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Lipid-lowering with statins reduces disease progression, prevents myocardial infarction and other hard end points, and prolongs survival. Data from large-scale trials with these agents further show that lowering low-density lipoprotein (LDL) cholesterol in patients with coronary artery disease reduces the incidence of cardiovascular events and that the lower the LDL cholesterol achieved, the lower the event rate. Currently available evidence supports the National Cholesterol Education Program (NCEP) recommendations for reduction of LDL-cholesterol levels to at least 100 mg/dL in patients with coronary artery disease. The Treating to New Targets study, which will evaluate the effects of LDL-cholesterol lowering to < or = 75 mg/dL with atorvastatin, may help clarify if additional benefit accrues with further reductions. However, up to 82% of patients with proven coronary disease are not even at the current NCEP lipid goal. Up to 55% need a > 30-mg/dL reduction in LDL cholesterol to reach that goal. These data suggest that many patients are not receiving a statin or are receiving an inadequate dose. Aggressive lipid lowering, although a desirable goal, does not yet appear to be standard practice. [ABSTRACT FROM AUTHOR]

Coronary heart disease (CHD) is a major cause of morbidity and mortality in Western countries, and is associated with significant healthcare costs. Epidemiological studies have shown that elevated cholesterol levels, particularly elevated low density lipoprotein (LDL) cholesterol, are a major established risk factor for the development of CHD. There is a large amount of clinical data available to indicate that lowering total or LDL-cholesterol levels reduces the risk of cardiovascular events and mortality. The most recent cholesterol treatment guidelines from the US and Europe recommend intensive treatment (usually pharmacological) for patients at highest risk for CHD. Results from a number of landmark primary and secondary prevention studies are in support of these guidelines and also suggest that the lower the level of LDL-cholesterol achieved with treatment, the better clinical benefit attained. Thus, these findings indicate that even more aggressive lipid lowering than that recommended by available treatment guidelines may be warranted. Finding and treating all individuals at risk for CHD would be expected to increase the overall treatment costs of hypercholesterolaemia because many patients may not otherwise be treated; however, targeting high risk patients, rather than treating all patients or treating inappropriately, would be expected to reduce other healthcare costs and the indirect costs of lost productivity due to cardiovascular morbidity and mortality. Studies with the HMG-CoA reductase inhibitors, which show that these drugs substantially lower LDL-cholesterol, are the most convincing since they have consistently shown reductions in cardiovascular morbidity and mortality. As a result, statins are now well-established agents for the treatment of dyslipidaemia. [ABSTRACT FROM AUTHOR]

Heterotermes ferox (Froggatt) auctt. is shown to be a complex of species, each characterized by the composition of cuticular hydrocarbons in the worker, by canonical variate scores calculated from eight measurements of the soldier, and by small differences in the size and shape of the alate. H.ferox is redefined and two species are described, H.brevicatena sp.n. and H.longicatena sp.n. [ABSTRACT FROM AUTHOR]

Hypocholesterolemia reported in patients with myeloproliferative disorders prompted our investigation of lipoprotein metabolism in these patients. The production and fractional catabolic rates of very-low-density lipoprotein (VLDL) apoprotein-B were measured using 131I-VLDL; those of VLDL triglyceride, using 3H-glycerol; and those of low-density lipoprotein (LDL) apoprotein-B, using 125I-LDL. Plasma total and LDL cholesterol levels (mean +/- SD) were significantly reduced in seven patients with myeloproliferative diseases, compared to five normal subjects (93.1 +/- 20.3 mg/dL versus 166.8 +/- 24.6 mg/dL and 50.3 +/- 14.8 mg/dL versus 107 +/- 20.8 mg/dL, respectively). The production rates of VLDL apoprotein-B and VLDL triglyceride were normal in the patients. The fractional catabolic rate of LDL apoprotein-B was increased in the patients with myeloproliferative diseases (0.89 +/- 0.32/d versus 0.52 +/- 0.10/d; p less than 0.05); this increased rate was associated with reduced plasma LDL apoprotein-B levels (41.7 +/- 7.1 mg/dL versus 57.0 +/- 11.3 mg/dL; p less than 0.05) despite normal or elevated LDL apoprotein-B production (16.7 +/- 5.3 mg/kg body weight . d versus 12.9 +/- 1.2 mg/kg body weight . d). The site (or sites) of increased LDL catabolism in these hypocholesterolemic patients with myeloproliferative disorders is under investigation. [ABSTRACT FROM AUTHOR]