| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Ratio of low-density lipoprotein cholesterol to ubiquinone as a coronary risk factor Hanaki, Y., S. Sugiyama, et al. (1991), N Engl J Med 325(11): 814-5. |
| Ratio of remnant-like particle cholesterol to serum total triglycerides is a reliable screening test for type III dyslipidaemia Devaraj, S., S. Hirany, et al. (2000), Ann Clin Biochem 37 (Pt 6): 790-1. |
| Ratio of remnant-like particle-cholesterol to serum total triglycerides is an effective alternative to ultracentrifugal and electrophoretic methods in the diagnosis of familial type III hyperlipoproteinemia Wang, T., K. Nakajima, et al. (1999), Clin Chem 45(11): 1981-7. Abstract: BACKGROUND: Familial type III hyperlipoproteinemia (HLP) is characterized by the presence of beta-migrating VLDL (beta-VLDL) and increased risk of cardiovascular disease. Assessment of plasma beta-VLDL is achieved by measuring the ratio of VLDL-cholesterol (VLDL-C) to total plasma triglycerides (TGs) or by detecting beta-VLDL in total VLDL. The objective of this study was to compare the clinical utility of the ratio of remnant-like particle-cholesterol (RLP-C) to total TGs with that of the current methods for diagnosing type III HLP. METHODS: Detection of beta-VLDL by electrophoresis of VLDL was used to define type III HLP. Twenty-eight patients with type III HLP and 43 subjects lacking beta-VLDL were investigated. Fasting TG concentrations were >2.26 mmol/L in all subjects. Subjects were separated into three groups: group 1, serum total cholesterol 5.18 mmol/L and TGs between 2.26 and 9.04 mmol/L (n = 51); and group 3, TGs >9.04 mmol/L (n = 9). RESULTS: In group 2, a RLP-C-to-total TG molar ratio >/=0.23 (>/=0.10 when using mg/dL) and a VLDL-C-to-total TG molar ratio >/=0.69 (>/=0.30 when using mg/dL) correctly classified 94% and 90% of the subjects, respectively. The utility of the RLP-C-to-total TG ratio in diagnosing type III HLP decreased in patients in the other two groups. CONCLUSION: When used in an appropriate target population, the RLP-C-to-total TG ratio is a convenient and effective alternative to ultracentrifugal and electrophoretic methods for diagnosing type III HLP. |
| Ratio of triglycerides to HDL cholesterol is an indicator of LDL particle size in patients with type 2 diabetes and normal HDL cholesterol levels Boizel, R., P. Y. Benhamou, et al. (2000), Diabetes Care 23(11): 1679-85. Abstract: OBJECTIVE: In patients with type 2 diabetes, a normal HDL cholesterol level does not rule out that LDL particles may be small. Although techniques for analyzing LDL subfractions are not likely to be used in clinical practice, a prediction of LDL size based on a regular lipid profile may be useful for assessment of cardiovascular risk. RESEARCH DESIGN AND METHODS: Sixty patients with type 2 diabetes with acceptable glycemic control and an HDL cholesterol level > or = 1 mmol/l were recruited after cessation of lipid-altering treatments. LDL size was determined by 2-20% PAGE; patients having small LDL (n = 30) were compared with those having intermediate or large LDL (n = 30). RESULTS: Clinical characteristics, pharmacological therapies, lifestyle, and prevalence of diabetes-related complications were similar in both patient groups. LDL size correlated negatively with plasma triglycerides (TGs) (R2 = 0.52) and positively with HDL cholesterol (R2 = 0.14). However, an inverse correlation between the TG-to-HDL cholesterol molar ratio and LDL size was even stronger (R2 = 0.59). The ratio was > 1.33 in 90% of the patients with small LDL particles (95% CI 79.3-100) and 16.5% of those with larger LDL particles. A cutoff point of 1.33 for the TG-to-HDL cholesterol ratio distinguishes between patients having small LDL values better than TG cutoff of 1.70 and 1.45 mmol/l. CONCLUSIONS: The TG-to-HDL cholesterol ratio may be related to the processes involved in LDL size pathophysiology and relevant with regard to the risk of clinical vascular disease. It may be suitable for the selection of patients needing an earlier and aggressive treatment of lipid abnormalities. |
| Rational approach to pharmacologic reduction of cholesterol levels in children Sprecher, D. L. and S. R. Daniels (1996), J Pediatr 129(1): 4-7. |
| Rationale and design features of a clinical trial examining the effects of cholesterol lowering and angiotensin-converting enzyme inhibition on coronary atherosclerosis: Simvastatin/Enalapril Coronary Atherosclerosis Trial (SCAT). SCAT Investigators Teo, K. K., J. R. Burton, et al. (1997), Can J Cardiol 13(6): 591-9. Abstract: BACKGROUND: In the treatment of coronary atherosclerotic artery disease (CAD), the mechanisms by which lipid lowering, a proven therapy, produces beneficial clinical effects remain unclear. Moreover, although potential mechanisms of benefit are well known and increasingly applied clinically, there are no conclusive data from clinical trials studying primarily the antiischemic effects of angiotensin-converting enzyme (ACE) inhibition in patients with normal heart function. The Simvastatin/Enalapril Coronary Atherosclerosis Trial (SCAT) is designed to clarify some of these issues in CAD patients with normal or mildly elevated cholesterol. DESIGN AND OBJECTIVES: SCAT is a three- to five-year, multicentre, randomized, double-blind, placebo controlled, 2 x 2 factorial trial evaluating the effects of cholesterol lowering therapy by simvastatin and/or ACE inhibition by enalapril on anatomic coronary atherosclerosis progression assessed by quantitative coronary angiography in CAD patients with preserved left ventricular function and total cholesterol levels between 4.1 and 6.2 mmol/L. PATIENTS: Of 460 patients (age 61 +/- 9 years; 409 males, 51 females) enrolled between June 1991 and July 1995, 230 were randomized to simvastatin and 230 to placebo, and 229 to enalapril and 231 to placebo. Average baseline total cholesterol level was 5.20 +/- 0.61 mmol/L, high density lipoprotein cholesterol was 0.99 +/- 0.25 mmol/L, low density lipoprotein cholesterol was 3.36 +/- 0.57 mmol/L and triglycerides were 1.82 +/- 0.75 mmol/L. The trial will be completed in June 1998. SIGNIFICANCE: Insights gained from this long term angiographic trial will lead to a better understanding of the mechanisms of benefits of these two treatments, both alone and in combination. Of particular interest is that this trial will be able to examine a suspected beneficial interaction, if present, between these two treatments. |
| Rationale and design of a secondary prevention trial of increasing serum high-density lipoprotein cholesterol and reducing triglycerides in patients with clinically manifest atherosclerotic heart disease (the Bezafibrate Infarction Prevention Trial) Goldbourt, U., S. Behar, et al. (1993), Am J Cardiol 71(11): 909-15. Abstract: Controlled clinical trials have demonstrated the efficacy of reducing the blood levels of low-density lipoprotein cholesterol in reducing the incidence of coronary artery disease in hypercholesterolemic middle-aged men. However, a similar reversibility of the risk of coronary artery disease has not been demonstrated for high-density lipoprotein cholesterol elevation and triglyceride reduction. Therefore, the effect of administering 400 mg of bezafibrate retard daily versus placebo (double blind) to patients with myocardial infarction preceding randomization by 6 months to 5 years, or a clinically manifest anginal syndrome documented by objective evidence of dynamic myocardial ischemia, or both, is being investigated. Three thousand subjects (aged 45 to 74 years) are being enrolled from 19 cardiac departments in Israel, with total serum cholesterol between 180 and 250 mg/dl, high-density lipoprotein cholesterol < or = 45 mg/dl and triglycerides < or = 300 mg/dl. In addition, low-density lipoprotein cholesterol concentrations are required to be < or = 180 mg/dl (< or = 160 mg/dl for patients aged < 50 years). Patients needing lipid-modifying therapy, exhibiting > or = 1 prespecified exclusion criterion or not giving informed consent, or a combination, are not randomized. The primary end points for evaluating efficacy are the incidence of fatal and nonfatal myocardial infarction, and sudden death. The hypothesized effect of bezafibrate administration under the aforementioned protocol is to reduce an estimated cumulative end point event incidence of > or = 15% by 20 to 25% over an average follow-up period of 6.25 years, through early 1998, when the last patient recruited will have completed 5 years.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Rationale and design of a secondary prevention trial of lowering normal plasma cholesterol levels after acute myocardial infarction: the Cholesterol and Recurrent Events trial (CARE) Sacks, F. M., M. A. Pfeffer, et al. (1991), Am J Cardiol 68(15): 1436-46. Abstract: Recent clinical trials of primary and secondary prevention of cardiovascular disease have demonstrated that lowering plasma cholesterol decreases the incidence of coronary heart disease in patients with elevated plasma cholesterol. However, it is not known whether patients with established coronary artery disease and normal plasma cholesterol can be benefited. Several previous prevention trials reviewed in this report found that patients who had plasma cholesterol levels at baseline in the upper portion of the eligibility range (e.g., greater than 240 mg/dl) received greater benefit from hypolipidemic diet or drug therapy than patients who had lower plasma cholesterol levels at baseline. The recent availability of drugs that are more potent and less prone to cause adverse reactions than previous regimens permits this important question to be addressed. The Cholesterol and Recurrent Events trial is testing whether pravastatin, a hydroxymethylglutaryl coenzyme A reductase inhibitor, will decrease the sum of fatal coronary heart disease and nonfatal myocardial infarction (MI) in patients who have recovered from a MI and who have normal total cholesterol levels. Fatal cardiovascular disease and total mortality are important secondary end points. The trial is enrolling 4,000 men and women from 80 centers throughout North America, age 21 to 75 years, who have survived MI for 3 to 20 months, who have plasma total cholesterol less than 240 mg/dl (6.2 mmol/liter) and low-density cholesterol of 115 to 174 mg/dl (3.0 to 4.5 mmol/liter), and who are representative of the general population of patients with MI. Patients are randomized to either active or inactive drug therapy. Active therapy consists of pravastatin, 40 mg/day, designed to achieve an average decrease in low-density lipoprotein cholesterol of approximately 30%, and an increase in high-density lipoprotein of 5%. The average duration of follow-up will be greater than or equal to 5 years. To protect against a lower than expected rate of recurrent events, the trial will be continued until a predetermined fixed number of coronary heart disease events occurs in the entire cohort so that the original sensitivity of the trial will be maintained. |
| Rationale and design of the Department of Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial (HIT) for secondary prevention of coronary artery disease in men with low high-density lipoprotein cholesterol and desirable low-density lipoprotein cholesterol Rubins, H. B., S. J. Robins, et al. (1993), Am J Cardiol 71(1): 45-52. Abstract: Although a large body of epidemiologic evidence suggests that low levels of high-density lipoprotein (HDL) cholesterol are strongly associated with an increased risk of coronary artery disease (CAD), no large-scale clinical trials focusing on this association have been reported. This report describes the rationale and design of the Department of Veterans Affairs HDL Intervention Trial (HIT), a multicenter, randomized, controlled clinical trial designed to determine whether lipid therapy reduces the combined incidence of CAD death and nonfatal myocardial infarction in men with established CAD who have low levels of HDL cholesterol with "desirable" levels of low-density lipoprotein (LDL) cholesterol. Twenty-five hundred men with CAD and HDL cholesterol < or = 40 mg/dl, LDL cholesterol < or = 140 mg/dl, and triglycerides < or = 300 mg/dl are being recruited at 20 Department of Veterans Affairs medical centers, randomized to either gemfibrozil or placebo, and followed in a double-blind manner for an average of 6 years. In this population, gemfibrozil is expected to increase HDL cholesterol by 10 to 15%, have a negligible effect on LDL cholesterol, and lower triglycerides by 30 to 40%. Because an estimated 20 to 30% of patients with CAD have a low HDL cholesterol as their primary lipid abnormality, the results of this trial are expected to have far-reaching clinical implications. |
| Rationale and design of the Myocardial Ischemia Reduction With Aggressive Cholesterol lowering (MIRACL) Study that evaluates atorvastatin in unstable angina pectoris and in non-Q-wave acute myocardial infarction Ghali, J. K. (1998), Am J Cardiol 82(5): 703. |
| Rationale for cholesterol-lowering strategies Grundy, S. M. and D. Friedman (1995), Curr Probl Cardiol 20(5): 281-357. |
| Rationale for new American Diabetes Association Guidelines: are national cholesterol education program goals adequate for the patient with diabetes mellitus? Haffner, S. (2005), Am J Cardiol 96(4A): 33E-36E. Abstract: Both the American Diabetes Association (ADA) and the National Cholesterol Education Program (NCEP) consider type 2 diabetes mellitus to be a coronary artery disease (CAD) risk equivalent and thus suggest that patients with either diabetes or CAD should have their plasma levels of low-density lipoprotein (LDL) cholesterol lowered to <2.59 mmol/L (<100 mg/dL). Recently the NCEP issued a white paper suggesting an even lower plasma LDL cholesterol goal of <1.81 mmol/L (<70 mg/dL) for patients at high cardiovascular risk, including patients with diabetes. This rationale was based partly on the higher risk of future cardiovascular disease seen in patients who have diabetes with or without preexisting cardiovascular disease than in nondiabetic subjects with preexisting cardiovascular disease. Additionally, as reported in the Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT) study, high-dose lipid-lowering therapy has been shown to further reduce CAD event rates compared with conventional therapy. |
| Rationale for use of non-high-density lipoprotein cholesterol rather than low-density lipoprotein cholesterol as a tool for lipoprotein cholesterol screening and assessment of risk and therapy Frost, P. H. and R. J. Havel (1998), Am J Cardiol 81(4A): 26B-31B. Abstract: The plasma level of low-density lipoprotein (LDL) cholesterol is the "gold standard" for estimating the lipoprotein-related risk for complications of atherosclerotic vascular disease. LDL cholesterol concentrations are commonly estimated by the Friedewald formula that requires only the measurement (after overnight fasting) of plasma cholesterol and triglycerides along with high-density lipoprotein (HDL) cholesterol. This value, however, is not in fact a true estimate of LDL cholesterol but rather of LDL cholesterol along with variable, usually smaller, amounts of intermediate-density lipoprotein (IDL) cholesterol and lipoprotein(a). Estimation of LDL cholesterol levels by the Friedewald formula becomes progressively less accurate as plasma triglyceride concentrations increase, and the formula is generally considered inapplicable when triglyceride levels exceed 400 mg/dL. We believe that a very simple measurement-non-HDL cholesterol (serum cholesterol minus HDL cholesterol)-has considerable potential as a screening tool for identifying dyslipoproteinemias, for risk assessment, and for assessing the results of hypolipidemic therapy. Unlike the estimation of LDL cholesterol levels by the Friedewald formula, the estimation of non-HDL cholesterol concentrations requires no assumptions about the relation of very-low-density (VLDL) cholesterol levels to plasma triglyceride concentrations. This method includes all of the cholesterol present in lipoprotein particles now considered to be potentially atherogenic VLDL, IDL, LDL, and lipoprotein(a). This article provides examples of the utility of non-HDL cholesterol concentrations in clinical medicine. |
| RCS rat retinal rod outer segment membranes exhibit different cholesterol distributions than those of normal rats Boesze-Battaglia, K., D. T. Organisciak, et al. (1994), Exp Eye Res 58(3): 293-300. Abstract: Royal College of Surgeons (RCS) rats exhibit an hereditary defect in phagocytosis of the tips of the photoreceptor cell rod outer segments (ROS) which leads to degeneration of the retinal visual cells. The lipid composition of outer segment membranes of these rats was analysed and compared to those of normal rats to determine whether there are differences between the normal and mutant rat ROS. The cholesterol distribution in ROS disk membranes from normal and RCS rats was investigated using a digitonin induced change in membrane density. Normal rat ROS disks varied in cholesterol to phospholipid mole ratio from 0.36 to 0.03. The disk membranes from RCS rats, however, do not exhibit the same marked cholesterol heterogeneity. The mean molar ratio of cholesterol to phospholipid in the disk membranes of normal rats is 0.11 while that found in the RCS rats is 0.14. The ROS plasma membrane of dystrophic rats also has a lower cholesterol to phospholipid ratio (0.20) than is found in the normal rat (0.40). The phospholipid headgroup composition of RCS disks and plasma membrane were determined. RCS disks were shown to differ from those of normal animals. The cholesterol content of ROS disks may be governed by the phospholipid composition. |
| Re: "Dietary cholesterol and incidence of lung cancer: the Western Electric Study" Stockwell, H. G. and E. C. Candelora (1992), Am J Epidemiol 136(9): 1167; author reply 1169-70. |
| Re: "Orbitofrontal cholesterol granuloma: distinct diagnostic features and management" Selva, D. (2004), Ophthal Plast Reconstr Surg 20(5): 406; author reply 406. |
| Re: "Precursors of essential hypertension: pulmonary function, heart rate, uric acid, serum cholesterol, and other serum chemistries" Richards, S. M., M. G. Clark, et al. (1991), Am J Epidemiol 133(7): 753. |
| Re: "Sex difference in high density lipoprotein cholesterol in six countries" Kesteloot, H. and S. Sasaki (1997), Am J Epidemiol 146(4): 365-6. |
| Re: "The effect of dietary cholesterol and fat on the risk of lung cancer in Hawaii" Shekelle, R. B. (1990), Am J Epidemiol 131(3): 575-7. |
| Re: "Total cholesterol and high density lipoprotein cholesterol as important predictors of erectile dysfunction" Holmqvist, O. H. (1995), Am J Epidemiol 142(11): 1246-7. |