Cholesterol Journal Articles

Record 3701 to 3720

Cord blood cholesterol in term and preterm newborns
Singh, J., M. Purohit, et al. (1994), Indian Pediatr 31(10): 1278-81.

Corn fiber oil lowers plasma cholesterol by altering hepatic cholesterol metabolism and up-regulating LDL receptors in guinea pigs
Ramjiganesh, T., S. Roy, et al. (2002), J Nutr 132(3): 335-40.
Abstract: To evaluate some of the mechanisms involved in the hypocholesterolemic effects of corn fiber oil (CFO), male Hartley guinea pigs were fed diets containing increasing doses of CFO 0 (control), 5, 10 or 15 g/100 g. Total fat was adjusted to 15 g/100 g in all diets with regular corn oil. Diets contained 0.25 g/100 g cholesterol. A positive control group (LC) with low dietary cholesterol (0.04 g/100 g) was also included. Plasma LDL cholesterol concentrations were 32, 55 and 57% (P < 0.0005) lower with increasing doses of CFO. Compared with controls, intake of CFO resulted in 27-32% lower hepatic microsomal cholesterol (P < 0.0001), the regulatory pool of LDL receptor (LDL-R) expression. CFO intake resulted in favorable plasma and hepatic cholesterol concentrations, similar to those in guinea pigs fed the LC diet. Hepatic cholesterol 7alpha-hydroxylase (CYP7) activity was approximately 88% higher in guinea pigs fed the two higher dosages of CFO (P < 0.05). In parallel, CYP7 mRNA abundance was approximately 88% higher in guinea pigs fed all three CFO diets. CFO treatment also induced hepatic LDLR mRNA by 66-150% with significant differences at the highest CFO dose. These results suggest that CFO, as a result of decreased bile acid absorption, increased mRNA abundance and activity of CYP7. Because hepatic cholesterol is the substrate for CYP7, a lowering of cholesterol concentrations in the total and microsomal pools was observed. As a response to the depleted microsomal free cholesterol pool, the LDL receptor was up-regulated, drawing more cholesterol from plasma, thus leading to the observed decrease in plasma LDL cholesterol concentrations.

Corn oil and beef tallow elicit different postprandial responses in triglycerides and cholesterol, but similar changes in constituents of high-density lipoprotein
Muesing, R. A., P. Griffin, et al. (1995), J Am Coll Nutr 14(1): 53-60.
Abstract: OBJECTIVE: The study was designed to compare, in a homogeneous, normolipidemic population, the postprandial responses of plasma lipids, in particular, high-density lipoprotein (HDL) constituents, after administration of a polyunsaturated fat and a more saturated fat. METHODOLOGY: Emulsions of 100 g corn oil (CO) and 100 g beef tallow (BT) were given in a crossover protocol to 12 male subjects (21-24 years). Plasma cholesterol (TC), triglycerides (TG), and HDL lipid and protein constituents were measured at 0, 2, 4, 7 and 10 hours. RESULTS: A postprandial increase in TG at 2 hours after CO ingestion (96%) was twice that with BT (48%); TG returned to near fasting levels at 10 hours after ingestion of either fat. Areas under the TG response curves for CO and BT were 6.29 +/- 1.67 and 1.75 +/- 0.60 mmol x hour/L (mean +/- SE), respectively. TC and low-density lipoprotein cholesterol (LDL-C) levels were unchanged at 10 hours after CO ingestion, but they were increased 8.1% and 9.3%, respectively, with BT. Both fats increased HDL TG at 2-4 hours, and both similarly increased HDL free cholesterol, cholesterol ester, phospholipid, apolipoproteins A-I and A-II, and lipoprotein (A-I) levels at 7-10 hours. Changes in HDL were predominantly in HDL3. CONCLUSIONS: The increase in LDL-C with BT at 10 hours suggests that levels may be abnormally elevated in "fasting" samples, dependent on the amount and type of fat in a prior meal. The increase in LDL-C is consistent with short-term regulation of hepatic LDL-receptor activity and/or LDL synthesis. Similar increases in HDL constituents at 7-10 hours after CO or BT, despite the difference in TG responses, suggests differences in the metabolism of chylomicrons and/or HDL due to the type of fat ingested.

Coronaries, cholesterol and children. The 1989 Long Fox lecture
Lloyd, J. K. (1990), West Engl Med J 105(1): 7-11.

Coronary arteriography as a cause of disseminated cholesterol emboli
Peten, E., J. P. Cosyns, et al. (1990), Nephrol Dial Transplant 5(2): 155-7.

Coronary artery calcification and dietary cholesterol intake in Korean men
Oh, K. W., C. M. Nam, et al. (2002), Acta Cardiol 57(1): 5-11.
Abstract: OBJECTIVE: This study was performed to examine the relationship between dietary cholesterol intake and coronary artery calcification (CAC) score in healthy men. METHODS: Electron beam computed tomography (EBCT) was used to examine the CAC score in 135 Korean men aged 40-81 years who did not have clinical illness. Dietary cholesterol intake was assessed by a nutritionist using a semiquantitative food frequency method. Body mass index (BMI), serum lipid levels, cigarette use, alcohol intake, exercise, and a past history of cardiovascular disease were determined during interview and examination. RESULTS: The resultant median CAC score among those who experienced CAC was 22.5 (1-697) and average intakes of total fat and cholesterol were 22.4% (13.8-40.7) of total energy intake and 306.0 mg/day (84-1191). When the participants were classified into high (> or = 75 percentile) and low (< 75 percentile) CAC score groups, multiple logistic analysis showed that the cholesterol intake (per 10 mg/1000 kcal of energy) was significantly related to a high CAC score (OR 1.12: 95% CI 1.02-1.24), after adjustment for age, BMI, serum triglyceride level, past history of hypertension, past history of hyperlipidaemia, and energy intake. Also, when participants were classified into 2 groups (CAC score > or = 100 vs. < 100), cholesterol intake was found to be significantly related to CAC score. However, fatty acid intakes were not significantly related to the CAC score. CONCLUSION: These results suggest that in a population with a relatively low risk of coronary heart disease, higher cholesterol intake may increase the level of CAC.

Coronary artery disease risk predicted by plasma concentrations of high-density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B, and lipoprotein(a) in a general Chinese population
Wu, J. H., J. T. Kao, et al. (1993), Clin Chem 39(2): 209-12.
Abstract: We measured lipid and lipoprotein concentrations in blood samples from control subjects and patients with coronary artery disease (CAD) in Taiwan. We found significant differences (P < 0.01) in the concentrations of high-density lipoprotein cholesterol (HDLC), apolipoprotein AI (ApoAI), apolipoprotein B (ApoB), and lipoprotein(a) Lp(a). Concentrations of HDLC < 350 mg/L, ApoAI < 900 mg/L, ApoB > 800 mg/L, and Lp(a) > 200 mg/L occurred, respectively, 2.8, 5.2, 1.7, and 2.3 times more frequently in the patients than in the control group. If one considers HDLC at < 350 mg/L, ApoAI at < 900 mg/L, ApoB at > 800 mg/L, and Lp(a) at > 200 mg/L as separate risk factors for CAD, the ratio of individual patients to control subjects having 4, 3, 2, 1, or 0 risk factors was symbol: see text 9.4, 2.1, 0.2, 0.2, respectively. Individuals displaying three or more risk factors were found 15 times more frequently in the CAD group than in the control group. These risk factors may be used clinically for the prediction and prevention of CAD in the general population.

Coronary artery disease, hypertension, ApoE, and cholesterol: a link to Alzheimer's disease?
Sparks, D. L. (1997), Ann N Y Acad Sci 826: 128-46.
Abstract: The premature presence of senile plaques (SP) in coronary artery disease (CAD), and neurofibrillary tangles (NFT) as well as SP in hypertension (HyperT), suggest a neuropathologic link between CAD, HyperT, and AD. Previous MI, CAD and HyperT often occur in and may increase the risk of AD. Expression of Apo-E4 likely increases risk of CAD by elevating blood cholesterol and the risk of AD via proposed interactions with beta-amyloid and/or free radicals (FRs). Any Apo-E4 effect is vague, but FRs probably mediate vascular damage in HyperT. Increasing FR content in the blood is related to increasing CAD severity, while the severity of elevated FR level correlates with how deep into a blood vessel there is activation of the FR scavenger enzyme, superoxide dismutase (SOD). The ApoE genotype and SP/NFT areal densities were determined in a large population of non-demented CAD, HyperT and non-heart disease (non-HD) control subjects, and compared to findings in a similar number of AD patients. ApoE immunoreactivity was determined in many individuals. Cholesterol content in cortex was determined by HPLC in a small, loosely age-matched group of Apo-E4 genotype-matched AD, CAD and non-HD subjects. SOD immunoreactivity was also assessed in a number of subjects. The Apo-E4 genotype frequency was increased in CAD, HyperT and AD compared to non-HD controls. Dose of Apo-E4 correlated with SP densities, but not NFT, and only in the non-demented groups. Essentially all SP in CAD, HyperT and non-HD subjects were ApoE-immunoreactive. Cortical cholesterol was increased in CAD and AD compared to controls. SOD immunoreactivity was similar in HyperT and AD; SP were immunodecorated in both. AD, CAD and HyperT may be linked, while CAD and HyperT subjects may die of heart disease before showing cognitive change.

Coronary event secondary prevention with statins irrespective of LDL-cholesterol
Kerst, L. L. and V. F. Mauro (2004), Ann Pharmacother 38(6): 1060-4.
Abstract: OBJECTIVE: To review the evidence for statin secondary prevention of coronary artery disease in patients with near-optimal or optimal low-density lipoprotein cholesterol (LDL-C). DATA SOURCES: A MEDLINE search (1966-October 2003) was conducted using the search terms HMG-CoA reductase inhibitor, statins, coronary disease, post-myocardial infarction, and average cholesterol. DATA SYNTHESIS: Secondary prevention trials enrolling subjects with near-optimal (<130 mg/dL) or optimal (<100 mg/dL) baseline LDL-C were included. Early statin secondary prevention studies suggested attenuated benefit, but more recent trials challenge this finding. CONCLUSIONS: Statin secondary prevention of coronary artery disease in patients near goal LDL-C is controversial, but recent trial results show promise.

Coronary heart disease in patients with low LDL-cholesterol: benefit of pravastatin in diabetics and enhanced role for HDL-cholesterol and triglycerides as risk factors
Sacks, F. M., A. M. Tonkin, et al. (2002), Circulation 105(12): 1424-8.
Abstract: BACKGROUND: In two large secondary prevention trials of pravastatin, risk reduction was not significant in participants who had low baseline LDL-C concentrations (that is, <125 mg/dL). We conducted exploratory analyses of participant characteristics, lipid risk factors, and risk reduction in this group. METHODS AND RESULTS: Among 13 173 participants with coronary heart disease (CHD), 2607 had baseline LDL-C <125 mg/dL. Those with LDL-C <125 compared with > or =125 mg/dL were more likely to be diabetic (15% versus 9%), hypertensive (46 versus 41%), and male (89% versus 83%); they had higher triglycerides (169 versus 154 mg/dL), lower HDL-C (36.5 versus 38 mg/dL), and similar body mass index (27 kg/m2); and pravastatin lowered their LDL-C by 36 mg/dL (32%) versus 45 mg/dL (29%). During 5.8-year (mean) follow-up, HDL-C and triglycerides were both significantly stronger predictors of recurrent CHD events in participants with LDL-C <125 than > or =125 mg/dL. In diabetic participants with low LDL-C, pravastatin decreased CHD events from 34% to 22% (relative risk, 0.56; 95% CI, 0.37 to 0.83; P=0.004), significantly different from the effect in nondiabetic participants with low LDL-C (P interaction, 0.005) (event rate, 21%; relative risk, 1.06 95% CI, 0.89 to 1.27). There were trends toward risk reduction in smokers and in those with low HDL-C, <40 mg/dL. CONCLUSIONS: Among patients with CHD who have low LDL-C, diabetics have much higher subsequent CHD event rates than do nondiabetics. Pravastatin reduced the event rate in diabetics to that of nondiabetic participants. The results also suggest enhanced therapeutic potential for improving HDL-C and triglycerides in patients with CHD who have low LDL-C concentrations.

Coronary heart disease prediction from lipoprotein cholesterol levels, triglycerides, lipoprotein(a), apolipoproteins A-I and B, and HDL density subfractions: The Atherosclerosis Risk in Communities (ARIC) Study
Sharrett, A. R., C. M. Ballantyne, et al. (2001), Circulation 104(10): 1108-13.
Abstract: BACKGROUND: Despite consensus on the need for blood cholesterol reductions to prevent coronary heart disease (CHD), available evidence on optimal cholesterol levels or the added predictive value of additional lipids is sparse. METHODS AND RESULTS: After 10 years follow-up of 12 339 middle-aged participants free of CHD in the Atherosclerosis Risk in Communities Study (ARIC), 725 CHD events occurred. The lowest incidence was observed in those at the lowest LDL cholesterol (LDL-C) quintile, with medians of 88 mg/dL in women and 95 mg/dL in men, and risk accelerated at higher levels, with relative risks (RRs) for the highest quintile of 2.7 in women and 2.5 in men. LDL-C, HDL-C, lipoprotein(a) Lp(a), and in women but not men, triglycerides (TG) were all independent CHD predictors, providing an RR, together with blood pressure, smoking, and diabetes, of 13.5 in women and 4.9 in men. Lp(a) was less significant in blacks than whites. Prediction was not enhanced by HDL-C density subfractions or apolipoproteins (apo) A-I or B. Despite strong univariate associations, apoB did not contribute to risk prediction in subgroups with elevated TG, with lower LDL-C, or with high apoB relative to LDL-C. CONCLUSIONS: Optimal LDL-C values are <100 mg/dL in both women and men. LDL-C, HDL-C, TG, and Lp(a), without additional apolipoproteins or lipid subfractions, provide substantial CHD prediction, with much higher RR in women than men.

Coronary heart disease prevention. Are there differences in cholesterol synthesis inhibitors?
Muller-Wieland, D., M. Faust, et al. (2000), MMW Fortschr Med 142(30): 26-8.
Abstract: All statins have been shown to reduce plasma cholesterol concentrations significantly. Cardioprotective effects of these drugs appear to be mainly due to cholesterol lowering. It remains unclear whether pharmacokinetic differences of statins are of clinical relevance. The clinical studies with statins performed on more than 30,000 individuals demonstrate that lipid lowering drug therapy not only reduces cardiovascular complications but also is a safe and well tolerated long-term therapy. However, the majority of patients who should be treated according to appropriate guidelines, still do not receive any cholesterol lowering therapy. Therefore, it is a main goal that at least high-risk patients (e.g. with coronary heart disease or diabetes mellitus type 2) should be treated with statins.

Coronary revascularization with reduction of serum cholesterol level using LDL apheresis in patient with homozygous familial hypercholesterolemia
Takahashi, T., K. Ihara, et al. (1990), Kokyu To Junkan 38(9): 925-30.
Abstract: We reported a case of a 48-year-old male with homozygous familial hypercholesterolemia who underwent coronary revascularization successfully. Coronary artery bypass grafting (CABG) utilizing internal mammary artery graft to LAD, and percutaneous transluminal angioplasty for residual stenosis after CABG was able to relieve symptomatic myocardial ischemia. LDL apheresis every two weeks in addition to combined drug treatment had maintained total cholesterol at an acceptable level (120-280 mg/dl) before and after CABG. It was confirmed by repetition of coronary angiography at one year after CABG that all grafts were widely patent, and the native coronary artery did not accelerate the atherosclerotic lesion. It was important in patients with homozygous familial hypercholesterolemia, to carry out active coronary revascularization with reduction of serum cholesterol level by using LDL apheresis.

Coronary risk assessment methods and cholesterol lowering
Ramsay, L. E., E. J. Wallis, et al. (1999), Lancet 353(9158): 1095; author reply 1096-7.

Coronary risk assessment methods and cholesterol lowering
Robson, J. (1999), Lancet 353(9158): 1097.

Coronary risk assessment methods and cholesterol lowering
Wight, J. (1999), Lancet 353(9158): 1096-7.

Correction of hypertriglyceridemia with low high-density lipoprotein cholesterol by the novel compound NO-1886, a lipoprotein lipase-promoting agent, in STZ-induced diabetic rats
Tsutsumi, K., Y. Inoue, et al. (1995), Diabetes 44(4): 414-7.
Abstract: We have previously reported that the novel compound NO-1886 increased lipoprotein lipase (LPL) activity, with resulting elevation of high-density lipoprotein (HDL) cholesterol in normal rats (J Clin Invest 92:411-417, 1993). The aim of this study was to ascertain whether the compound has the same action in diabetes, because hypertriglyceridemia with low HDL cholesterol is an extremely common concomitant condition in diabetes. Streptozotocin-induced diabetic rats showed marked elevation of plasma triglyceride and reduction of HDL cholesterol. Both single and repeated administration of NO-1886 increased postheparin plasma LPL activity, with resulting reduction of plasma triglyceride and elevation of HDL cholesterol. Repeated administration increased the amount of LPL mRNA in adipose tissue and myocardium. The compound had no effects on plasma glucose and insulin levels. Our study indicates that the compound is potentially beneficial for the treatment of hypertriglyceridemia with low HDL cholesterol in diabetes.

Correction of increased thrombogenic potential with cholesterol reduction is mainly due to vascular wall
Karanikas, G., H. Kritz, et al. (1997), Circulation 96(6): 2097-9.

Correlates of high HDL cholesterol among women with coronary heart disease
Bittner, V., J. A. Simon, et al. (2000), Am Heart J 139(2 Pt 1): 288-96.
Abstract: BACKGROUND: The National Cholesterol Education Program (NCEP) has designated high-density lipoprotein cholesterol (HDL-C) > or =60 mg/dL a "negative" coronary heart disease (CHD) risk factor, but a substantial proportion of coronary events occur among women despite high HDL-C levels. METHODS AND RESULTS: The objective of this study was to characterize postmenopausal women with prevalent CHD despite HDL-C > or =60 mg/dL and to identify factors that may attenuate the protective effect of high HDL-C. We analyzed baseline data from a randomized, double-blind study of estrogen/progestin replacement therapy in 2763 postmenopausal women <80 years old with CHD. Demographics, CHD risk factors, medications, anthropometrics, and lipid levels were compared among women with low, normal, and high HDL-C by NCEP criteria with and without stratification by use of lipid-lowering medications. Independent correlates of high HDL-C were determined by logistic regression analysis. HDL-C > or =60 mg/dL was present in 20% of participants. Women with high HDL-C were older, better educated, had fewer CHD risk factors, lower triglyceride levels and total cholesterol/HDL-C ratio, and were more likely to report past estrogen and current calcium antagonist, niacin, and statin use. beta-Blocker, diuretic, and fibrate use was less common. Older age, alcohol consumption, niacin, and calcium antagonist use and prior estrogen use were independently associated with high HDL-C, whereas waist-to-hip ratio, smoking, triglyceride level, and beta-blocker and fibrate use were inversely associated (all P <.05). CONCLUSIONS: High HDL-C, as defined by the NCEP, occurred in 20% of women with CHD in this cohort without a concomitantly higher prevalence of other CHD risk factors. Redefinition of "high" HDL-C levels for women may be warranted.

Correlates of high-density lipoprotein cholesterol in a sample of healthy workers
Jossa, F., M. Trevisan, et al. (1991), Prev Med 20(6): 700-12.
Abstract: METHODS. Correlates of high-density lipoprotein cholesterol are analyzed in a sample of 797 male workers in southern Italy participating in the Olivetti Heart Study. At the univariate level high-density lipoprotein cholesterol concentrations are positively related to alcohol consumption (r = 0.127; P less than or equal to 0.001) and sport activity (r = 0.074; P less than or equal to 0.05) and inversely related to body mass index (r = -0.160; P less than or equal to 0.001), serum triglycerides (r = -0.349; P less than or equal to 0.001), cigarette smoking (r = -0.227; P less than or equal to 0.001), and coffee consumption (r = -0.153; P less than or equal to 0.001). RESULTS. In the group as a whole, body mass index, alcohol consumption, cigarette smoking, and serum triglycerides remain significantly related to high-density lipoprotein cholesterol in the multivariate model, while the association with coffee intake and sport activity loses statistical significance. A significant negative interaction is reported between physical activity and cigarette smoking, and a positive significant linear trend between high-density lipoprotein cholesterol and sport activity is observed only in nonsmokers. CONCLUSION. These findings suggest that body mass index, alcohol consumption, cigarette smoking, serum triglycerides, and sport activity are important correlates of high-density lipoprotein cholesterol but that the positive significant association between sport activity and high-density lipoprotein cholesterol is absent in smokers.

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