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Lipid-lowering for peripheral arterial disease of the lower limb.
Aung, PP, Maxwell, HG, Jepson, RG, Price, JF, Leng, GC
The Cochrane database of systematic reviews. 2007;(4):CD000123
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Abstract
BACKGROUND Lipid-lowering therapy is recommended for secondary prevention in people with coronary artery disease. It may also reduce cardiovascular events and/or local disease progression in people with lower limb peripheral arterial disease (PAD). OBJECTIVES To assess the effects of lipid-lowering therapy on all-cause mortality, cardiovascular events and local disease progression in patients with PAD of the lower limb. SEARCH STRATEGY The authors searched The Cochrane Peripheral Vascular Diseases Group's Specialised Register (last searched February 2007) and the Cochrane Central Register of Controlled Trials (CENTRAL) (last searched Issue 2, 2007) for publications describing randomised controlled trials of lipid-lowering therapy in peripheral arterial disease of the lower limb. SELECTION CRITERIA Randomised controlled trials of lipid-lowering therapy in patients with PAD of the lower limb. DATA COLLECTION AND ANALYSIS Three authors independently assessed trial quality and extracted data. MAIN RESULTS Eighteen trials were included, involving a total of 10,049 participants. Trials differed considerably in their inclusion criteria, outcomes measured, and type of lipid-lowering therapy used. Only one trial (PQRST) reported a detrimental effect of active treatment on blood lipid/lipoprotein levels. The pooled results from all eligible trials indicated that lipid-lowering therapy had no statistically significant effect on overall mortality (Odds Ratio (OR) 0.86; 95% Confidence Interval (CI) 0.49 to 1.50) or on total cardiovascular events (OR 0.8; 95% CI 0.59 to 1.09). However, subgroup analysis which excluded PQRST showed that lipid-lowering therapy significantly reduced the risk of total cardiovascular events (OR 0.74; CI 0.55 to 0.98). This was primarily due to a positive effect on total coronary events (OR 0.76; 95% CI 0.67 to 0.87). Greatest evidence of effectiveness came from the use of simvastatin in people with a blood cholesterol ≥ 3.5 mmol/litre (HPS). Pooling of the results from several small trials on a range of different lipid-lowering agents indicated an improvement in total walking distance (Weighted Mean Difference (WMD) 152 m; 95% CI 32.11 to 271.88) and pain-free walking distance (WMD 89.76 m; 95% CI 30.05 to 149.47) but no significant impact on ankle brachial index (WMD 0.04; 95% CI -0.01 to 0.09). AUTHORS' CONCLUSIONS Lipid-lowering therapy is effective in reducing cardiovascular mortality and morbidity in people with PAD. It may also improve local symptoms. Until further evidence on the relative effectiveness of different lipid-lowering agents is available, use of a statin in people with PAD and a blood cholesterol level ≥3.5 mmol/litre is most indicated.
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[Adipocytokines: link between obesity, type 2 diabetes and atherosclerosis].
Paquot, N, Tappy, L
Revue medicale de Liege. 2005;(5-6):369-73
Abstract
Adipose tissue, in addition to the storage of lipids function for lipids, plays active roles in normal metabolic homeostasis and in the development of several diseases, such as type 2 diabetes, dyslipaemia and atherosclerosis. These roles are mediated by adipocytokines, factors secreted by adipose tissue. These include tumor necrosis factors (TNF)-alpha, leptin, resistin, adiponectin or visfatin. Adipocytokines act in an autocrine, paracrine and endocrine manner. Adiponectin is a peculiar adipocytokine because in contrast to the markedly increased levels of leptin, resistin or TNF-alpha in obesity, its level is negatively correlated with body mass index, and is decreased in presence of insulin resistance and in type 2 diabetes. Adiponectin may play a crucial role in the development of diabetes mellitus and high adiponectin levels should protect against impairment of glucose metabolism. Moreover, adipocytokines are involved in the pathogenesis of vascular diseases and may represent a link between obesity, diabetes, inflammation and atherosclerosis. Weight loss, exercise and some antidiabetic drugs also influence plasma adipocytokines levels. For instance, thiazolidinediones treatment in patients with type 2 diabetes resulted in an increased in plasma adiponectin levels and a decrease in circulating TNF-alpha concentrations.
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3.
Iron and atherosclerosis.
Qayyum, R, Schulman, P
Clinical cardiology. 2005;(3):119-22
Abstract
Traditional risk factors fail to account for all deaths from coronary artery disease (CAD). Iron can inflict oxidative injury on components of the blood and arterial wall to incite the atherosclerotic process. Medical evidence suggests a role of elevated body iron stores as a risk factor for the development of atherosclerosis. Results of a clinical trial to determine the benefits of reducing body iron stores on cardiovascular mortality are pending.
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Patients with low levels of high-density lipoprotein cholesterol: to treat or not to treat?
Tavintharan, S, Lim, SC, Sum, CF
Singapore medical journal. 2005;(10):519-28
Abstract
Clinical evidence indicates that a low level of high-density lipoprotein cholesterol (HDL-C) is a major risk of atherosclerosis. Raising HDL-C reduces this risk significantly, making HDL-C levels an important target of treatment for dyslipidaemia, especially in pre-existent atherosclerosis. HDL-C is protective against atherosclerosis, largely due to its function of reverse cholesterol transport. Additionally, some important roles include fibrinolysis, antioxidant functions, and reduction of platelet aggregability. A number of agents potentially modify HDL favourably. Niacin is the most potent HDL-C raising agent currently available in clinical practice, followed by fibrates. CETP inhibitors show greater HDL-C rising, but are still used in trial settings only. HDL mimetic agents are another group of agents that offer much promise. Clinical outcome data are awaited for these newer therapeutic agents.
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Postprandial hyperlipidemia and atherosclerosis.
Tanaka, A
Journal of atherosclerosis and thrombosis. 2004;(6):322-9
Abstract
The development of the remnant like particle (RLP) method for conveniently measuring serum remnant lipoprotein levels in 1993 promoted much research on atherogenic significance and metabolism of remnant lipoproteins. This research brought about many results as the following. A novel apolipoprotein B48 receptor incorporating remnant lipoproteins into macrophages in arterial wall was discovered and the structure of the gene of the receptor was clarified. The expression of apolipoprotein B100 was recognized in the human small intestine, suggesting that dietary very low density lipoproteins (VLDL) might be synthesized in the human small intestine and converted into VLDL remnants and low density lipoproteins (LDL). It is recognized that the atherosclerotic risk of postprandial hyperlipidemia is derived from an increase of remnant lipoproteins and that measurement of serum RLP levels in postprandial state is more sensitive and necessary for evaluating an atherosclerotic risk because serum RLP levels remain high all day in patients with diabetes mellitus or coronary heart disease. The relation between postprandial hyperlipidemia and insulin resistance was clarified.
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Non-HDL cholesterol as a measure of atherosclerotic risk.
Packard, CJ, Saito, Y
Journal of atherosclerosis and thrombosis. 2004;(1):6-14
Abstract
Elevated triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) levels, hallmarks of the atherogenic lipid profile found in the metabolic syndrome and type 2 diabetes, are commonly seen in Japanese patients with coronary heart disease (CHD). In the setting of mildly to moderately elevated plasma TG (150-500 mg/dl), very-low-density lipoprotein (VLDL) accumulates and so do high levels of atherogenic TG-rich, cholesterol-enriched remnant particles. Indeed, in hypertriglyceridemia, abnormalities are seen in the quantity and quality of all lipoprotein B-containing lipoproteins. Non-HDL-C (total cholesterol minus HDL-C) provides a convenient measure of the cholesterol content of all atherogenic lipoproteins, and thus incorporates the potential risk conferred by elevated levels of atherogenic TG-rich remnants that is additional to the risk associated with low-density lipoprotein cholesterol (LDL-C). Non-HDL-C level has been found to be a strong predictor of future cardiovascular risk among patients whether or not they exhibit symptoms of vascular disease, and was recently recommended as a secondary treatment target (after LDL-C) in patients with elevated TG by the National Cholesterol Education Program Adult Treatment Panel III. Adoption of this readily available measure to assess risk and response to treatment in patients with elevated TG would improve treatment of dyslipidemia in a substantial number at risk for CHD.
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[Oxysterols: metabolism, biological role and associated diseases].
Souidi, M, Dubrac, S, Parquet, M, Volle, DH, Lobaccaro, JM, Mathé, D, Combes, O, Scanff, P, Lutton, C, Aigueperse, J
Gastroenterologie clinique et biologique. 2004;(3):279-93
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[Low density lipoprotein apheresis].
Zaliūnas, R, Slapikas, R, Gustiene, O, Siurkus, J, Vaitkus, E
Medicina (Kaunas, Lithuania). 2003;(12):1158-64
Abstract
Increased blood cholesterol concentration is one of the main factors in ischemic heart disease, development of which is determined by atherosclerotic changes in coronary vessels. Diet and treatment with 3-hydroxi-3-metilglutaril coenzyme A (HMG-CoA) reductase inhibitors helps to reduce low density lipoprotein cholesterol (LDL-Ch) blood concentration up to recommended level of 3.0 mmol/l in most patients but in some patients particularly with familial dyslipidemias cholesterol concentration remains increased even after treatment with maximal doses of lipid-regulating agents or their combinations. The most frequently used mechanical methods of cholesterol removal from blood include the procedures of extracorporeal apheresis. Low density lipoprotein (LDL) apheresis not only significantly reduces the blood concentrations of total cholesterol (TCh), and LDL-Ch, lipoprotein (a) (Lp(a) and fibrinogen but also stops the progression of atherosclerosis in coronary vessels.
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Antioxidant therapy for atherosclerotic vascular disease: the promise and the pitfalls.
Shihabi, A, Li, WG, Miller, FJ, Weintraub, NL
American journal of physiology. Heart and circulatory physiology. 2002;(3):H797-802
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Carboxyl ester lipase: structure-function relationship and physiological role in lipoprotein metabolism and atherosclerosis.
Hui, DY, Howles, PN
Journal of lipid research. 2002;(12):2017-30
Abstract
Carboxyl ester lipase (CEL), previously named cholesterol esterase or bile salt-stimulated (or dependent) lipase, is a lipolytic enzyme capable of hydrolyzing cholesteryl esters, tri-, di-, and mono-acylglycerols, phospholipids, lysophospholipids, and ceramide. The active site catalytic triad of serine-histidine-aspartate is centrally located within the enzyme structure and is partially covered by a surface loop. The carboxyl terminus of the protein regulates enzymatic activity by forming hydrogen bonds with the surface loop to partially shield the active site. Bile salt binding to the loop domain frees the active site for accessibility by water-insoluble substrates. CEL is synthesized primarily in the pancreas and lactating mammary gland, but the enzyme is also expressed in liver, macrophages, and in the vessel wall. In the gastrointestinal tract, CEL serves as a compensatory protein to other lipolytic enzymes for complete digestion and absorption of lipid nutrients. Importantly, CEL also participates in chylomicron assembly and secretion, in a mechanism mediated through its ceramide hydrolytic activity. Cell culture studies suggest a role for CEL in lipoprotein metabolism and oxidized LDL-induced atherosclerosis. Thus, this enzyme, which has a wide substrate reactivity and diffuse anatomic distribution, may have multiple functions in lipid and lipoprotein metabolism, and atherosclerosis.