505 research outputs found
Ctenarytaina bipartita Burckhardt, Farnier, Queiroz, Taylor & Steinbauer, 2013, sp. n.
No full textCtenarytaina bipartita sp. n. (Figs 1–13) Material examined. Holotype 3, Australia: Victoria, Battery Creek, 146 ° 7 ’ 42.3 ”E, 38 ° 42 ’ 51.5 ”S, 144 m above sea level, 7 March 2012, planted Eucalyptus kitsoniana (K. Farnier & M.J. Steinbauer), bred in greenhouse in LTUV (ANIC, dry mounted). Paratypes. Australia: Australian Capital Territory: 1 3, 1 Ƥ, Canberra, 13 September 1959 (V.F. Eastop), 1960 - 144 (BMNH, slide mounted). – New South Wales: 6 3, 2 Ƥ, Orange, Dalton Street roundabout, 149 ° 6 ’ 25.8 ”E, 33 ° 16 ’ 31.1 ”S, 866 m above sea level, 15 March 2012, Eucalyptus viminalis (D. Burckhardt) (NHMB, dry mounted); – Tasmania: 3 3, 5 Ƥ, Hobart, 3 December 1986, Eucalyptus viminalis (D. Burckhardt) (MHNG, NHMB, dry and slide mounted); 4 3, 1 Ƥ, same but Marion Bay, West of Copping, 13 December 1986, various trees (MHNG, dry mounted); 2 Ƥ, same but 10 km South of Bronte, 10 December 1986, Eucalyptus spp. (MHNG, dry mounted); 1 Ƥ, Weegena, 9 June 1959, Eucalyptus (V.F. Eastop) VFE 7674, 1960- 144 (BMNH, slide mounted). – Victoria: 8 3, 12 Ƥ, 26 larvae, same data as holotype (ANIC, ELEF, LTUV, MHNG, NHMB, dry and slide mounted and in ethanol); 13 3, 12 Ƥ, same data but (G.S. Taylor & M.J. Steinbauer) (WINC, dry mounted and in ethanol); 8 Ƥ, 22 larvae (5 th instar 12, 4th instar 1, 3rd 4, 2nd 1, 1st 4), Hoddle Range, 146 ° 7 ’ 55.6 ”E, 38 ° 43 ’ 0.9 ”S, 254 m above sea level, 19 October 2011, planted E. kitsoniana (K. Farnier & M.J. Steinbauer) (LTUV, dry mounted); 5 3, 5 Ƥ, 125 larvae, nr Portland, Oakleys Rd, 141 ° 31 ’ 6.4 ”E, 38 ° 19 ’ 55.5 ”S, 7 May 2012, roadside reveg planting of E. kitsoniana and E. viminalis (M.J. Steinbauer), (WINC, in ethanol); 1 3, 110 larvae, same but 7 May 2012; 1 larva, nr Portland, Post Office Rd, 147 ° 20 ’ 33.1 ”E, 38 ° 12 ’6.0”S, 8 May 2012, naturally seeded seedling of E. kitsoniana (M.J. Steinbauer) (WINC, in ethanol). Description. Adult (Figs 1–4). Colouration. When alive bright orange to light brown (Fig. 14); eyes reddish. In dry mounted specimens head and pronotum light orange-brown, preocular tubercule and genal processes yellowish. Antennal segments 1 and 2 yellowish, 5–7 light brown, 8–10 dark brown to almost black. Thorax light reddish brown. Forewing with yellow to light brown veins; membrane semitransparent, indistinctly yellowish. Hindwing transparent, whitish. Legs brown, tibiae whitish, abdominal tergites brown, ventrites dirty whitish or yellowish, membranes reddish. Terminalia yellowish to light ochreous. Young specimens generally lighter in colour. Structure. Head (Fig. 5) strongly deflexed from longitudinal body axis; preocular sclerite forming distinct tubercule; genal processes about one third as long as vertex along mid-line, conical, subacute, contiguous in the middle in basal half; completely enveloping the median ocellus basally. Antenna short, 0.87–0.95 times head width, with a single subapical rhinarium on each of segments 4, 6, 8 and 9; segment 10 with one long curved apical seta, which is about as long as segment 10, and a very short truncate seta. Forewing (Fig. 6) oblong-oval, 2.54–2.84 times as long as head width, 2.64 – 2.28 times as long as broad, more or less evenly rounded apically; pterostigma relatively broad, broadest near the middle; costal break present. Vein C+Sc very weakly, evenly curved, cell c+sc narrow; vein Rs almost straight, vein M long with short, widely diverging branches, vein Cu 1 b relatively long, evenly curved, in males reaching the margin at the point of bifurcation of vein M, in females often beyond point of bifurcation. Surface spinules present in all cells, forming irregular cellular pattern. Mesotibia with a subapical, longitudinal row of stout setae. Metacoxa with small, straight, weakly narrowing, apically blunt meracanthus. Metatibia longer than metafemur, 0.54–0.56 times as long as head width, with 5 almost equidistant short, strongly sclerotised apical spurs. Metabasitarsus with 2 small lateral sclerotised spurs. Male terminalia (Figs. 7, 8) with basal segment of proctiger, in profile, without conspicuous stout pointed seta at the distal posterior angle; apical segment thin, tubular, 0.54–0.62 times length of basal segment; subgenital plate relatively small, triangular, in profile, with concave dorsal margin and longitudinal row of lateral setae. Paramere (Figs. 9, 14) lamellar, weakly curved forward with small finger-like process in basal third of hind margin, subacute apically; outer face sparsely covered in long setae, inner face with a group of thick setae apically and along fore margin, as well as a row of closely spaced peg-like setae starting from about apical third of the hind margin to the base; from behind, fingerlike process visible as narrow lobe with straight inner margin. Distal portion of aedeagus (Figs. 10, 15) with apical third or half imperceptibly inflated, apex narrowly rounded, sclerotised end tube of ductus ejaculatorius small, sshaped. Female terminalia (Fig. 11) with proctiger 0.77 – 0.70 times as long as head width, 2.83–3.27 times as long as circumanal ring, 1.75–1.89 times as long as subgenital plate; dorsal margin of proctiger strongly concave, apical half of proctiger forming narrow process, truncate at apex, and bearing two lateral rows of small peg-like setae over four fifths of its length. Subgenital plate 0.44–0.57 times as long as proctiger, in profile broadly triangular at base, strongly narrowing in apical third. Valvulae dorsalis and ventralis moderately curved. Measurements in mm (3 3, 3 Ƥ). Head width 0.49–0.58, Antenna length 0.46–0.51, forewing length 1.29–1.60, length of basal segment of male proctiger 0.16, length of distal segment of male proctiger 0.09–0.10, paramere length 0.11–0.14, length of distal portion of aeeagus 0.18–0.21, female proctiger length 0.43–0.45. Fifth instar larva (Fig. 16). Coloration. Larvae orange when alive; dirty whitish with yellowish or greyish sclerites when preserved in 70 % ethanol. Tip of antenna and tarsi dark brown, compound eyes red. Dorsum of head yellowish anteriorly. Abdomen with yellow mycetome visible in basal third. Structure. Body (Fig. 13) elongate, weakly sclerotised, 1.63–1.72 times as long as wide. Antenna indistinctly 9 -segmented, a single rhinarium present on each of segments 3, 5, 7 and 8. Forewing pad 1.58–1.60 times as long as antenna. Tarsal arolium oval, lacking pedicel and unguitractor, shorter than claws. Caudal plate (Fig. 12) angular, truncate apically, 0.71–0.91 times as long as wide. Circumanal ring terminal, small, consisting of a single row of pores. Additional pore fields present in the form of circular groups of 6–20 pores each; groups arranged in two irregular half circles on either side of caudal plate (Figs. 12 (large arrows), 16), anterior semicircle in anterior third of caudal plate, posterior in posterior third. Lanceolate marginal setae (Figs. 12 (small arrows), 16) forming three irregular groups in about basal third, in the middle and adjacent to circumanal ring. Measurements in mm (4 larvae). Body length 1.04–1.29, antenna length 0.28–0.31. Etymology. From Latin bipartitus = divided in two parts, referring to the paramere consisting of two lobes. Biology. In southern Victoria, adults were found on native and planted Eucalyptus kitsoniana and E. viminalis between October (mid spring) and early May (mid autumn). In Tasmania, adults were collected in December on Eucalyptus viminalis and by general sweeping on various plants including Eucalyptus pauciflora and unidentified eucalypt species. A single female was collected in June on Eucalyptus sp. The series from the ACT was found in September and that from New South Wales in March on E. viminalis. Adults appear feeding on juvenile foliage and are usually most abundant in opening leaf buds and on very recently expanded leaves. Adults spend most of the time feeding and usually disperse only when disturbed. Mating occurs at feeding sites (Fig. 17). Eggs are most often deposited inside closed apical buds. Females may be induced to lay by insertion of the ovipositor into tight crevices, e.g. between pairs of leaves. In the field, on planted hosts in Victoria, larvae were found between October and May inside apical buds and never on expanding leaves. Densities are typically low (5.9 ± 0.8 larvae per bud, n = 63 observations from seven trees), only rarely reaching high numbers (e.g. 38 larvae in a bud). Larvae produce wax strands (Figs. 18, 19) similar to those of C. eucalypti. Honeydew is encapsulated in the flocculent waxy material (Figs. 18, 19). High numbers of larvae in closed apical leaf pairs induce leaf rolls (Fig. 20). Condensation can be observed inside leaf rolls when opened indicating that they provide larvae with high humidity microhabitats in which to develop. Severely distorted young leaves often do not expand normally (Fig. 20). Leaf rolling was not observed in the field when larval densities were low, e.g. <5 larvae per leaf. In the laboratory larvae reach maturity within three weeks when reared under a 20: 10 °C for 12: 12 hours temperature regime. Mummified larvae with serrated exit holes have been observed in the wild suggesting that the species is attacked by parasitoid wasps. A regular psyllid infestation of small E. kitsoniana seedlings was observed in a nursery (F. Smolders, pers comm.). This population is currently in greenhouse culture at LTUV.Published as part of Burckhardt, Daniel, Farnier, Kevin, Queiroz, Dalva L., Taylor, Gary S. & Steinbauer, Martin J., 2013, Ctenarytaina bipartita sp. n. (Hemiptera, Psylloidea), a new eucalypt psyllid from Southeast Australia, pp. 589-596 in Zootaxa 3613 (6) on pages 590-594, DOI: 10.11646/zootaxa.3613.6.5, http://zenodo.org/record/22171
Colesevelam hydrochloride : usefulness of a specifically engineered bile acid sequestrant for lowering LDL-cholesterol
No full textSeveral recent meta-analyses of numerous lipid-lowering outcome trials confirm the direct relationship between low-density lipoprotein-cholesterol (LDL-C) lowering and cardiovascular risk reduction. As a consequence, LDL-C goals are continuously being set lower. To achieve lipid lowering, several efficient drugs are available, however, the current pharmacopoeia remains limited for some critical patient situations. Colesevelam hydrochloride is a specifically engineered bile acid sequestrant that features a more favourable tolerability and drug interaction profile than traditional bile acid sequestrants, because of a better affinity and binding capacity to bile acids. In addition, colesevelam retains the nonsystemic mode of action of bile acid sequestrants. Moreover, colesevelam lowers LDL-C by 15-19% and 10-16%, respectively, in monotherapy and in combination to various lipid-lowering drugs, such as statins, ezetimibe and fenofibrates. Along with an efficient and sustainable effect on lipid profiles, colesevelam - as other bile acid sequestrants - has been shown to lower the glycosylated haemoglobin HbA1c by 0.5% on average in patients with type 2 diabetes. Overall, colesevelam represents an interesting add-on treatment to be used in high-risk patients with hypercholesterolaemia for whom standard lipid-lowering therapies are not enough or not well tolerate
Effect of co-administering ezetimibe with on-going simvastatin treatment on LDL-C goal attainment in hypercholesterolemic patients with coronary heart disease
No full textOBJECTIVE: To determine whether co-administering ezetimibe with on-going simvastatin treatment was more effective than placebo plus on-going simvastatin in achieving an LDL-C treatment target of or = 18 years) with documented CHD and on a stable dose of simvastatin 10 mg or 20 mg for at least 6 weeks were recruited for this study. After a 4-week simvastatin 10 or 20 mg plus placebo and diet run-in period, patients were eligible for randomization if LDL-C > 2.60 and < or = 4.20 mmol/l and triglycerides (TG) < or = 4.00 mmol/l. Eligible patients were randomized to a double-blind comparative study with ezetimibe 10 mg co-administered with on-going simvastatin 10 mg or 20 mg (n=181) versus placebo to match ezetimibe co-administered with simvastatin 10 mg or 20 mg (n=191) for 6 weeks. RESULTS: At baseline, mean LDL-C was comparable between the ezetimibe (3.14 mmol/l) and placebo (3.19 mmol/l) groups. With the addition of ezetimibe or placebo to on-going simvastatin therapy, the percentage of patients achieving the LDL-C goal of < or = 2.60 mmol/l after 6 weeks of treatment was significantly (p < or = 0.001) greater in the ezetimibe group (74.3%) than in the placebo group (16.7%). The addition of ezetimibe to on-going simvastatin treatment also resulted in a significantly (p < or = 0.001) larger mean percent reduction in LDL-C from baseline (25.2%) compared with placebo (0.9%). Ezetimibe was generally well tolerated compared to placebo when added to on-going simvastatin treatment. CONCLUSIONS: Co-administering ezetimibe with on-going simvastatin 10 or 20 mg treatment allowed more hypercholesterolemic patients with CHD to reach the LDL-C treatment target of < or = 2.60 mmol/l
Ctenarytaina bipartita sp. n. (Hemiptera, Psylloidea), a new eucalypt psyllid from Southeast Australia
No full textCtenarytaina bipartita sp.n., associated with Eucalyptus kitsoniana and E. viminalis, is described from the Australian Capital Territory, New South Wales, Tasmania and Victoria. It differs from other described Ctenarytaina species in the paramere which bears a small posterior lobe. Taxonomically relevant morphological details are illustrated and the species is diagnosed from other eucalypt inhabiting congeners. Information on the biology is also given. C. bipartita has the potential to become an exported pest species to countries with significant eucalypt plantations.Daniel Burckhardt, Kevin Farnier, Dalva L. Queiroz, Gary S. Taylor & Martin J. Steinbauerhttp://www.mapress.com/zootaxa/2013/f/z03613p596f.pd
Efficacy and safety of adding alirocumab to rosuvastatin versus adding ezetimibe or doubling the rosuvastatin dose in high cardiovascular-risk patients:The ODYSSEY OPTIONS II randomized trial
No full textOBJECTIVE: To compare lipid-lowering efficacy of adding alirocumab to rosuvastatin versus other treatment strategies (NCT01730053).METHODS: Patients receiving baseline rosuvastatin regimens (10 or 20 mg) were randomized to: add-on alirocumab 75 mg every-2-weeks (Q2W) (1-mL subcutaneous injection via pre-filled pen); add-on ezetimibe 10 mg/day; or double-dose rosuvastatin. Patients had cardiovascular disease (CVD) and low-density lipoprotein cholesterol (LDL-C) ≥70 mg/dL (1.8 mmol/L) or CVD risk factors and LDL-C ≥100 mg/dL (2.6 mmol/L). In the alirocumab group, dose was blindly increased at Week 12 to 150 mg Q2W (also 1-mL volume) in patients not achieving their LDL-C target. Primary endpoint was percent change in calculated LDL-C from baseline to 24 weeks (intent-to-treat).RESULTS: 305 patients were randomized. In the baseline rosuvastatin 10 mg group, significantly greater LDL-C reductions were observed with add-on alirocumab (-50.6%) versus ezetimibe (-14.4%; p < 0.0001) and double-dose rosuvastatin (-16.3%; p < 0.0001). In the baseline rosuvastatin 20 mg group, LDL-C reduction with add-on alirocumab was -36.3% compared with -11.0% with ezetimibe and -15.9% with double-dose rosuvastatin (p = 0.0136 and 0.0453, respectively; pre-specified threshold for significance p < 0.0125). Overall, ∼80% alirocumab patients were maintained on 75 mg Q2W. Of alirocumab-treated patients, 84.9% and 66.7% in the baseline rosuvastatin 10 and 20 mg groups, respectively, achieved risk-based LDL-C targets. Treatment-emergent adverse events occurred in 56.3% of alirocumab patients versus 53.5% ezetimibe and 67.3% double-dose rosuvastatin (pooled data).CONCLUSIONS: The addition of alirocumab to rosuvastatin provided incremental LDL-C lowering versus adding ezetimibe or doubling the rosuvastatin dose.</p
Not all fibrates are made equal: Learning from biology and clinical trials
No full text: Atherogenic dyslipidemia is an important risk factor for cardiovascular disease (CVD) in patients with type 2 diabetes, obesity, and metabolic disorders. Statin therapy, the standard treatment for dyslipidemia management, falls short of controlling the residual risk of adverse cardiovascular events, even with good control of low-density lipoprotein cholesterol (LDL-C). Apolipoprotein B (apoB), in addition to non-high-density lipoprotein cholesterol (non-HDL-C), is considered a better measure of residual risk and a more comprehensive treatment target in atherogenic dyslipidemia. Fibrates in combination with statins represent a proven therapeutic modality for atherogenic dyslipidemia. Fibrates lower triglyceride-rich lipoproteins (TRL), TRL remnants, and small dense LDL particles while increasing HDL-C levels. However, only fenofibrate appears to reduce apoB, whereas gemfibrozil and pemafibrate do not. This leads to a reduction in atherogenic lipids, as measured by a significant decrease in apoB/non-HDL-C levels, and a corresponding reduction in CVD risk. Real-world efficacy studies and CVD outcome trials have shown that fenofibrate may be an option in combination with statins compared to other fibrates and is well tolerated. Additionally, evidence from real-world studies of the fenofibrate-statin combination in patients over a period of up to 20 years has dispelled safety concerns regarding long-term use of fenofibrate
Combination therapy in dyslipidemia : where are we now?
No full textLowering low-density lipoprotein cholesterol (LDL-C) reduces the risk of cardiovascular disease: each 1.0mmol/L (38.7mg/dL) reduction in LDL-C reduces the incidence of major coronary events, coronary revascularizations, and ischemic stroke by approximately 20%. Statins are a well-established treatment option for dyslipidemia, with LDL-C reduction in the range of 27-55%.Several lipid goal-driven guidelines recommend reducing LDL-C to <2.59mmol/L (100mg/dL) or <1.81mmol/L (70mg/dL) in very high-risk patients. Many patients treated with statins do not reach these goals, and remain at risk of future cardiovascular events. The 2013 American College of Cardiology/American Heart Association guidelines move away from advocating LDL-C treatment targets with focus placed on identifying patients most likely to benefit from high-intensity or moderate-intensity statin therapy.While increasing the statin dose can prove efficacious in some patients, this approach typically offers limited additional LDL-C lowering, and is associated with increased incidence of adverse side effects. Indeed, this has led to the investigation of statins in combination with other lipid-modifying agents for the treatment of dyslipidemia.This review of the evidence for statin use in combination with fibrates, niacin, bile acid sequestrants, and the cholesterol absorption inhibitor, ezetimibe, in dyslipidemic patients at increased risk of cardiovascular disease, explores the impact of such combination therapies on lipids, attainment of lipid targets, inflammatory markers, and on cardiovascular outcomes and pathology. Additionally, new and emerging dyslipidemia treatments are summarized
Efficacy and Safety of Ezetimibe Added to Atorvastatin Versus Atorvastatin Uptitration or Switching to Rosuvastatin in Patients With Primary Hypercholesterolemia
No full textHypercholesterolemic patients (n = 1,547) at high atherosclerotic cardiovascular disease risk with low-density lipoprotein cholesterol (LDL-C) levels ≥100 and ≤160 mg/dl while treated with atorvastatin 10 mg/day entered a multicenter, randomized, double-blind, active-controlled, clinical trial using two 6-week study periods. Period I compared the efficacy/safety of (1) adding ezetimibe 10 mg (ezetimibe) to stable atorvastatin 10 mg, (2) doubling atorvastatin to 20 mg, or (3) switching to rosuvastatin 10 mg. Subjects in the latter 2 groups who persisted with elevated LDL-C levels (≥100 and ≤160 mg/dl) after period I, entered period II; subjects on atorvastatin 20 mg had ezetimibe added to their atorvastatin 20 mg, or uptitrated their atorvastatin to 40 mg; subjects on rosuvastatin 10 mg switched to atorvastatin 20 mg plus ezetimibe or uptitrated their rosuvastatin to 20 mg. Some subjects on atorvastatin 10 mg plus ezetimibe continued the same treatment into period II. At the end of period I, ezetimibe plus atorvastatin 10 mg reduced LDL-C significantly more than atorvastatin 20 mg or rosuvastatin 10 mg (22.2% vs 9.5% or 13.0%, respectively, p <0.001). At the end of period II, ezetimibe plus atorvastatin 20 mg reduced LDL-C significantly more than atorvastatin 40 mg (17.4% vs 6.9%, p <0.001); switching from rosuvastatin 10 mg to ezetimibe plus atorvastatin 20 mg reduced LDL-C significantly more than uptitrating to rosuvastatin 20 mg (17.1% vs 7.5%, p <0.001). Relative to comparative treatments, ezetimibe added to atorvastatin 10 mg (period I) or atorvastatin 20 mg (period II) produced significantly greater percent attainment of LDL-C targets <100 or <70 mg/dl, and significantly greater percent reductions in total cholesterol, non-high-density lipoprotein cholesterol, most lipid and lipoprotein ratios, and apolipoprotein B (except ezetimibe plus atorvastatin 20 vs atorvastatin 40 mg). Reports of adverse experiences were generally similar among groups. In conclusion, treatment of hypercholesterolemic subjects at high cardiovascular risk with ezetimibe added to atorvastatin 10 or 20 mg produced significantly greater improvements in key lipid parameters and significantly greater attainment of LDL-C treatment targets than doubling atorvastatin or switching to (or doubling) rosuvastatin at the compared doses
Ezetimibe/Simvastatin 10/20 mg versus Rosuvastatin 10 mg in high-risk hypercholesterolemic patients stratified by prior statin treatment potency
No full textAbstract Objective This post-hoc analysis compared the lipid-altering efficacy of Ezetimibe/Simvastatin 10/20 mg (EZ/Simva) versus Rosuvastatin 10 mg (Rosuva) in patients stratified by statin potency/dose prior to randomization. Methods Patients with elevated low-density lipoprotein cholesterol (LDL-C) despite prior statin treatment (n = 618) were randomized 1:1 to EZ/Simva 10/20 mg or Rosuva 10 mg for 6 weeks. Percent change from baseline in lipids and attainment of lipid targets were assessed within each subgroup (low potency n = 369, high potency n = 249). Consistency of the treatment effect across subgroups was evaluated by testing for treatment-by-subgroup interaction. No multiplicity adjustments were made. Results Significant treatment-by-subgroup interaction occurred for LDL-C (p = 0.013), total cholesterol (p = 0.025), non-HDL-C (p = 0.032), and apolipoprotein B (p = 0.016) with greater between-treatment differences in favor of EZ/Simva observed in patients from the high potency stratum vs low potency stratum. Individual and triple target attainment was higher for Eze/Simva compared with Rosuva in both strata. Conclusions Compared with Rosuva, switching to EZ/Simva provided greater reductions in LDL-C, total cholesterol, non-HDL-C and apolipoprotein B and higher target attainment in patients on prior statin treatment, regardless of potency, although patients treated with higher potency statins prior to randomization experienced greater between treatment differences in favor of EZ/Simva. Trial Registration Registered at ClinicalTrials.gov: NCT00479713</p
SWITCHING FROM STATIN MONOTHERAPY TO EZETIMIBE/SIMVASTATIN OR ROSUVASTATIN MODIFIES THE RELATIONSHIPS BETWEEN APOLIPOPROTEIN B, LDL CHOLESTEROL, ANC NON-HDL CHOLETEROL IN PATIENTS AT HIGH RISK OF CORONARY DISEASE
No full textOBJECTIVE:
To evaluate relationships between apolipoprotein B (Apo B), LDL cholesterol (LDL-C), and non-HDL-C in high-risk patients treated with lipid-lowering therapy.
DESIGN AND METHODS:
This post-hoc analysis calculated LDL-C and non-HDL-C levels corresponding to an Apo B of 0.9 g/L following treatment with 1) statin monotherapy (baseline) and 2) ezetimibe/simvastatin 10/20mg or rosuvastatin 10mg (study end). The percentages of patients reaching LDL-C, non-HDL-C, and Apo B targets were calculated at study end.
RESULTS:
After switching to ezetimibe/simvastatin or rosuvastatin, the LDL-C and non-HDL-C corresponding to Apo B=0.9 g/L were closer to the more aggressive LDL-C and non-HDL-C goals (1.81 and 2.59 mmol/L, respectively). Only slightly >50% of the patients who reached minimum recommended LDL-C or non-HDL-C at study end also had an Apo B level <0.9 g/L with both treatments.
CONCLUSION:
The use of Apo B for monitoring the efficacy of lipid-altering therapy would likely lead to more stringent criteria for lipid lowering
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