necrosis, as reflected by a higher peak troponin I concentration (AMI 32.03 ± 29.46 vs. SCM 2.68 ± 2.6 ng/ml, p < 0.05). AMI and SCM patients had equivalent reductions in left ventricular ejection fraction [LVEF (%) 39 ± 12 vs. 37 ± 12, p = 0.479]. In follow-up, women with SCM had a greater improvement in cardiac function [LVEF (%) 60 ± 7 vs. 45 ± 13, p < 0.001]. No differentially expressed proteins were detected (absolute log2-fold change >1; q < 0.05) between AMI and SCM in the acute or recovery phase. However, when we compared normal controls to patients with AMI, there was differential expression of 35 proteins. When we compared normal controls to patients with SCM, 45 proteins were differentially expressed. In comparison to normal controls, biological processes such as complement, coagulation, and inflammation were activated in both AMI and SCM. There were four proteins that showed a non-significant trend to be increased in acute SCM vs. AMI (netrin-1, follistatin-like 3, kallikrein 7, kynureninase). Despite a lesser degree of myocardial necrosis than AMI, SCM is characterized by a similar activation of inflammatory, complement, and coagulation pathways. These findings may explain reported thromboembolic complications in the short term and elevated risk of mortality in the long term of SCM.

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Aims Despite three decades of study, it is still challenging to discriminate acute apical variant stress cardiomyopathy (AVSCM) from acute left anterior descending‐myocardial infarction (LAD‐MI) at the time of presentation. A biomarker or practical imaging modality that can differentiate these two entities is highly desirable. Our objective was to characterize left ventricular (LV) mechanical deformation using 2‐dimensional (2D) echocardiographic strain imaging in an attempt to discriminate AVSCM from LAD‐MI at presentation. Methods and Results We studied 108 women (60 AVSCM, 48 ST segment elevation LAD‐MI). All underwent echocardiography within 48 hours of presentation. 2D longitudinal strain (LS) from an 18‐segment LV model was performed, with global LS (GLS) taken as the average of all 18 segments. GLS was abnormal, but did not differentiate AVSCM from LAD‐MI. Mean LS of the basal and mid‐anterior, basal, and mid‐anteroseptum segments were significantly lower in LAD‐MI vs AVSCM group (−14 ± 9% vs −20 ± 8%; −11 ± 7% vs −14 ± 6%; −9 ± 8% vs −14 ± 8%; −9 ± 7% vs −13 ± 5%, respectively, all P ≤ .05). Mean LS of the basal inferior and inferolateral segments was significantly higher in the LAD‐MI vs. AVSCM group (−19 ± 9% vs −13 ± 7%; −23 ± 11% vs −18 ± 7%, respectively, all P ≤ .05). Using ROC curve analysis, segmental strain ratio of average basal inferior and inferolateral segments LS to average mid‐ and basal anterior and anteroseptum segments LS of ≥1.58 was 90% specific for LAD‐MI [area under the curve (AUC) 0.87; P < .001]. Conclusion Longitudinal strain patterns are useful in discriminating AVSCM from LAD‐MI patients at presentation and may be valuable in stratifying patients for invasive evaluation.

Introduction The main objective of this study was to characterise an animal model of colon cancer in the F344-ApcPircUwm rat through the analysis of microRNAs expressed in plasma by Next Generation Sequencing. Methods Colonoscopic follow-ups of the colon cancer model were performed for 10 months (n=60). At each follow-up, 2 ml of whole blood was collected in EDTA tubes, centrifuged for plasma extraction and frozen at - 80 °C. After euthanasia of the animals the different regions of the colon and their respective findings were analysed by histopathological analysis to obtain a ground truth. After this, 14 plasma samples were analysed by Next Generation Sequencing to observe the different expressions of microRNAs between the animals corresponding to the Neoplasia group and the healthy animals (n=6/8). Results After the corresponding functional analysis of the microRNAs deregulated in the animals of the colonic adenoma group and the healthy animals, we highlight rno-miR-192–5p, rno-miR-125b-5p and rno-miR-29c-3p, which appear underexpressed in the animals with adenomatous and adenocarcinomatous lesions in the colon. Conclusions The microRNAs deregulated in this animal model compared to their healthy counterpart without lesions obtained by liquid biopsy are miR-125b-5p, miR-192–5p and miR-29c-3p and their study could open the door to novel therapeutic strategies for prognosis and diagnosis by studying their expression in animal models that could be transferred to humans in the fight against colon cancer.

INTRODUCTION New endoscopic technologies developed to improve colorectal cancer diagnosis need to be validated on animal models, which already exist for neoplastic polyps, but not for hyperplasia. For that, a hyperplastic model of growth in colon has been created on murine animal. For its characterization, a first pilot study was performed, and this study aims to validate the results. MATERIALS AND METHODS 30 Pirc (Polyposis In the Rat Colon) rats, wild type strain (F344/NTac-Apcam1137), were used. The hyperplastic model was induced by laparotomy with a non-resorbable suture, not stenosing, placed through the colon wall. Then, colonic biopsies were extracted weekly from the growth around the suture. RESULTS After the second follow-up, hyperplastic growths are already found. The reproducibility of the model has been obtained and the optimal time determined, after induction of the model. According to our knowledge, this is the first induced colonic hyperplasia model in rats. It solves limitations of other traditional models that only produce hypertrophy, where hyperplasia appears when iatrogenic effects occur as undesired results in a non-standardised or reproducible form. CONCLUSIONS This work has successfully developed a preclinical model of colonic hyperplasia in rats that recreates important characteristics of human hyperplasia, such as the generation of new cells in the colonic mucosa and tissue growth, as well as the corresponding angiogenesis. The new hyperplastic model created could be used for the validation of endoscopic technology, and other studies. It would be useful to improve optical biomarkers of colorectal cancer and to discriminate between endoscopic findings.