Effect of statins on coronary bifurcation atherosclerosis: an intravascular ultrasound virtual histology study

This study is aimed at assessing by intravascular ultrasound virtual histology (VH-IVUS) the effect of statins on coronary bifurcation atherosclerosis in non-culprit vessels. In this non-randomized study, in 48 patients, 51 bifurcation atherosclerotic sites in non-culprit vessels without significant angiographic stenosis, underwent baseline and 12 months follow-up VH-IVUS. Patients received treatment with either simvastatin (20 mg daily, n = 24) or rosuvastatin (10 mg daily, n = 24) for the same period. VH-IVUS analysis of bifurcation lesions included the 5-mm proximal, bifurcation only (side-branch point) and 5-mm distal subsegments. Overall plaque and external elastic membrane volume decreased after 1 year (115.7 ± 35.5 to 106.1 ± 29.3 mm3, P < 0.001; and 241.0 ± 57.0 to 232.4 ± 54.2 mm3, P = 0.005, respectively). Similarly, overall dense calcium volume significantly increased (7.1 ± 5.3 to 11.0 ± 8.5 mm3, P < 0.010), while fibrous and fibrofatty volumes significantly decreased (36.9 ± 19.2 to 24.1 ± 11.7 mm3, P < 0.001; and 5.1 ± 3.8 to 2.3 ± 2.0 mm3, P < 0.001, respectively), and necrotic core volume did not change significantly (17.0 ± 11.1 to 19.8 ± 13.5 mm3, P = 0.053). There were no significant differences in compositional analysis between the simvastatin and rosuvastatin treatment groups. However, within groups, necrotic core volume significantly increased in the simvastatin treatment group (19.7 ± 13.9 to 24.3 ± 16.1 mm3, P = 0.029) but not in the rosuvastatin treatment group. (14.3 ± 6.7 to 15.6 ± 8.7 mm3, P = 0.423). The independent clinical predictors for reduction of necrotic core volume by multiple stepwise logistic regression analysis were the percent change of HDL-cholesterol level (P = 0.041, odds ratio: 1.052, 95% confidence interval (CI): 1.002 to 1.104) and the percent change of hsCRP level (P = 0.021, odds ratio: 0.989, 95% CI: 0.980 to 0.998). After 1 year, overall dense calcium volume significantly increased whilst fibrous and fibrofatty volumes significantly decreased; no significant change in the content of necrotic core was observed. Although changes in the volumes of all plaque components were not significantly different between the simvastatin and rosuvastatin treatment groups, halting of necrotic core progression was apparent in the rosuvastatin group

In vitro assessment of six aspiration catheters using a distal protection filter

Background: We assessed performance of 6 aspiration catheters for distal embolization using a distal protection filter in an in vitro experiment. In acute myocardial infarction, a distal protection filter is used for lesions likely to induce a distal embolism. Which aspiration cathether is most effective when used with a distal protection filter remains still unclear.Methods: A 0.5-cm3 bolus of gelatin as a model of stagnant pools of coronary plaque debris was captured in the distal protection filter and aspirated by 6 aspiration catheters. We measured and compared the length of the suspended embolus matter.Results: Among the 6 catheters evaluated, the use of the Export Advance catheter (Medtronic) resulted in significantly shorter lengths of the suspended embolus matter compared to the use of the TVAC II (Nipro), Thrombuster III SL (Kaneka), and Rebirth Pro (Goodman) catheters (p &lt; 0.01). The residual embolus matter in all cases had drained distally to the distal protection filter when the filter was retrieved.Conclusions: The use of the Export Advance catheter showed better performance using a distal protection filter in this in vitro experiment, and its use might be more effective in preventing distal embolisms in combination with a distal protection filter

Phosphorylation of proteins and apoptosis induced by c-Jun N-terminal kinase1 activation in rat cardiomyocytes by H2O2 stimulation

AbstractCytokines and various cellular stresses are known to activate c-Jun N-terminal kinase-1 (JNK1), which is involved in physiological function. Here, we investigate the activation of JNK1 by oxidative stress in H9c2 cells derived from rat cardiomyocytes. H2O2 (100 μM) significantly induces the tyrosine phosphorylation of JNK1 with a peak 25 min after the stimulation. The amount of JNK1 protein remains almost constant during stimulation. Immunocytochemical observation shows that JNK1 staining in the nucleus is enhanced after H2O2 stimulation. To clarify the physiological role of JNK1 activation under these conditions, we transfected antisense JNK1 DNA into H9c2 cells. The antisense DNA (2 μM) inhibits JNK1 expression by 80% as compared with expression in the presence of the sense DNA, and significantly blocks H2O2-induced cell death. Consistent with the decrease in cell number, we detected condensation of the nuclei, a hallmark of apoptosis, 3 h after H2O2 stimulation in the presence of the sense DNA for JNK1. The antisense DNA of JNK1 inhibits the condensation of nuclei by H2O2. Under these conditions, the H2O2-induced phosphorylation of proteins with molecular masses of 55, 72, and 78 kDa is blocked by treatment with the antisense DNA for JNK1 as compared with the sense DNA for JNK1. These findings suggest that JNK1 induces apoptotic cell death in response to H2O2, and that the cell death may be involved in the phosphorylations of 55, 72, and 78 kDa proteins induced by JNK1 activation

Hierarchies of conditional beliefs and interactive epistemology in dynamic games

Digitised version produced by the EUI Library and made available online in 2020

Do neutrophil extracellular traps implicate in atheromatous plaques from carotid endarterectomy? Re-analyzes of cDNA microarray data by surgeons

BackgroundCarotid artery stenosis is the cause of 15% of strokes. Neutrophil extracellular traps (NETs) and peptidyl arginine deiminase 4 (PAD4) are believed to be involved in thrombosis. This pilot study described the differential expression profile of NETs between atheromatous plaques and surrounding tissues.MethodsMicroarray datasets of carotid plaques were obtained from Gene Expression Omnibus. The normalized data were processed into comma-separated value matrix files using spreadsheet software. Analyzes of microarray data were conducted using integrated differential expression and pathway analysis.ResultThe clustering results illustrated that the classifications of plaque and control had reasonable biological validity. Pathway analysis revealed the relevance of immune response, cell signaling, and other pathways. Differentially expressed genes were detected between carotid plaques and control specimens. However, enrichment analyzes did not reveal a difference in PAD4 expression between the groups and that NET implication was only found in one cDNA microarray dataset.DiscussionThis pilot study does not necessarily dismiss the possibility of a relationship between NETs and atherothrombotic stroke. Gene expression could differ between endothelial cells and atheromas, and further studies are needed