Beneficial effects of rosuvastatin alone and in combination with extended-release niacin in patients with a combined hyperlipidemia and low high-density lipoprotein cholesterol levels

Capuzzi, David M.; Morgan, John; Weiss, Robert; Chitra, Rohini; Hutchinson, Howard G.; Cressman, Michael D.

doi:10.1016/s0002-9149(03)00318-7

Cited by 68 publications

(53 citation statements)

References 25 publications

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“…Unexpectedly, rosuvastatin decreased ApoA-I mRNA, although clinical studies have shown an increase in ApoA-I levels. [34][35][36][37] Marchesi et al 38 reported that rosuvastatin did not increase ApoA-I transcription or hepatic secretion. The unexpected result obtained in our study, that is, rosuvastatin reduced hepatic ApoA-I mRNA, could be a consequence of hepatic cholesterol depletion attributable to the inhibition of statin, which may reduce hepatic HDL production.…”

Section: Discussionmentioning

confidence: 99%

Rosuvastatin Activates ATP-Binding Cassette Transporter A1–Dependent Efflux Ex Vivo and Promotes Reverse Cholesterol Transport in Macrophage Cells in Mice Fed a High-Fat Diet

Shimizu

Miura

Tanigawa

et al. 2014

ATVB

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Objective— It is controversial whether statins improve high-density lipoprotein (HDL) function, which plays an important role in reverse cholesterol transport in vivo. The aim of the present study was to clarify the effects of rosuvastatin and atorvastatin on reverse cholesterol transport in macrophage cells in vivo and their underlying mechanisms. Approach and Results— Male C57BL mice were divided into 3 groups (rosuvastatin, atorvastatin, and control groups) and orally administered rosuvastatin, atorvastatin, or placebo for 6 weeks under feeding with a 0.5% cholesterol+10% coconut oil diet. After administration, although there were no changes in plasma HDL cholesterol levels among the groups, plasma from the rosuvastatin group showed an increased ability to promote ATP-binding cassette transporter A1–mediated cholesterol efflux ex vivo. In addition, capillary electrophoresis revealed a shift in HDL toward the pre-β HDL fraction only in the rosuvastatin group. Mice in all 3 groups were intraperitoneally injected with 3 H-cholesterol–labeled and cholesterol-loaded macrophages and then were monitored for the appearance of 3 H-tracer in plasma and feces. The amount of 3 H-tracer excreted into feces during 48 hours in the rosuvastatin group was greater than that in the control group. Finally, 3 H-cholesteryl oleate-HDL was intravenously injected into all groups, blood samples were taken, and the count of 3 H-cholesterol was analyzed. Plasma 3 H-cholesteryl oleate-HDL changed similarly, and no differences in fractional catabolic rates were observed. Conclusions— Rosuvastatin enhanced the ATP-binding cassette transporter A1–dependent HDL efflux function of reverse cholesterol transport, and this finding highlights the potential of rosuvastatin for the regression of atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Rosuvastatin Activates ATP-Binding Cassette Transporter A1–Dependent Efflux Ex Vivo and Promotes Reverse Cholesterol Transport in Macrophage Cells in Mice Fed a High-Fat Diet

Shimizu

Miura

Tanigawa

et al. 2014

ATVB

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“…Given the pharmacological profile of nicotinic acid, its addition to statin monotherapy should provide an optimal strategy for raising HDL-cholesterol and improving the typical lipid profile of older patients. 63,64 Clinical evidence from the ARterial Biology for the Investigation of the Treatment Effects of Reducing cholesterol (ARBITER) 2 study in men with CVD (mean age 68 years) supports this rationale. 65 Although patients in ARBITER 2 had already achieved a mean LDL-cholesterol value of less than 2.6 mmol/L (100 mg/dL) on statin monotherapy, atherosclerosis continued to progress, as assessed by a significant increase in the intima media thickness of the carotid arteries (a valid surrogate cardiovascular end point).…”

Section: Hdl-cholesterol In An Ageing Societymentioning

confidence: 99%

The significance of low HDL-cholesterol levels in an ageing society at increased risk for cardiovascular disease

Windler

Schöffauer

Zyriax

2007

Diabetes and Vascular Disease Research

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I n most developed and developing countries, the proportion of the population aged 60 years or more is growing faster than any other age group. Given that the vast majority of cardiovascular events occur in older individuals, new thinking is needed to reduce their risk. Epidemiological studies have shown an increasing prevalence of the metabolic syndrome with age, driven by nutrition inappropriate for a modern sedentary lifestyle. A low level of high-density lipoprotein (HDL)-cholesterol, a component of the atherogenic dyslipidaemia of the metabolic syndrome, has been shown to be an important determinant of coronary risk, which rises in prevalence with increasing age. Thus, raising HDLcholesterol, in addition to lowering the level of low-density lipoprotein (LDL)-cholesterol, seems a plausible approach to reduce cardiovascular risk in an ageing population.Clinical studies have shown that adding nicotinic acid, which raises HDL-cholesterol by 20-25%, to a statin enhances the reduction in progression of atherosclerosis. Results of the ongoing Atherothrombosis Intervention in Metabolic syndrome with low HDL/High triglyceride and Impact on Global Health Outcomes (AIM-HIGH) study are awaited with interest to see whether such theoretical benefit translates into clinical outcome. 2007;4:136-42 doi:10.3132/dvdr.2007.032 Key words: cardiovascular disease, combination therapy, coronary heart disease, fibrate, HDL-cholesterol, lipidlowering therapy, metabolic syndrome, nicotinic acid, statin. Diabetes Vasc Dis Res IntroductionCardiovascular disease (CVD) has become the most important cause of morbidity and mortality in the developed world.1 Risk factors have been identified that explain the great majority of cardiovascular events in many countries, independently of ethnic origin: these include smoking, hypertension, dyslipidaemia and insulin resistance.2 In Western industrialised countries, and increasingly in Asian and developing countries, there has been an increase in the prevalence of the metabolic syndrome (figure 1), resulting from a sedentary lifestyle and inappropriate nutrition. The populations of these societies are also developing a longer life expectancy, with the proportion of individuals aged 60 years or more growing faster than any other age group.1 As a result, the incidence of important cardiovascular risk factors, such as hypertension, insulin resistance and dyslipidaemia, is accelerating. More than 50% of older subjects have two or more cardiovascular risk factors and might benefit from specific intervention. 3,4The central role of dyslipidaemia in cardiovascular disease Dyslipidaemia is one of the prominent risk factors for CVD in any population, as identified by the INTERHEART study, a global case control study.2 Specifically, the imbalance between atherogenic and atheroprotective lipoproteins was the most powerful potentially modifiable risk factor for CVD. The highest odds ratio for myocardial infarction was provided by the ratio of apolipoproteins B to A-I, indicative of the ratio of con...

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“…Treatment with niacin ER plus a statin administered as separate tablets has been shown to have beneficial effects on lipids in a number of randomized, controlled, double-blind, [5][6][7][8] or open-label [3,[9][10][11] clinical trials in patients with dyslipidemia. In a 24-week trial, [3] patients receiving atorvastatin or rosuvastatin plus niacin ER had significantly greater improvements in several lipid parameters compared with those receiving simvastatin plus ezetimibe or rosuvastatin alone.…”

Section: What Is the Efficacy Of Niacin Extended Release Plus A Statimentioning

confidence: 99%

“…[10] In other trials, the lipid-modifying effects of ER were often additive when used in combination with lovastatin, [5,6] rosuvastatin, [9] or atorvastatin.…”

Section: Potential Drug Interactionsmentioning

confidence: 99%

Niacin Extended Release (ER)/Simvastatin (Simcor®)

Lyseng‐Williamson

2010

Drugs R D

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Beneficial effects of rosuvastatin alone and in combination with extended-release niacin in patients with a combined hyperlipidemia and low high-density lipoprotein cholesterol levels

Cited by 68 publications

References 25 publications

Rosuvastatin Activates ATP-Binding Cassette Transporter A1–Dependent Efflux Ex Vivo and Promotes Reverse Cholesterol Transport in Macrophage Cells in Mice Fed a High-Fat Diet

Rosuvastatin Activates ATP-Binding Cassette Transporter A1–Dependent Efflux Ex Vivo and Promotes Reverse Cholesterol Transport in Macrophage Cells in Mice Fed a High-Fat Diet

The significance of low HDL-cholesterol levels in an ageing society at increased risk for cardiovascular disease

Niacin Extended Release (ER)/Simvastatin (Simcor®)

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