Dose-dependent Effect of Rosuvastatin Treatment on HDL-subfraction Phenotype in Patients With Primary Hyperlipidemia

Kostapanos, Michael S.; Milionis, Haralampos; Filippatos, Theodosios D.; Christogiannis, Leonidas; Bairaktari, Eleni; Tselepis, Alexandros D.; Elisaf, Moses

doi:10.1177/1074248408331031

Cited by 29 publications

(29 citation statements)

References 35 publications

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“…This finding is in line with the results of previous studies 33,34) showing the beneficial effects of statins via an increase in the level of large HDL particles. Indeed, statin therapy induces a minor increase in the HDL-C level (by 5-10%), consistent with a reduction in the cholesteryl ester transfer protein activity and stimulation of apolipoprotein A-Ⅰ production 35) .…”

Section: Acknowledgements and Notice Of Grant Supportsupporting

confidence: 83%

Interrelated Cathepsin S-Lowering and LDL Subclass Profile Improvements Induced by Atorvastatin in the Plasma of Stable Angina Patients

Mirjanic-Azaric

Vekić

Zeljković

et al. 2014

JAT

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Aim:We hypothesized that, in stable angina patients, atorvastatin therapy lowers the cathepsin S (CTSS) concentrations, as assessed non-invasively according to a plasma analysis. In addition, the low-density lipoprotein (LDL) and high-density lipoprotein (HDL) size and subclasses in the plasma were analysed to establish the association between CTSS and lipoprotein metabolism and determine whether this association is atorvastatin-sensitive. Methods: A total of 43 patients with stable angina received atorvastatin therapy (20 mg/day, 10 weeks). The plasma CTSS mRNA levels, CTSS protein concentrations and CTSS activity, as well as LDL and HDL size and subclasses, were analysed before and after treatment. Results: Atorvastatin treatment did not change the plasma CTSS mRNA levels, although it lowered the plasma CTSS concentrations and activity. An increased plasma CTSS concentration and activity were found to be associated with a more atherogenic LDL subclass profile (a decreased dominant LDL size and increased percentage of small, dense LDL particles). The atorvastatin-induced CTSSlowering effect was concomitant with an improvement in the LDL subclass profile, and the changes were found to be interrelated. Concomitant, interrelated changes in the CTSS levels and LDL subclass profiles were found in the LDL phenotype B patients only (a dominant LDL diameter of ≤ 25.5 nm at the start of the study). In this subgroup, lowering of the plasma CTSS mRNA level also correlated with lowering of the proportion of small, dense LDL particles. Conclusions: Atorvastatin-induced CTSS-lowering and LDL subclass profile improvements in the plasma of LDL phenotype B patients with stable angina are concomitant and interrelated. J Atheroscler Thromb, 2014; 21:868-877.

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Section: Acknowledgements and Notice Of Grant Supportsupporting

confidence: 83%

Interrelated Cathepsin S-Lowering and LDL Subclass Profile Improvements Induced by Atorvastatin in the Plasma of Stable Angina Patients

Mirjanic-Azaric

Vekić

Zeljković

et al. 2014

JAT

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“…Surprisingly, only a few studies investigated the effect of statins on HDL subclasses, and the results are not concordant. Results of the clinical studies are summarized in Table 2 [29][30][31][32][33][34][35][36][37][38][39][40][41][42]. Unfortunately, different statins have been administered in different doses for various patient populations.…”

Section: Effect Of Statins On Hdl Subfractionsmentioning

confidence: 99%

Benefits and Difficulties in Measuring HDL Subfractions and Human Paraoxonase-1 Activity During Statin Treatment

Harangi

Serés

Harangi³

et al. 2009

Cardiovasc Drugs Ther

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Dyslipidaemia including decreased high density lipoprotein cholesterol concentration is one of several factors that have been implicated in increased cardiovascular risk. Since their introduction in the 1980s, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have emerged as the one of the best-selling class of medications to date, with numerous trials demonstrating powerful efficacy in preventing cardiovascular diseases. Although statins have been shown to modestly raise or not alter HDL-cholesterol, their effect on HDL subfractions and on HDL-associated enzymes including human paraoxonase-1 (PON1) has not yet been fully explored. This review summarizes the currently available data on the effect of statins on HDL subfractions and on PON1 activity with a particular emphasis on the clinical relevance of these effects. Moreover, methodological problems of HDL subfraction and PON1 activity determinations are also discussed.

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“…Our randomised placebo-controlled study showed that 8-week treatment with simvastatin, bezafibrate and their combination does not affect serum PON-I activity in type 2 diabetes [84]. Since the appearance of our paper, it was reported that administration of various doses of rosuvastatin does not affect serum PON-I activity in primary dyslipidemic subjects [87]. PON-I activity was also unchanged after 3-month treatment with 5-10 mg simvastatin in hypercholesterolemic type 2 diabetic patients [88].…”

Section: (Farouk Mookadam and Kathryn Boyle)mentioning

confidence: 93%

Research update for articles published in EJCI in 2009

Abed

Adlbrecht

Señarís

et al. 2011

European Journal of Clinical Investigation

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Dose-dependent Effect of Rosuvastatin Treatment on HDL-subfraction Phenotype in Patients With Primary Hyperlipidemia

Cited by 29 publications

References 35 publications

Interrelated Cathepsin S-Lowering and LDL Subclass Profile Improvements Induced by Atorvastatin in the Plasma of Stable Angina Patients

Interrelated Cathepsin S-Lowering and LDL Subclass Profile Improvements Induced by Atorvastatin in the Plasma of Stable Angina Patients

Benefits and Difficulties in Measuring HDL Subfractions and Human Paraoxonase-1 Activity During Statin Treatment

Research update for articles published in EJCI in 2009

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