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.