Dyslipidemia, more specifically, high-serum low-density lipoproteins and low-serum high-density lipoproteins, are known risk factors for cardiovascular disease. The current clinical treatment of dyslipidemia represents the outcome of a large body of fundamental basic science research on lipids, lipid metabolism, and the effects of different lipids on cellular components of the artery, inflammatory cells, and platelets. In general, lower density lipids activate intracellular pathways to increase local and systemic inflammation, monocyte adhesion, endothelial cell dysfunction and apoptosis, and smooth muscle cell proliferation, resulting in foam cell formation and genesis of atherosclerotic plaque. In contrast, higher density lipids prevent or attenuate atherosclerosis. This article is part 1 of a 2-part review, with part 1 focusing on lipid metabolism and the downstream effects of lipids on the development of atherosclerosis, and part 2 on the clinical treatment of dyslipidemia and the role of these drugs for patients with arterial disease exclusive of the coronary arteries.

HDL will inhibit and LDL will augment TSP-1-induced VSMC chemotaxis. VSMC chemotaxis will be inhibited by the HDL moiety, S1P, through the S1PR1 receptor, and augmented by the LDL component, LPA, through the LPAR1 receptor. The goal of this study was to determine the effect of HDL and LDL and their receptors on TSP-1-induced VSMC chemotaxis. For VSMC chemotaxis to TSP-1 cells received the following pretreatments: low (25 µg/ml) or optimal (75 µg/ml) concentration of HDL, S1P, optimal (75 µg/ml) or high (175 µg/ml) concentration of LDL, or LPA. For the receptor studies, VSMCs were transfected with siRNA to S1PR1, S1PR3, LPAR1, LPAR2, LPAR3, or a S1PR2 receptor antagonist. The TSP-1-induced chemotaxis results were (1) HDL (25 µg/ml) or LDL (75 µg/ml) exhibited no effect on chemotaxis; (2) HDL (75 µg/ml) inhibited chemotaxis by 50.9 ± 8 % and S1P by 43.4 ± 11.6 %; (3) LDL (175 µg/ml) augmented chemotaxis by 30 ± 10.4 % and LPA by 25.6 ± 12.3 %; (4) S1PR1 and S1PR3 knockdown and S1PR2 antagonist-treated cells augmented chemotaxis; and (5) LPAR1 and LPAR2 knockdown inhibited and LPAR3 knockdown had no effect on chemotaxis. In conclusion, HDL/S1P inhibits, while LDL/LPA stimulates TSP-1-induced VSMC chemotaxis. The HDL/S1P effect is mediated by the S1PR1-3 receptors. The LDL/LPA effects are mediated by the LPAR1 and LPAR2 receptors, but not LPAR3. Therefore, lipids have significant effects on TSP-1-induced VSMC chemotaxis.

Objective(s):In an attempt to identify the concerns of vascular fellows regarding their training in vascular surgery, we conducted an anonymous survey consisting of 22 questions at an annual national meeting held yearly in March from 2004 to 2010.Methods: The fellows were asked to assess their endovascular, open, and vascular laboratory experience as excellent, satisfactory, or mixed. They were queried about who trained them in their endovascular skills, the quality of their didactics, and amount of small cases that yielded no learning experience. Of the 466 attendees, 376 (80%) completed the survey. Up to 84% of those surveyed were men. Second-year fellows comprised up to 66% of those surveyed.Results: Most (79%) were satisfied with their endovascular experience during their fellowship, and 81% were satisfied with their experience with open cases. Interventional skills were obtained from a vascular surgeon (84%), an interventional radiologist (9%), a cardiologist (1%), or a mixture (5%). The didactics were felt to be excellent, satisfactory, or required some or much improvement in 20%, 64%, 11%, and 4% respectively. The distribution of nonlearning cases was felt to be excellent, satisfactory, or required some or much improvement in 42%, 45%, 10%, and 3% respectively. However, only 64% thought their vascular laboratory experience was excellent or satisfactory. Only 36% actually performed the vascular duplex examination, and only 47% felt that they would feel comfortable in managing a vascular laboratory. Forty-six percent suggested that finding the type of job they wanted was easy in 46% or moderately difficult in 46%. Most (72%) felt that future demand for manpower in vascular surgery will exceed available manpower. In the 2004 survey, the primary source of training for interventional skill was a vascular surgeon in 77% and this increased to 100% in 2010. No other major significant differences were noted from year to year.Conclusions: The results of this survey suggest that several significant issues are reflected in the minds of vascular trainees. These data suggest that vascular fellows are not being adequately trained in the vascular laboratory. Because the trainees represent the future of our field, we suggest that the vascular laboratory become a specific area of focus in the fellowship training.