Right Ventricular Dysfunction following Acute Myocardial Infarction in the Absence of Pulmonary Hypertension in the Mouse

Background Cardiac remodelling after AMI is characterized by molecular and cellular mechanisms involving both the ischemic and non-ischemic myocardium. The extent of right ventricular (RV) dilatation and dysfunction and its relation to pulmonary hypertension (PH) following AMI are unknown. The aim of the current study was to evaluate changes in dimensions and function of the RV following acute myocardial infarction (AMI) involving the left ventricle (LV). Methods We assessed changes in RV dimensions and function 1 week following experimental AMI involving the LV free wall in 10 mice and assessed for LV and RV dimensions and function and for the presence and degree of PH. Results RV fractional area change and tricuspidal annular plane systolic excursion significantly declined by 33% (P = 0.021) and 28% (P = 0.001) respectively. Right ventricular systolic pressure measured invasively in the mouse was within the normal values and unchanged following AMI. Conclusion AMI involving the LV and sparing the RV induces a significant acute decline in RV systolic function in the absence of pulmonary hypertension in the mouse indicating that RV dysfunction developed independent of changes in RV afterload

Silicic conduits as supersized tuffisites:Clastogenic influences on shifting eruption styles at Cordón Caulle volcano (Chile)

Understanding the processes that drive explosive-effusive transitions during large silicic eruptions is crucial to hazard mitigation. Conduit models usually treat magma ascent and degassing as a gradual, unidirectional progression from bubble nucleation through magmatic fragmentation. However, there is growing evidence for the importance of bi-directional clastogenic processes that sinter fragmented materials into coherent clastogenic magmas. Bombs that were ejected immediately before the first emergence of lava in the 2011–2012 eruption at Cordón Caulle volcano (Chile) are texturally heterogeneous composite assemblages of welded pyroclastic material. Although diverse in density and appearance, SEM and X-ray tomographic analysis show them all to have been formed by multi-generational viscous sintering of fine ash. Sintering created discrete clasts ranging from obsidian to pumice and formed a pervasive clast-supporting matrix that assembled these clasts into a conduit-sealing plug. An evaluation of sintering timescales reveals texturally disparate bomb components to represent only minutes of difference in residence time within the conduit. Permeability modelling indicates that the plug was an effective conduit seal, with outgassing potential—even from high-porosity regions—being limited by the inability of gas to flow across tendrils of densely sintered inter-clast matrix. Contrary to traditional perspectives, declining expressions of explosivity at the surface need not be preceded or accompanied by a decline in fragmentation efficiency. Instead, they result from tips in balance between the opposing processes of fragmentation and sintering that occur in countless cycles within volcanic conduits. These processes may be particularly enhanced at silicic fissure volcanoes, which have laterally extensive subsurface plumbing systems that require complex magma ascent pathways. The textures investigated here reveal the processes occurring within silicic fissures to be phenomenologically identical to those that have been inferred to occur in tuffisite veins: silicic conduits are essentially supersized examples of edifice-penetrating tuffisites

Alterations in the Interleukin-1/Interleukin-1 Receptor Antagonist Balance Modulate Cardiac Remodeling following Myocardial Infarction in the Mouse

Background Healing after acute myocardial infarction (AMI) is characterized by an intense inflammatory response and increased Interleukin-1 (IL-1) tissue activity. Genetically engineered mice lacking the IL-1 receptor (IL-1R1-/-, not responsive to IL-1) or the IL-1 receptor antagonist (IL-1Ra, enhanced response to IL-1) have an altered IL-1/IL-1Ra balance that we hypothesize modulates infarct healing and cardiac remodeling after AMI. Methods IL-1R1-/- and IL-1Ra-/- male mice and their correspondent wild-types (WT) were subjected to permanent coronary artery ligation or sham surgery. Infarct size (trichrome scar size), apoptotic cell death (TUNEL) and left ventricular (LV) dimensions and function (echocardiography) were measured prior to and 7 days after surgery. Results When compared with the corresponding WT, IL-1R1-/- mice had significantly smaller infarcts (−25%), less cardiomyocyte apoptosis (−50%), and reduced LV enlargement (LV end-diastolic diameter increase [LVEDD], −20%) and dysfunction (LV ejection fraction [LVEF] decrease, −50%), whereas IL-1Ra-/- mice had significantly larger infarcts (+75%), more apoptosis (5-fold increase), and more severe LV enlargement (LVEDD increase,+30%) and dysfunction (LVEF decrease, +70%)(all P values \u3c0.05). Conclusions An imbalance in IL-1/IL-1Ra signaling at the IL-1R1 level modulates the severity of cardiac remodeling after AMI in the mouse, with reduced IL-1R1 signaling providing protection and unopposed IL-1R1 signaling providing harm

Unexpected large eruptions from buoyant magma bodies within viscoelastic crust

Large volume effusive eruptions with relatively minor observed precursory signals are at odds with widely used models to interpret volcano deformation. Here we propose a new modelling framework that resolves this discrepancy by accounting for magma buoyancy, viscoelastic crustal properties, and sustained magma channels. At low magma accumulation rates, the stability of deep magma bodies is governed by the magma-host rock density contrast and the magma body thickness. During eruptions, inelastic processes including magma mush erosion and thermal effects, can form a sustained channel that supports magma flow, driven by the pressure difference between the magma body and surface vents. At failure onset, it may be difficult to forecast the final eruption volume; pressure in a magma body may drop well below the lithostatic load, create under-pressure and initiate a caldera collapse, despite only modest precursors

Chronic systemic glucocorticoid therapy is associated with increased risk of major vascular complications and cardiac tamponade after transcatheter aortic valve implantation: a systematic review and meta-analysis

INTRODUCTION: TAVI-related complications, such as conduction disturbances, vascular complications or death may be related to increased inflammatory response. The aim of this study was to elucidate the efficacy and safety of the systemic glucocorticoid therapy regarding the adverse events after TAVI deployment. EVIDENCE ACQUISITION: We conducted a systemic search of PubMed, a reference list of relevant articles, and Medline. The main efficacy outcomes of interest were all-cause death, cardiac and non-cardiac death, permanent pacemaker implantation (PPM), new left bundle branch block (LBBB), stroke, and myocardial infarction (MI). Safety endpoints were major vascular complications, major bleeding events, and cardiac tamponade. EVIDENCE SYNTHESIS: A total of 7 studies including data from 3439 patients with a median follow-up was 30 days. Systemic glucocorticoid compared to the control group were associated with an increased risk of non-cardiac death (Relative Risk [RR] 5.90 95%CI [2.95; 11.80], P<0.001) major vascular complications (RR 1.78, 95%CI [1.22 - 2.61], P=0.003) and cardiac tamponade (RR 3.42, 95%CI [1.69 - 6.92], P<0.001). However, there were no differences in all-cause death, cardiac death, new LBBB, stroke, MI, or major bleeding events (all P values >0.05). CONCLUSIONS: Glucocorticoid therapy before the TAVI procedure was associated with an increase in non-cardiac death, major vascular events and cardiac tamponade. There were no differences in the risk of all-cause death, cardiac death, PPM or LBBB, stroke, or MI