| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Is cholesterol lowering with statins the gold standard for treating patients with cardiovascular risk and disease? Sinatra, S. T. (2003), South Med J 96(3): 220-2. |
| Is cholesterol reduction always safe? Oliver, M. F. (1992), Eur J Clin Invest 22(7): 441-2. |
| Is cholesterol testing/treatment really beneficial? Barratt, A. and L. Irwig (1993), Med J Aust 159(10): 644-7. |
| Is cholesterol testing/treatment really beneficial? d'Emden, M. (1994), Med J Aust 160(4): 237. |
| Is cholesterol testing/treatment really beneficial? Sullivan, D. (1994), Med J Aust 160(7): 450-1. |
| Is cholesterol testing/treatment really beneficial? Wurth, P. (1994), Med J Aust 160(4): 238. |
| Is cholesterol testing/treatment really beneficial? Wurth, P. J. (1994), Med J Aust 161(9): 575. |
| Is elevated cholesterol the cause of arteriosclerosis? Kaltenbach, M. (1995), Versicherungsmedizin 47(4): 112-6. Abstract: In post mortem studies the alterations produced by arteriosclerosis present a panorama of structural changes that defies the determination of an orderly sequence of events (Netter). Proliferation of fibromuscular vascular wall cell elements and over-production of extracellular matrix is quantitatively predominant. Lipid dispositions comprise less than 5% of the average plaque volume. Arteriosclerosis induced experimentally by cholesterol feeding and vessel wall traumatisation shows dependency in plaque composition from cholesterol feeding. The resulting vessel lumen narrowing is predominantly caused by overproliferation and equal with and without cholesterol feeding. The vision of arteriosclerosis as a "Proliferation disease" therefore appears more adequate than that as a "cholesterol storage disease". When patient groups are separated from coronary arteriography into those with normal coronary arteries and into those with coronary arteriosclerosis differences in cholesterol values are found below the age of 50 years, while above the age of 60 years no difference exists. In all groups the overlap is large and the individual risk can not be determined on the base of cholesterol levels. Between extend of angiographic changes and plasma lipid levels no correlation exists. Angiographic progression of disease which is closely correlated with clinical progression is independent of plasma cholesterol levels determined at the beginning of the observation period. The rate of restenosis after PTCA has been found to be independent of plasma cholesterol levels and can not be influenced by cholesterol lowering. In the report from the NHLBI on more than 600 000 individuals total mortality was independent from plasma cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Is elevated serum cholesterol level a risk factor for coronary heart disease in the elderly? Benfante, R. and D. Reed (1990), Jama 263(3): 393-6. Abstract: Since serum cholesterol is a major component in the causal pathway of atherosclerosis, a pathological process that usually progresses with age, we have evaluated reported findings of a diminished association between serum cholesterol level and coronary heart disease in the elderly. In the Honolulu (Hawaii) Heart Program, 1480 men aged 65 years and older and free of coronary heart disease were followed up for an average of 12 years. Incidence rates of coronary heart disease increased progressively from the lowest to the highest quartile of serum cholesterol level. The independent role of serum cholesterol level as a predictor of coronary heart disease risk was evaluated with other major risk factors using a Cox multivariate regression model. The upper-lower quartile relative risk for serum cholesterol level was 1.64 (95% confidence interval, 1.14 to 2.36). The relative risk for middle-aged men was also 1.64. The results suggest that serum cholesterol level is an independent predictor of coronary heart disease, even among men older than 65 years. Thus, an elevated serum cholesterol level in the elderly should be regarded, as in middle-aged men, to be an indicator for further evaluation of lipoprotein levels and possible intervention. |
| Is good cholesterol always good? Thompson, G. R. (2004), Bmj 329(7464): 471-2. |
| Is high density lipoprotein cholesterol useful in diagnosis of metabolic syndrome in native Africans with type 2 diabetes? Isezuo, S. A. (2005), Ethn Dis 15(1): 6-10. Abstract: BACKGROUND: High-density lipoprotein (HDL) hypocholesterolemia predicts metabolic syndrome among Caucasians and is one of the World Health Organization (WHO) diagnostic criteria of the syndrome. Plasma lipid levels are, however, influenced by genetic and environmental factors. OBJECTIVE: To determine the relationship between HDL cholesterol and metabolic syndrome among native Africans with type 2 diabetes. METHODS: Indigenous Nigerians with type 2 diabetes (N = 254) aged 35-80 years (mean: 52.0 +/- 11.7 years) with male:female ratio of 1.5:1 were studied prospectively. Outcome measures included anthropometric indices, plasma lipid concentrations, uric acid, microalbuminuria, and predictive values. RESULTS: Of the 254 diabetic patients, 150 (54.3%) had metabolic syndrome. Dyslipidemia occurred in 184 (72.4%) patients. Of these, 54 (29.4%) had HDL hypocholesterolemia. Mean HDL cholesterol among patients with HDL hypocolesterolemia and those with normocholesterolemia were 32.4 +/- 5.7 mg/dL and 51.3 +/- 9.9 mg/dL, respectively. Prevalence of metabolic syndrome did not differ significantly between the two groups (56% vs 70.4%; P =.08). Linear regression analysis showed no association between HDL cholesterol and metabolic syndrome (r = 0.01; P =.2), body mass index (r = 0.02; P =.4), waist circumference (r = 0.07; P =.42) and microalbuminuria (r = 0.03; P =.8). A positive correlation occurred between HDL cholesterol and triglyceride concentrations (r = 0.6). The sensitivity, specificity, and positive and negative predictive values of HDL hypocholesterolemia in the diagnosis of metabolic syndrome were 25%, 84.6%, 70.4%, and 44%, respectively. CONCLUSION: High-density lipoprotein cholesterol may not be a reliable diagnostic tool of metabolic syndrome among native Africans with type 2 diabetes. |
| Is it dangerous to lower the cholesterol level? Angelin, B. (1993), Lakartidningen 90(28-29): 2509-12. |
| Is it time to modify the reverse cholesterol transport model? Tall, A. R., N. Wang, et al. (2001), J Clin Invest 108(9): 1273-5. |
| Is knowing your cholesterol number harmful? Irvine, M. J. and A. G. Logan (1994), J Clin Epidemiol 47(2): 131-45. Abstract: To examine the potential adverse psychological effects of screening for hypercholesterolemia, 287 men working at a motor-car assembly or steel-making plant who were ultimately diagnosed as having hypercholesterolemia and 236 randomly selected normal cholesterol controls from the same plants completed psychological questionnaires at the initial screen and 1-year later. At baseline and before diagnosis, hypercholesterolemic men scored higher on mental health and lower on negative affect than controls (p values < 0.05). One year later no adverse changes on the psychological measures were found irrespective of the type of follow-up care that they were randomly assigned to receive. Surprisingly only about half of the hypercholesterolemic men believed they had hypercholesterolemia at follow-up despite being told otherwise. Baseline scores of those who did not accept the label (n = 122) classified as deniers were higher on measures of positive affect and lower on measures of negative effect than those of hypercholesterolemic men who accepted the disease label (n = 73) (p values < 0.05). Moreover they held more negative attitudes towards dietary change at baseline (p < 0.03), made fewer dietary changes (p values < 0.05), and had a lesser change in total cholesterol. We conclude that a hypercholesterolemia detection and treatment program conducted in a working adult population had no adverse psychological consequences. It did, however, reveal a large subset of hypercholesterolemic men who did not accept the label despite being told they had this problem. Denial was a significant barrier to health behaviour change and may represent a maladaptive coping style for men at risk of cardiovascular disease. High cholesterol appears to be associated with better mental health and those who deny having hypercholesterolemia have the best mental health. The multifarious relationship between cholesterol, mental health, and denial deserves further study. |
| Is LCAT activity a determinant of HDL cholesterol concentrations? Terpstra, A. H., A. van Tol, et al. (1995), Nutrition 11(5): 469-70. |
| Is lipoprotein(a) cholesterol a significant indicator of cardiovascular risk? Nauck, M., W. Marz, et al. (2000), Clin Chem 46(3): 436-7. |
| Is lipoprotein(a)-cholesterol a better predictor of vascular disease events than total lipoprotein(a) mass? A nested case control study from the West of Scotland Coronary Prevention Study Gaw, A., E. A. Brown, et al. (2000), Atherosclerosis 148(1): 95-100. Abstract: The clinical utility of a new assay for plasma lipoprotein(a)-cholesterol (Lp(a)-C) was assessed in parallel with our routine Lp(a) mass measurements in a nested-case control study of subjects within the placebo arm of the West of Scotland Coronary Prevention Study (WOSCOPS). A total of 238 control patients and 108 patients who had suffered a serious vascular event during the course of the WOSCOPS were examined. Lp(a) mass was assessed within 2 years of sampling by an ELISA method on baseline EDTA plasma samples which had been stored at -70 degrees C. Subsequently, the Lp(a) mass was re-measured by an immunoturbidimetric assay approximately 8 years after sampling. On the same stored aliquot the Lp(a)-C was measured. These analyses allowed us to assess whether the Lp(a)-C assay could provide any additional information over and above that which would be obtained from our Lp(a) mass assays. In addition the apo(a) isoform sizes of these subjects were measured using a high resolution immunoblotting system. The Lp(a)-C and Lp(a) mass measurements provided exactly the same information in the study, as they were equally non-discriminatory between cases and controls. The only difference between the two patient groups was the percentage of 'null' apo(a) alleles (control: 25.6% versus cases: 19.4%). We conclude that these results reinforce the concordance of the two assay systems and confirm that the Lp(a)-C assay provides no added information over and above that gained from traditional Lp(a) mass assays, which may be faster and less expensive. |
| Is reverse cholesterol transport a misnomer for suggesting its role in the prevention of atheroma formation? Quintao, E. C. (1995), Atherosclerosis 116(1): 1-14. Abstract: Reverse cholesterol transport from peripheral tissues, including the arterial wall, involves high density lipoprotein (HDL) uptake of unesterified cell cholesterol, its esterification by lecithin-cholesterol-acyl-transferase (LCAT), direct HDL-cholesteryl ester uptake by the liver and the indirect pathway consisting of the cholesteryl ester transfer protein (CETP)-mediated transfer of HDL-cholesteryl ester to apolipoprotein (apo) B-containing lipoproteins (very low density lipoprotein (VLDL) and LDL). Although the first route should be regarded as anti-atherogenic, ambiguous interpretations are drawn from the indirect pathway since it is potentially atherogenic to the extent that it may raise the plasma cholesteryl ester concentration in lipoproteins that are taken up by arterial wall macrophages. In addition, controversial roles are played in reverse cholesterol transport by LCAT and liver uptake of HDL-cholesteryl ester mediated by hepatic lipase (HL). HDL may exert several antiatherogenic effects unrelated to its role in cell cholesterol removal. |
| Is serum cholesterol associated with progression of diabetic retinopathy or macular edema in persons with younger-onset diabetes of long duration? Klein, B. E., R. Klein, et al. (1999), Am J Ophthalmol 128(5): 652-4. Abstract: PURPOSE: To quantitate the relationships of total cholesterol and high-density lipoprotein cholesterol to the incidence and progression of diabetic retinopathy and macular edema 5 years later in those with younger-onset diabetes of long duration. METHODS: Casual serum specimens for lipid values and fundus photography at the time of the lipid determinations were evaluated with regard to retinal lesions in photographs taken 5 years later during the course of a population-based cohort study. RESULTS: Univariable associations were significant for associations of incident retinal lesions with total cholesterol/high-density lipoprotein cholesterol, but multivariable associations considering covariates were not significant. CONCLUSION: Our data suggest that lowering cholesterol by therapeutic means may not be indicated for the sole purpose of decreasing the incidence or progression of these retinal lesions. |
| Is the cholesterol-lowering effect of simvastatin influenced by CYP2D6 polymorphism? Nordin, C., M. L. Dahl, et al. (1997), Lancet 350(9070): 29-30. |