Differential effects of simvastatin and atorvastatin on high‐density lipoprotein cholesterol and apolipoprotein A‐I are consistent across hypercholesterolemic patient subgroups

Davidson, Michael; Ose, Leiv; Fröhlich, Jiří; Scott, Russell S.; Dujovne, Carlos A.; Escobar, Iván Darío; Bertolami, Marcelo Chiara; Cihon, Frank; Maccubbin, Darbie; Mercuri, Michele

doi:10.1002/clc.4960261106

Cited by 15 publications

(14 citation statements)

References 31 publications

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“…Patients who were started on statin therapy or had undergone doubling of a statin dose experienced a decrease in HDL-C levels. This unexpected effect was also reported in other studies [18,19]. The results of three randomized, multicenter clinical studies comparing the effects of atorvastatin and simvastatin on HDL-C were analyzed by Davidson et al (2003); who found that both drugs increased HDL-C consistently at low doses but at higher doses, simvastatin retained its raising effect on HDL-C while atorvastatin showed a negative dose response pattern [18], this may explain our results bearing in mind that majority of our study population were on atorvastatin.…”

Section: Discussionsupporting

confidence: 75%

“…This unexpected effect was also reported in other studies [18,19]. The results of three randomized, multicenter clinical studies comparing the effects of atorvastatin and simvastatin on HDL-C were analyzed by Davidson et al (2003); who found that both drugs increased HDL-C consistently at low doses but at higher doses, simvastatin retained its raising effect on HDL-C while atorvastatin showed a negative dose response pattern [18], this may explain our results bearing in mind that majority of our study population were on atorvastatin. Moreover, we noticed that patients who experienced transient reductions in HDL-C level experienced an increase afterwards which can be attributed to distributing brochures on life style modifications that can help increase HDL-C levels; however, we were not able to measure this effect due to study duration.…”

Section: Discussionsupporting

confidence: 75%

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The role of clinical pharmacist on lipid control in dyslipidemic patients in North of Jordan

et al. 2011

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Section: Discussionsupporting

confidence: 75%

Section: Discussionsupporting

confidence: 75%

The role of clinical pharmacist on lipid control in dyslipidemic patients in North of Jordan

et al. 2011

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“…One possible explanation is the relatively greater increase in HDL cholesterol in patients treated with high-dose simvastatin compared with those treated with high-dose atorvastatin, a finding consistent with previous studies. 16,17 Patients who have survived 4 months after ACS without a recurrent event could be considered to be patients with "stable coronary artery disease (CAD)." Data from the Treating to New Targets (TNT) and the Incremental Decrease in End points through Aggressive Lipid lowering (IDEAL) trials are consistent with the findings 18,19 in the chronic phases of A to Z and PROVE IT.…”

Section: Long-term Benefitmentioning

confidence: 99%

A Tale of Two Trials

et al. 2006

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Background-The Aggrastat to Zocor (A to Z) and Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE IT) trials compared intensive and moderate statin therapy after acute coronary syndromes, with seemingly disparate results. We analyzed the design, implementation, and results of the two trials in an attempt to clarify the effects of early intensive statin therapy. Methods and Results-Study design, end points, and definitions were compared. In each trial, comparisons were made between intensive and moderate arms for both trials' primary end points and death/myocardial infarction. Analyses were performed over various time points: at the end of the trials, Յ4 months, and Ͼ4 months. Subjects in A to Z had higher-risk demographics. More PROVE IT subjects were enrolled in the United States and underwent prerandomization revascularization. The low-density lipoprotein (LDL) difference was greater in A to Z than in PROVE IT early (Յ4 months) but less late. Significant C-reactive protein reduction was earlier in PROVE IT. With common end points, event rates were higher in A to Z, and early favorable separation of event curves was seen in PROVE IT but not in A to Z. Clinical end point rates and reductions were similar in both trials after 4 months. Conclusions-An early benefit was seen in PROVE IT but not in A to Z. Late-phase results were similar. Factors that may explain this disparity include the intensity of therapy in the early phase, timing, and magnitude of LDL and C-reactive protein lowering, differences in early revascularization, and the play of chance. Taken together, the results of these trials support a strategy of early intensive statin therapy coupled with revascularization when appropriate in patients after acute coronary syndrome.

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“…Whilst statins are able to reduce LDL cholesterol levels by 40% or more, their effects on HDL cholesterol levels are much more limited with elevations in efficacy trials usually reported to be in the 5-15% range [1][2][3]. Use of these agents in long term clinical trials has generally resulted in increases toward the lower end of this range.…”

Section: Hmg Coa Reductase Inhibitorsmentioning

confidence: 95%

Pharmacotherapy and HDL Cholesterol

Dart¹

2005

CMCIEMA

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The concentration of HDL cholesterol is a powerful predictor of the occurrence of cardiovascular events, with a possible causal relationship between these variables. As such, the ability of pharmacological agents to influence HDL levels, and to affect the related processes such as reverse cholesterol transport, is of considerable relevance to the prevention and treatment of cardiovascular disease.Whilst currently available lipid modifying therapy does influence HDL cholesterol levels, and those of its sub-fractions, the effects are generally modest in comparison with the effects which can be achieved in reducing levels of LDL cholesterol. Thus, HMG CoA reductase inhibitors at the prevailing doses generally increase HDL cholesterol by no more than 10%. Fibrates induce a somewhat similar response. Somewhat larger effects are seen with niacin, and smaller effects with ezetemibe. CETP inhibition by agents such as torcetrapib are able to produce more marked effects. Knowledge of the effects of these agents on functional processes in man, such as reverse cholesterol transport is limited.Evidence that elevation of plasma HDL levels can causally influence cardiovascular outcomes is largely dependent on studies with agents which principally influence HDL and triglyceride levels, rather than LDL, and in subjects with low HDL cholesterol levels at baseline. Trial data does not suggest that HDL modification is a major contributor to the clear beneficial effects of HMG CoA reductase inhibitions. Outcome trials with agents, such as torcetrapib, which effect larger changes in HDL cholesterol should give clearer insight into the potential therapeutic benefits of such strategies. However, newer approaches will be required to evaluate the efficacy of agents designed to improve functional aspects of HDL cholesterol such as cellular cholesterol efflux, as distinct from functions directly dependent on HDL cholesterol levels.

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Differential effects of simvastatin and atorvastatin on high‐density lipoprotein cholesterol and apolipoprotein A‐I are consistent across hypercholesterolemic patient subgroups

Cited by 15 publications

References 31 publications

The role of clinical pharmacist on lipid control in dyslipidemic patients in North of Jordan

The role of clinical pharmacist on lipid control in dyslipidemic patients in North of Jordan

A Tale of Two Trials

Pharmacotherapy and HDL Cholesterol

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