Cholesterol Journal Articles

Record 1001 to 1020

Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2: a double-blind, placebo-controlled study of extended-release niacin on atherosclerosis progression in secondary prevention patients treated with statins
Taylor, A. J., L. E. Sullenberger, et al. (2004), Circulation 110(23): 3512-7.
Abstract: BACKGROUND: Niacin reduces coronary heart disease morbidity and mortality when taken either alone or in combination with statins; however, the incremental impact of adding niacin to background statin therapy is unknown. METHODS AND RESULTS: This was a double-blind randomized placebo-controlled study of once-daily extended-release niacin (1000 mg) added to background statin therapy in 167 patients (mean age 67 years) with known coronary heart disease and low levels of high-density lipoprotein cholesterol (HDL-C; <45 mg/dL). The primary end point was the change in common carotid intima-media thickness (CIMT) after 1 year. Baseline CIMT (0.884+/-0.234 mm), low-density lipoprotein cholesterol (89+/-20 mg/dL), and HDL-C (40+/-7 mg/dL) were comparable in the placebo and niacin groups. Adherence to niacin exceeded 90%, and 149 patients (89.2%) completed the study. HDL-C increased 21% (39 to 47 mg/dL) in the niacin group. After 12 months, mean CIMT increased significantly in the placebo group (0.044+/-0.100 mm; P<0.001) and was unchanged in the niacin group (0.014+/-0.104 mm; P=0.23). Although the overall difference in IMT progression between the niacin and placebo groups was not statistically significant (P=0.08), niacin significantly reduced the rate of IMT progression in subjects without insulin resistance (P=0.026). Clinical cardiovascular events occurred in 3 patients treated with niacin (3.8%) and 7 patients treated with placebo (9.6%; P=0.20). CONCLUSIONS: The addition of extended-release niacin to statin therapy slowed the progression of atherosclerosis among individuals with known coronary heart disease and moderately low HDL-C.

Arterial encasement and cranial nerve displacement in a case of cholesterol granuloma of the petrous apex
Hardjasudarma, M., K. R. Parker, et al. (1996), AJR Am J Roentgenol 167(1): 284-5.

Arterial injury by cholesterol oxidation products causes endothelial dysfunction and arterial wall cholesterol accumulation
Rong, J. X., S. Rangaswamy, et al. (1998), Arterioscler Thromb Vasc Biol 18(12): 1885-94.
Abstract: Cholesterol oxidation products (ChOx) have been reported to cause acute vascular injury in vivo; however, the pharmacokinetics of ChOx after administration and the mechanisms by which they cause chronic vascular injury are not well understood. To further study the pharmacokinetics and atherogenic properties of ChOx, New Zealand White rabbits were injected intravenously (70 mg per injection, 20 injections per animal) with a ChOx mixture having a composition similar to that found in vivo during a 70-day period. Total ChOx concentrations in plasma peaked almost immediately after a single injection, declined rapidly, and returned to preinjection levels in 2 hours. After multiple injections, the ChOx concentrations rose gradually to levels 2- to 3-fold above baseline levels, increasing mostly in the cholesteryl ester fraction of LDL and VLDL. Rabbit serum and the isolated LDL/VLDL fraction containing elevated ChOx concentrations were cytotoxic to V79 fibroblasts and rabbit aortic endothelial cells. At the time of killing, cholesterol levels in the aortas from ChOx-injected rabbits were significantly elevated despite the fact that plasma cholesterol levels remained in the normal range. In addition, aortas from the ChOx-injected rabbits retained more 125I-labeled horseradish peroxidase, measured 20 minutes after intravenous injection. Transmural concentration profiles across the arterial wall also showed increased horseradish peroxidase accumulation in the inner half of the media from the thoracic aorta in ChOx-injected rabbits. In conclusion, ChOx injection resulted in accumulation of circulating ChOx and induced increased vascular permeability and accumulation of lipids and macromolecules. This study reveals that even under normocholesterolemic conditions, ChOx can cause endothelial dysfunction, increased macromolecular permeability, and increased cholesterol accumulation, parameters believed to be involved in the development of early atherosclerotic lesions.

Arterial remodeling in the left coronary system: the role of high-density lipoprotein cholesterol
Taylor, A. J., A. P. Burke, et al. (1999), J Am Coll Cardiol 34(3): 760-7.
Abstract: OBJECTIVES: We sought to evaluate the plaque and patient variables related to arterial remodeling responses of early, de novo atherosclerotic lesions involving the left coronary artery. BACKGROUND: Coronary artery remodeling is a lesion-specific process involving either enlargement or shrinkage of atherosclerotic coronary arteries. There are little histologic data available correlating plaque morphologic and patient clinical characteristics with the degree and type of arterial remodeling in early atherosclerosis. METHODS: We studied 736 serial arterial sections from the left coronary system of 97 autopsy cases (mean age 33 +/- 11 years) by correlating the arterial remodeling response to plaque with demographic, serologic and histologic variables. Using the most proximal section as a reference, and considering the expected degree of internal elastic lamina tapering, remodeling was classified as positive (including neutral remodeling or compensatory enlargement) or negative. RESULTS: Remodeling was classified as positive in 84.3% (compensatory in 30.6%) and negative in 15.7% of sections with an overall mean luminal stenosis of 10.4 +/- 9.9%. In the lesions with the greatest arterial cross-sectional narrowing from each case, compensatory enlargement was associated with higher high-density lipoprotein (HDL) cholesterol (59.4 +/- 27.2 mg/dl) compared with either neutral (49.3 +/- 15.5 mg/dl) or negative remodeling (30.4 +/- 5.2 mg/dl; p = 0.019). In subjects with advanced atherosclerosis (maximum American Heart Association histologic grade 5 atherosclerosis), there was a modest linear relationship between higher HDL cholesterol and the propensity for positive remodeling (r2 = 0.37; p = 0.025). On multivariate analysis, only HDL cholesterol was related to the arterial remodeling response. CONCLUSIONS: Negative arterial remodeling occurs in early atherosclerosis. Higher HDL cholesterol may favor positive remodeling.

Arteriosclerotic lesions of the distal small coronary artery in cholesterol-fed rabbits differ from those in watanabe heritable-hyperlipidemic rabbits
Nakamura, M. and S. Abe (1997), Ann N Y Acad Sci 811: 420-3.

Artery interposed to vein did not develop atherosclerosis and underwent atrophic remodeling in cholesterol-fed rabbits
Zhang, H., A. Sun, et al. (2004), Atherosclerosis 177(1): 37-41.
Abstract: Autologous vein grafts interposed to arteries are susceptible to the development of accelerated atherosclerosis. The effect of grafted artery interposed to vein on the atherosclerosis development and vascular remodeling is unknown. We investigated, therefore, the morphologic changes of artery grafts to vein in hyperlipidemic rabbits. Left common carotid artery grafts, approximately 5 cm long, were placed in the right external jugular vein position of 24 New Zealand White rabbits. After surgery, rabbits were fed with high lipid diet for 1, 2, 4 and 12 weeks, respectively. Serum lipid levels were measured and the right common carotid artery and grafted left common carotid artery were harvested at above mentioned time points. Serum lipid levels were also measured in six rabbits receiving normal chow. Vessel wall thickness was measured and analyzed by image processing system. Hyperlipidemia occurred in all rabbits fed with high lipid diet. Fatty streak and atherosclerotic plaques were observed and lipid drops enriched in medial smooth muscle cells in control right common carotid arteries 4 weeks after surgery. In the grafted arteries, no fatty streak and atherosclerotic plaque were seen and the vessel wall thickness decreased continuously after surgery (before surgery: 107.32 +/- 4.57 microm; 1 week: 94.50 +/- 5.78 microm*; 2 weeks: 87.00 +/- 5.32 microm*; 4 weeks: 40.17 +/- 5.11 microm*;12 weeks: 18.00 +/- 4.93 microm*, *p <0.05 versus before surgery). Three months after surgery, grafted arteries possess similar structures as that of veins. The artery interposed to vein did not develop atherosclerosis and underwent atrophic remodeling in cholesterol-fed rabbits suggesting that local hemodynamic load was the most important determinant influencing the development of atherosclerosis.

Artifactual oxidation of cholesterol during the analysis of cholesterol oxidation products: protective effect of antioxidants
Guardiola, F., S. Garcia-Cruset, et al. (2004), J AOAC Int 87(2): 493-8.
Abstract: To study the influence of the addition of various antioxidants and their combinations on the artifactual oxidation of cholesterol during analysis, 2 factorial experiments were performed in duplicate. In the first experiment, 2 amounts of the following antioxidants were assayed: ethylenediaminetetraacetic acid (EDTA) disodium salt (0 and 1 mg), pyrogallol (0 and 600 microg), and butylated hydroxytoluene (BHT; 0 and 600 microg); in the second, EDTA disodium salt (0 and 1 mg), ascorbyl palmitate (0 and 600 microg), and BHT (0 and 600 microg). Under low oxidative conditions of dim light, evaporation of solvents at low temperatures, and cold saponification in darkness under nitrogen atmosphere, the addition of antioxidants showed no further protective effect. Furthermore, the presence of ascorbyl palmitate significantly increased the formation of cholesterol-5beta,6beta-epoxide, and 7beta-hydroxycholesterol.

Artifactual undetectable HDL-cholesterol with the Beckman synchron LX and vitros 950 assays temporally associated with a paraprotein
Baca, A., R. J. Haber, et al. (2004), Clin Chem 50(1): 255-6.

Artificial cell microcapsules containing genetically engineered E. coli DH5 cells for in-vitro lowering of plasma potassium, phosphate, magnesium, sodium, chloride, uric acid, cholesterol, and creatinine: a preliminary report
Prakash, S. and T. M. Chang (1999), Artif Cells Blood Substit Immobil Biotechnol 27(5-6): 475-81.
Abstract: Lowering of plasma Mg, P, Na, Cl, uric acid, cholesterol, and creatinine is required in renal failure and other diseases. In this preliminary report, we studied the ability of artificial cells microencapsulated genetically engineered E. coli DH5 cells in lower K, Mg, P, Na, Cl, uric acid, cholestrol, creatinine, and billirubin from plasma in-vitro. Result shows that this novel approach has the ability to significantly lower these metabolites from the plasma in-vitro.

Artificial lipid-protein complexes accelerate cholesterol crystallisation in model bile
Hrbasova, M., R. Vondruskova, et al. (2000), Int J Biochem Cell Biol 32(6): 609-19.
Abstract: Cholesterol gallstone disease is one of the major health problems in the world. Substances which can affect the crystallisation of cholesterol from human bile have been given considerable attention. Various substances (among them natural lipid-protein complexes) have been tested for cholesterol crystallisation-promoting activity. Various artificial lipid-albumin complexes have been prepared of which taurodeoxycholate-human serum albumin-calcium ions (TDC-HSA-Ca(2+)) had the highest cholesterol crystallisation-promoting activity. This cholesterol crystallisation-promoting activity is similar to that for the lipid-protein complex isolated from native human bile concanavalin A nonbinding fraction (con A(-) fraction). Addition of cholesterol to the TDC-HSA-Ca(2+) complex further increased the cholesterol crystallisation-promoting activity whereas the addition of lecithin had an opposite effect. The interaction of individual components of the TDC-HSA-Ca(2+) complex was followed using several methods. A new effect of Ca(2+) ions (increase in the number of binding sites for bile salts) on the interaction of TDC with HSA was found by equilibrium dialysis. Interaction of TDC with albumin and Ca(2+) did not induce any modification of the secondary structure of albumin. The results of fluorescence spectroscopy may indicate that TDC is at least partially bound to not essentially fatty acid free HSA somehow via admixtures, probably fatty acids. Difference absorption spectrum of the TDC-HSA-Ca(2+)-cholesterol complex was very similar to that of the "natural" lipid-protein complex (con A(-) fraction). From the three drugs with different albumin binding characteristics, only sulphadimethoxin had an observable effect on the cholesterol crystallisation-promoting activity. The action of the TDC-HSA-Ca(2+) complex decreased significantly after the addition of sulphadimethoxin. The addition of TDC modified the absorption spectrum of the sulphadimethoxin-HSA-Ca(2+) complex. It can be suggested that the complex of HSA with bile salts (TDC mainly) and Ca(2+) forms a nucleation centre for cholesterol crystallisation in bile.

Ascitic fluid cholesterol in differential diagnosis of ascites
Garg, R., A. Sood, et al. (1993), J Assoc Physicians India 41(10): 644-6.
Abstract: Cholesterol was estimated in ascitic fluid of 89 patients (29 malignant and 60 non-malignant ascites). Mean ascitic cholesterol level was significantly higher in malignant ascites (89.52 mg/dl) as compared to non-malignant ascites (29.93 mg/dl). At a cut off value of 48 mg/dl, the sensitivity, specificity, positive and negative predictive value and overall diagnostic accuracy for diagnosing malignant ascites is 96.5%, 96.6%, 93.3%, 98.3% and 96.6% respectively. Ascitic fluid cholesterol estimation is an easy and reliable test for differentiating malignant ascites from non-malignant ascites.

Ascitic fluid cholesterol in malignant and tubercular ascites
Sood, A., R. Garg, et al. (1995), J Assoc Physicians India 43(11): 745-7.
Abstract: Cholesterol was estimated in ascitic fluid of 44 patients (29 malignant and 15 tubercular). Mean ascitic cholesterol level was significantly higher in malignant ascites (89.52 mg/dl) as compared to tubercular ascites (35.07 mg/dl). At a cut off value of 54.5 mg/dl (mean in tubercular ascites + 2SD), the sensitivity, specificity, positive and negative predictive value and overall diagnostic accuracy for differentiating malignant from tubercular ascites was found to be 89.65%, 100%, 100%, 83.33% and 93.18% respectively. Ascitic fluid cholesterol estimation is a reliable and simple test for differentiating malignant ascites from tubercular ascites.

Ascitic fluid concentrations of fibronectin and cholesterol: comparison of differential diagnostic value with the conventional protein determination
Gerbes, A. L., Y. N. Xie, et al. (1990), Liver 10(3): 152-7.
Abstract: Ascitic fluid concentrations of fibronectin, cholesterol and protein were determined in 95 patients: 38 with cirrhosis of the liver, 10 with miscellaneous nonmalignant diseases, 43 with peritoneal carcinomatosis and 4 with liver metastases or hepatocellular carcinoma. Fibronectin, cholesterol and protein at discrimination values of 7.5 mg/100 ml, 45 mg/100 ml and 3.0 g/100 ml, respectively, separated patients with peritoneal carcinomatosis from patients with cirrhosis with an efficiency of 94%, 90% and 85%, respectively. Thus, ascitic fluid determinations of fibronectin and cholesterol offer good discrimination of cirrhotic ascites from ascites related to peritoneal carcinomatosis, superior to the conventional protein determination. However, the failure of all parameters to distinguish ascites caused by miscellaneous nonmalignant diseases from malignancy-related ascites underscores the importance of highly specific methods to confirm a suspected diagnosis of malignancy-related ascites.

Ascorbate administration to normal and cholesterol-fed rats inhibits in vitro TBARS formation in serum and liver homogenates
Santillo, M., P. Mondola, et al. (1996), Life Sci 58(14): 1101-8.
Abstract: We have recently shown that ascorbate has a hypocholesterolemic and hypotriglyceridemic effect on rats fed a diet enriched with 1.5% cholesterol and 25% hydrogenated coconut oil (Nath diet). In this study we evaluated the effect of intraperitoneal ascorbate administration on susceptibility to lipoperoxidation either in rats fed standard or Nath diet. In normal rats ascorbate treatment decreased (p<0.05) the susceptibility to lipoperoxidation induced by incubation of serum for 24 hours with 2.2 mM Cu++, without altering the normal serum fatty acid profile. In rats fed Nath diet we observed a reduced susceptibility of serum to CU++-induced lipoperoxidation (36%), according with their low levels of serum unsaturated fatty acids (40% less than rats fed standard diet). In these animals ascorbate administration affects serum fatty acid profile leading to a decrease of S/U ratio from 1.6 to 1.2 without significantly modifying the susceptibility of serum to lipoperoxidation. Moreover, the production of spontaneous lipid peroxides in liver homogenates, measured as TBARS levels, was strongly inhibited by ascorbate (p<0.01) in rats fed either standard or Nath diet. These data indicate that ascorbate administration exerts an antioxidant effect and that in hypercholesterolemic rats, in addition to a lipid lowering effect, ascorbate exerts a protective role against the peroxidative damage of lipids.

Ascorbic acid and cholesterol gallstones
Simon, J. A. (1993), Med Hypotheses 40(2): 81-4.
Abstract: Decreased activity of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in the catabolism of cholesterol to bile acids, is known to result in increased biliary cholesterol concentration and supersaturation of bile. Supersaturation of bile by cholesterol is a necessary condition for cholesterol gallstone formation. In guinea pigs, the hepatic concentration of ascorbic acid affects the catabolism of cholesterol: hypovitaminosis C reduces cholesterol 7 alpha-hydroxylase activity. Cholesterol gallstones are frequently found in ascorbic acid-deficient guinea pigs. Risk factors for cholesterol gallstones in humans include obesity, aging, estrogen treatment, pregnancy and diabetes. Plasma ascorbic acid levels are reduced in these groups. Vegetarian diets, which typically have high ascorbic acid contents, protect against gallstones. Since ascorbic acid effects the rate-limiting step in the catabolism of cholesterol in the guinea pig and many human risk groups for cholesterol gallstones are associated with reduced ascorbic acid levels, ascorbic acid may play a contributory role in human gallbladder disease.

Ascorbic acid deficiency elevates serum level of LDL-cholesterol in a rat mutant unable to synthesize ascorbic acid
Horio, F., N. Takahashi, et al. (1991), J Nutr Sci Vitaminol (Tokyo) 37(1): 63-71.
Abstract: The effect of ascorbic acid deficiency on serum levels of high density lipoprotein- (HDL-), low density lipoprotein- (LDL-), very low density lipoprotein- (VLDL-) and chylomicron-cholesterol was examined in ODS-od/od rat (ODS rat), that is a rat mutant unable to synthesize ascorbic acid. Male ODS rats were fed an ascrobic acid-free diet for 20 days. In another two groups, the diet supplemented with 300 mg ascorbic acid/kg diet was fed either ad libitum (ad libitum control) or in pair-feeding (pair-fed control). Pair-fed rats received the same amount of diet as rats fed the ascorbic acid-free diet. Serum level of total cholesterol in the ad libitum control rats, ascorbic acid-deficient rats, and the pair-fed control rats were 100.1 +/- 8.4 mg/dl, 92.8 +/- 6.2 mg/dl and 72.2 +/- 4.8 mg/dl, respectively. The level of LDL-cholesterol in ascorbic acid-deficient rats was significantly higher than that in the ad libitum control or that in the pair-fed control. The level of HDL-cholesterol in ascorbic acid-deficient rats was lower than that in the ad libitum control, but was not changed as compared with that in the pair-fed control. Ascorbic acid deficiency did not affect serum level of VLDL-cholesterol or chylomicron-cholesterol as compared with those in the controls. These results demonstrate that ascorbic acid deficiency causes the elevation of serum level of LDL-cholesterol both in ad libitum feeding condition and pair feeding condition.

Asialoganglioside enhances the efficiency of gene transfection mediated by cationic liposomes with a cationic cholesterol derivative
Noguchi, S., N. Hirashima, et al. (2003), Biol Pharm Bull 26(9): 1306-10.
Abstract: We investigated the transfection efficiency mediated by asialoganglioside-containing cationic liposomes. Previously we reported that monosialoganglioside GM(1) (GM(1a)) enhanced transfection efficiency. In this study, we investigated the effects of sialic acid in gangliosides on transfection efficiency. Two mammalian culture cell lines HeLa and HepG2 were transfected with luciferase plasmids (pGL3) using cationic liposomes which contain monosialoganglioside GM(1) (GM(1a)) or its asialic counterpart, asialoganglioside GM(1) (GA(1)). Both GM(1a) and GA(1) enhanced the efficiency of transfection mediated by cationic liposomes, and GA(1) exhibited higher efficiency than GM(1a) in both cell lines. Transfection efficiency of ganglioside-containing liposomes was also assessed by the effects of antisense oligonucleotides (AS-ODN) for bcl-2 gene, which suppresses apoptotic cell death. Western blotting analysis revealed that the expression of Bcl-2 was decreased by AS-ODN, and the reduction of protein expression in cells treated with GA(1)-containing liposomes was more remarkable than that with GM(1a)-containing liposomes. Furthermore, the induction rate of apoptosis was higher in cells treated with AS-ODN with GA(1)-containing liposomes. Together with the results obtained by luciferase assay mentioned above, the removal of sialic acid from ganglioside causes the enhancement of efficiency of transfection mediated by cationic liposomes.

Ask the doctor. At age 62 I'm a bit overweight and have diabetes. I take a statin, and my LDL cholesterol is good (84 mg/dL). But my HDL is low (30 mg/dL) and my triglycerides are above 300 mg/dL. Are high triglycerides a problem?
Lee, T. H. (2003), Harv Heart Lett 13(7): 8.

Ask the doctor. I am a 73-year-old woman and just found out that I have very high LDL cholesterol (197 mg/dL). I don't have any symptoms of heart disease and I hate taking pills, so I am reluctant to take cholesterol-lowering drugs. One doctor told me I should have a special CT scan of my heart to help decide whether to take medications, but I learned I would have to pay $750 for the test since it isn't covered by insurance. Should I do it?
Lee, T. H. (2001), Harv Heart Lett 11(12): 8.

Ask the doctor. I read somewhere that cocoa butter doesn't raise cholesterol levels even though it contains a lot of saturated fat. If this is true, can I eat dark chocolate without worrying about what it's doing to my heart and blood vessels?
Hosmer, C. (2003), Harv Heart Lett 14(3): 8.

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