Background-Statin therapy reduces adverse outcomes, with a minimal decrease in vessel stenosis. Magnetic resonance imaging (MRI) noninvasively detects atherosclerotic plaque (AP) reduction. We hypothesized that statin-induced AP regression can be monitored by MRI and detected earlier than previously reported and is significantly associated with its lipid-lowering effect. Methods and Results-APs in thoracic aorta were measured by combined surface/transesophageal MRI in 27 patients (treated with simvastatin 20 to 80 mg daily) before and after 6 months of therapy. AP volume and luminal dimensions were measured from 6 cross sections used to construct a 2.4-cm 3D volume of the aorta that included plaque and lumen. Method reproducibility was studied in 10 patients imaged twice, 1 week apart. AP volume was reduced from 3.3Ϯ0.1.4 to 2.9Ϯ1.4 cm 3 at 6 months (PϽ0.02), whereas luminal volume increase was less accentuated (from 12.0Ϯ3.9 to 12.2Ϯ3.7 cm 3 , PϽ0.06). LDL cholesterol decreased by 23% (from 125Ϯ32 to 97Ϯ27 mg/dL, PϽ0.05) in 6 months. AP regression (plaque volume/area reduction) was significantly related to LDL cholesterol reduction (PϽ0.02 and PϽ0.005, respectively), and luminal volume increase was inversely related to LDL cholesterol reduction (PϽ0.04). Plaque volume measurement was highly reproducible (intraclass correlation Rϭ0.98 and variabilityϭ4.8%). Intraobserver (0.91) and interobserver (0.81) concordances were documented for plaque volume assessment. Conclusions-AP regression and reverse remodeling can be detected accurately by MRI 6 months after statin therapy initiation, and it is strongly associated with LDL cholesterol reduction.

We found a 3-fold increased incidence of AMI more than 2 years after Hurricane Katrina. Even allowing for the loss of some local hospitals after the disaster, this represents a significant change in overall health of the study population and supports the need for further study into the health effects of chronic stress.

Atherosclerosis is an inflammatory arterial pathogenic condition, which leads to ischemic cardiovascular diseases, such as coronary artery disease and myocardial infarction, stroke, and peripheral arterial disease. Atherosclerosis is a multifactorial disorder and its pathophysiology is highly complex. Changes in expression of multiple genes coupled with environmental and lifestyle factors initiate cascades of adverse events involving multiple types of cells (e.g. vascular endothelial cells, smooth muscle cells, and macrophages). IGF-1 is a pleiotropic factor, which is found in the circulation (endocrine IGF-1) and is also produced locally in arteries (endothelial cells and smooth muscle cells). IGF-1 exerts a variety of effects on these cell types in the context of the pathogenesis of atherosclerosis. In fact, there is an increasing body of evidence suggesting that IGF-1 has beneficial effects on the biology of atherosclerosis. This review will discuss recent findings relating to clinical investigations on the relation between IGF-1 and cardiovascular disease and basic research using animal models of atherosclerosis that have elucidated some of the mechanisms underlying atheroprotective effects of IGF-1.

AF ablation with INR ≥ 2.0 provides a consistent anticoagulant milieu during the procedure, with lower heparin requirements that are important to anticipate.

Persistent inflammation promotes development and progression of heart failure (HF). TWEAK (TNF-Related WEAK Inducer Of Apoptosis), a NF-κB- and/or AP-1-responsive proinflammatory cytokine that signals via TWEAK receptor (TWEAKR), is expressed at high levels in human and preclinical models of HF. Since the adapter molecule TRAF3IP2 (TRAF3 Interacting Protein 2) is an upstream regulator of various proinflammatory pathways, including those activated by NF-κB and AP-1, we hypothesized that targeting TRAF3IP2 inhibits TWEAK-induced proinflammatory and pro-fibrotic responses in vitro and in vivo. Consistent with the hypothesis, forced expression of TRAF3IP2 upregulated TWEAK and its receptor expression in cultured adult mouse cardiac fibroblasts (CF). Further, exogenous TWEAK upregulated TRAF3IP2 expression in a time- and dose-dependent manner, suggesting a positive-feedback regulation of TRAF3IP2 and TWEAK. TWEAK also promoted TRAF3IP2 nuclear translocation. Confirming its critical role in TWEAK signaling, silencing TRAF3IP2 inhibited TWEAK autoregulation, TWEAKR upregulation, p38 MAPK, NF-κB and AP-1 activation, inflammatory cytokine expression, MMP and TIMP1 activation, collagen expression and secretion, and importantly, proliferation and migration. Recapitulating these in vitro results, continuous infusion of TWEAK for 7 days increased systolic blood pressure (SBP), upregulated TRAF3IP2 expression, activated p38 MAPK, NF-κB and AP-1, induced the expression of multiple proinflammatory and pro-fibrotic mediators, and interstitial fibrosis in hearts of wild type mice. These proinflammatory and pro-fibrotic changes occurred in conjunction with myocardial hypertrophy and contractile dysfunction. Importantly, genetic ablation of TRAF3IP2 inhibited these TWEAK-induced adverse cardiac changes independent of increases in SBP, indicating that TRAF3IP2 plays a causal role, and thus a therapeutic target, in chronic inflammatory and fibro-proliferative diseases.

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Purpose To compare the concentration of amino acids in subretinal and vitreous fluid of patients with primary rhegmatogenous retinal detachment to that of control vitreous. Methods This prospective, observational study measured amino-acid levels in subretinal fluid of patients undergoing scleral buckle placement (n ¼ 20) and vitreous fluid in patients undergoing pars plana vitrectomy (n ¼ 5) for primary retinal detachment. Vitreous fluid from patients undergoing vitrectomy for macular hole (n ¼ 7) or epiretinal membrane (n ¼ 3) served as a control. Subretinal fluid and control vitreous were analysed using high-pressure liquid chromatography. Retinal detachment vitreous was analysed using capillary electrophoresis-laser-induced fluorescence. Results Mean levels of glutamate (27.071.7 lM), aspartate (4.174.0 lM), and glycine (44.1731.0 lM) in subretinal fluid and glutamate (13.4711.9 lM) in the vitreous were significantly elevated in retinal detachment compared to control vitreous. A significant, positive association was observed between levels of aspartate and glutamate in subretinal fluid (Spearman's correlation coefficient: 0.74, Po0.01). Mean arginine levels did not differ significantly between subretinal fluid and control vitreous. Levels of alanine, tyrosine, valine, isoleucine, leucine, and phenylalanine were significantly lower in subretinal fluid compared to control vitreous (all Po0.01). Conclusions Glutamate levels in subretinal fluid and vitreous of patients with primary retinal detachment is significantly elevated in comparison to control vitreous. This finding lends further support to the hypothesis that elevated glutamate levels may result from ischaemia of the outer retina secondary to retinal detachment.

The use of antibiotic envelopes in CIED implant is associated with a significantly lower rate of infection.