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      Does high-density lipoprotein influence the development of saphenous vein graft disease after coronary bypass surgery?: exploratory analysis from the CASCADE trial

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          Abstract

          Background

          Low levels of high-density lipoprotein (HDL) purportedly increase the risk after coronary bypass surgery. This may relate to the development of saphenous vein graft (SVG) disease early postoperatively, but this premise has never been evaluated in the context of a prospective trial.

          Methods

          The CASCADE Trial was a multi-center study of 113 patients evaluating the use of postoperative clopidogrel. Patients received standard lipid management after surgery (96% statins). At 12 months, angiography and intravascular ultrasound was performed to assess SVG occlusion and intimal hyperplasia, respectively. In this exploratory analysis, we evaluated the influence of HDL levels on the development of SVG disease at 12 months, using the established cut-off of <40 mg/dL suggesting increased risk.

          Results

          While HDL levels increased over the time-period of the trial (P < 0.0001), 51.1% of patients had HDL levels <40 mg/dL 12 months after surgery. Slightly more SVG occlusions occurred amongst patients with HDL levels <40 mg/dL (6.8%), compared to patients with HDL levels >40 mg/dL (4.0%, P = 0.5). With multivariate adjustment, HDL level <40 mg/dL was associated with a trend towards more SVG occlusions (odds ratio: 3.2; P = 0.12). Lower HDL level was also associated with more intimal hyperplasia on ultrasound at 12 months (P = 0.10). Patients who had HDL levels >60 mg/dL had the least amount of intimal hyperplasia, significantly less than the remainder of the cohort (P = 0.01).

          Conclusions

          Within this population, lower HDL levels were associated with trends towards more graft occlusions and more vein intimal hyperplasia. Modulation of postoperative HDL levels may represent a valuable future strategy for the reduction of SVG disease.

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          Most cited references14

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          Aortocoronary Saphenous Vein Graft Disease: Pathogenesis, Predisposition, and Prevention

          Aortocoronary saphenous vein graft disease, with its increasing clinical sequelae, presents an important and unresolved dilemma in cardiological practice. During the 1st month after bypass surgery, vein graft attrition results from thrombotic occlusion, while later the dominant process is atherosclerotic obstruction occurring on a foundation of neointimal hyperplasia. Although the risk factors predisposing to vein graft atherosclerosis are broadly similar to those recognized for native coronary disease, the pathogenic effects of these risk factors are amplified by inherent deficiencies of the vein as a conduit when transposed into the coronary arterial circulation. A multifaceted strategy aimed at prevention of vein graft disease is emerging, elements of which include: continued improvements in surgical technique; more effective antiplatelet drugs; increasingly intensive risk factor modification, in particular early and aggressive lipid-lowering drug therapy; and a number of evolving therapies, such as gene transfer and nitric oxide donor administration, which target vein graft disease at an early and fundamental level. At present, a key measure is to circumvent the problem of vein graft disease by preferential selection of arterial conduits, in particular the internal mammary arteries, for coronary bypass surgery whenever possible.
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            Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis.

            Statins reduce low-density lipoprotein cholesterol (LDL-C) levels and slow progression of coronary atherosclerosis. However, no data exist describing the relationship between statin-induced changes in high-density lipoprotein cholesterol (HDL-C) and disease progression. To investigate the relationship between changes in LDL-C and HDL-C levels and atheroma burden. Post-hoc analysis combining raw data from 4 prospective randomized trials (performed in the United States, North America, Europe, and Australia between 1999 and 2005), in which 1455 patients with angiographic coronary disease underwent serial intravascular ultrasonography while receiving statin treatment for 18 months or for 24 months. Ultrasound analysis was performed in the same core laboratory for all of the studies. Relationship between changes in lipoprotein levels and coronary artery atheroma volume. During statin therapy, mean (SD) LDL-C levels were reduced from 124.0 (38.3) mg/dL (3.2 [0.99] mmol/L) to 87.5 (28.8) mg/dL (2.3 [0.75] mmol/L) (a 23.5% decrease; P or =5% reduction in atheroma volume) was observed in patients with levels of LDL-C less than the mean (87.5 mg/dL) during treatment and percentage increases of HDL-C greater than the mean (7.5%; P<.001). No significant differences were found with regard to clinical events. Statin therapy is associated with regression of coronary atherosclerosis when LDL-C is substantially reduced and HDL-C is increased by more than 7.5%. These findings suggest that statin benefits are derived from both reductions in atherogenic lipoprotein levels and increases in HDL-C, although it remains to be determined whether the atherosclerotic regression associated with these changes in lipid levels will translate to meaningful reductions in clinical events and improved clinical outcomes.
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              Extended-release niacin or ezetimibe and carotid intima-media thickness.

              Treatment added to statin monotherapy to further modify the lipid profile may include combination therapy to either raise the high-density lipoprotein (HDL) cholesterol level or further lower the low-density lipoprotein (LDL) cholesterol level. We enrolled patients who had coronary heart disease or a coronary heart disease risk equivalent, who were receiving long-term statin therapy, and in whom an LDL cholesterol level under 100 mg per deciliter (2.6 mmol per liter) and an HDL cholesterol level under 50 mg per deciliter for men or 55 mg per deciliter for women (1.3 or 1.4 mmol per liter, respectively) had been achieved. The patients were randomly assigned to receive extended-release niacin (target dose, 2000 mg per day) or ezetimibe (10 mg per day). The primary end point was the between-group difference in the change from baseline in the mean common carotid intima-media thickness after 14 months. The trial was terminated early, on the basis of efficacy, according to a prespecified analysis conducted after 208 patients had completed the trial. The mean HDL cholesterol level in the niacin group increased by 18.4% over the 14-month study period, to 50 mg per deciliter (P < 0.001), and the mean LDL cholesterol level in the ezetimibe group decreased by 19.2%, to 66 mg per deciliter (1.7 mmol per liter) (P < 0.001). Niacin therapy significantly reduced LDL cholesterol and triglyceride levels; ezetimibe reduced the HDL cholesterol and triglyceride levels. As compared with ezetimibe, niacin had greater efficacy regarding the change in mean carotid intima-media thickness over 14 months (P = 0.003), leading to significant reduction of both mean (P = 0.001) and maximal carotid intima-media thickness (P < or = 0.001 for all comparisons). Paradoxically, greater reductions in the LDL cholesterol level in association with ezetimibe were significantly associated with an increase in the carotid intima-media thickness (R = -0.31, P < 0.001). The incidence of major cardiovascular events was lower in the niacin group than in the ezetimibe group (1% vs. 5%, P = 0.04 by the chi-square test). This comparative-effectiveness trial shows that the use of extended-release niacin causes a significant regression of carotid intima-media thickness when combined with a statin and that niacin is superior to ezetimibe. (ClinicalTrials.gov number, NCT00397657.) 2009 Massachusetts Medical Society
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                Author and article information

                Contributors
                Journal
                J Cardiothorac Surg
                J Cardiothorac Surg
                Journal of Cardiothoracic Surgery
                BioMed Central
                1749-8090
                2013
                10 July 2013
                : 8
                : 172
                Affiliations
                [1 ]Lynn Heart and Vascular Institute, Boca Raton Regional Hospital, 801 Meadows Road, Suite 104, Boca Raton, Florida 33486, USA
                [2 ]The University of Ottawa Heart Institute, Ottawa, Ontario, Canada
                [3 ]Hôpital Laval, Quebec City, Quebec, Canada
                [4 ]Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, Florida, USA
                Article
                1749-8090-8-172
                10.1186/1749-8090-8-172
                3716982
                23842141
                d4b4bf3b-5e02-4f6c-9bf3-ab4637c76fa6
                Copyright © 2013 Jerzewski et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 5 April 2013
                : 8 July 2013
                Categories
                Research Article

                Surgery
                coronary artery bypass graft surgery,vein graft disease,hdl,graft patency,cholesterol
                Surgery
                coronary artery bypass graft surgery, vein graft disease, hdl, graft patency, cholesterol

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