485
Views
2
CrossRef citations to date
0
Altmetric
Reviews

Effects of pitavastatin on HDL metabolism

, &
Pages 55-68 | Published online: 18 Jan 2017

References

  • Nabel EG, Braunwald E. A tale of coronary artery disease and myocardial infarction. N. Engl. J. Med. 366(1), 54–63 (2012).
  • Cholesterol Treatment Trialists’ (CTT) Collaboration; Baigent C, Blackwell L et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet 376(9753), 1670–1681 (2010).
  • Emerging Risk Factors Collaboration; Di Angelantonio E, Sarwar N, P Perry et al. Major lipids, apolipoproteins, and risk of vascular disease. JAMA 302(18), 1993–2000 (2009).
  • Singh IM, Shishehbor MH, Ansell BJ. High-density lipoprotein as a therapeutic target: a systematic review. JAMA 298(7), 786–798 (2007).
  • Briel M, Ferreira-Gonzalez I, You JJ et al. Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis. BMJ 338, b92 (2009).
  • deGoma EM, deGoma RL, Rader DJ. Beyond high-density lipoprotein cholesterol levels evaluating high-density lipoprotein function as influenced by novel therapeutic approaches. J. Am. Coll. Cardiol. 51(23), 2199–2211 (2008).
  • Hill SA, McQueen MJ. Reverse cholesterol transport – a review of the process and its clinical implications. Clin. Biochem. 30(7), 517–525 (1997).
  • Matsuzawa Y, Yamashita S, Kameda K, Kubo M, Tarui S, Hara I. Marked hyper-HDL2-cholesterolemia associated with premature corneal opacity. A case report. Atherosclerosis 53(2), 207–212 (1984).
  • Yamashita S, Arai T, Hirano K et al. Molecular disorders of cholesteryl ester transfer protein. J. Atheroscler. Thromb. 3(1), 1–11 (1996).
  • Matsuzawa Y, Yamashita S, Funahashi T, Yamamoto A, Tarui S. Selective reduction of cholesterol in HDL2 fraction by probucol in familial hypercholesterolemia and hyperHDL2 cholesterolemia with abnormal cholesteryl ester transfer. Am. J. Cardiol. 62(3), B66–B72 (1988).
  • Yamashita S, Hbujo H, Arai H et al. Long-term probucol treatment prevents secondary cardiovascular events: a cohort study of patients with heterozygous familial hypercholesterolemia in Japan. J. Atheroscler. Thromb. 15(6), 292–303 (2008).
  • Duggan ST. Pitavastatin: a review of its use in the management of hypercholesterolaemia or mixed dyslipidaemia. Drugs 72(4), 565–584 (2012).
  • Sasaki J. Pitavastatin approved for treatment of primary hypercholesterolemia and combined dyslipidemia. Vasc. Health Risk Manag. 6, 997–1005 (2010).
  • Yamashita S, Tsubakio-Yamamoto K, Ohama T, Nakagawa-Toyama Y, Nishida M. Molecular mechanisms of HDL-cholesterol elevation by statins and its effects on HDL functions. J. Atheroscler. Thromb. 17(5), 436–451 (2010).
  • Teramoto T. The clinical impact of pitavastatin: comparative studies with other statins on LDL-C and HDL-C. Expert Opin. Pharmacother. 13(6), 859–865 (2012). ▪ Pitavastatin’s ability to significantly increase HDL cholesterol (HDL-C) levels suggests a particular benefit for patients with low baseline levels of HDL-C who fail to increase their HDL-C levels using alternative statins.
  • Saito Y. Pitavastatin: an overview. Atheroscler. Suppl. 12(3), 271–276 (2011).
  • Park S, Kang HJ, Rim SJ et al. A randomized, open-label study to evaluate the efficacy and safety of pitavastatin compared with simvastatin in Korean patients with hypercholesterolemia. Clin. Ther. 27(7), 1074–1082 (2005).
  • Lee SH, Chung N, Kwan J et al. Comparison of the efficacy and tolerability of pitavastatin and atorvastatin: an 8-week, multicenter, randomized, open-label, dosetitration study in Korean patients with hypercholesterolemia. Clin. Ther. 29(11), 2365–2373 (2007).
  • Gumprecht J, Gosho M, Budinski D, Hounslow N. Comparative long-term efficacy and tolerability of pitavastatin 4 mg and atorvastatin 20–40 mg in patients with Type 2 diabetes mellitus and combined (mixed) dyslipidaemia. Diabetes Obes. Metab. 13(11), 1047–1055 (2011).
  • Sasaki J, Ikeda Y, Kuribayashi T et al. A 52-week, randomized, open-label, parallelgroup comparison of the tolerability and effects of pitavastatin and atorvastatin on high-density lipoprotein cholesterol levels and glucose metabolism in Japanese patients with elevated levels of low-density lipoprotein cholesterol and glucose intolerance. Clin. Ther. 30(6), 1089–1101 (2008).
  • Teramoto T, Urashima M, Shimano H, Yokote K, Saito Y; LIVES Study Extension Group. A large-scale survey on cardiocerebrovascular events during pitavastatin (LIVALO tablet) therapy in Japanese patients with hypercholesterolemia – LIVALO Effectiveness and Safety Study Extension (LIVES Study Extension). Jpn Pharmacol Ther. 39(9), 789–803 (2011).
  • Maruyama T, Takada M, Nishibori Y et al. Comparison of preventive effect on cardiovascular events with different statins – the CIRCLE study. Circ. J. 75(8), 1951–1959 (2011). ▪ Differences in the effects of statins on the prevention of cardiac events are due to differences in their potency in elevating HDL-C levels.
  • AIM-HIGH Investigators; Boden WE, Probstfield JL, Anderson T et al. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N. Engl. J. Med. 365(24), 2255–2267 (2011).
  • Okamoto H, Yonemori F, Wakitani K, Minowa T, Maeda K, Shinkai H. A cholesteryl ester transfer protein inhibitor attenuates atherosclerosis in rabbits. Nature 406(6792), 203–207 (2000).
  • Fayad ZA, Mani V, Woodward M et al. Safety and efficacy of dalcetrapib on atherosclerotic disease using novel noninvasive multimodality imaging (dal-PLAQUE): a randomized clinical trial. Lancet 378(9802), 1547–1559 (2011).
  • Barter PJ, Caulfield M, Eriksson M et al. Effects of torcetrapib in patients at high risk for coronary events. N. Engl. J. Med. 357(21), 2109–2122 (2007).
  • Hooper AJ, Burnett JR. Dalcetrapib, a cholesteryl ester transfer protein modulator. Expert Opin. Investig. Drugs 21(9), 1427–1432 (2012). ▪ The newly developed dalcetrapib, a new CETP inhibitor, has been disappointing.
  • Thompson A, Di Angelantonio E, Sarwar N et al. Association of cholesteryl ester transfer protein genotypes with CETP mass and activity, lipid levels, and coronary risk. JAMA 299(23), 2777–2788 (2008).
  • Hirano K, Yamashita S, Nakajima N et al. Genetic cholesteryl ester transfer protein deficiency is extremely frequent in the Omagari area of Japan. Marked hyperalphalipoproteinemia caused by CETP gene mutation is not associated with longevity. Arterioscler. Thromb. Vasc. Biol. 17(6), 1053–1059 (1997).
  • Ishigami M, Yamashita S, Sakai N et al. Large and cholesteryl ester-rich high-density lipoproteins in cholesteryl ester transfer protein (CETP) deficiency cannot protect macrophages from cholesterol accumulation induced by acetylated low-density lipoproteins. J. Biochem. 116(2), 257–262 (1994).
  • Mackey RH, Greenland P, Goff DC Jr, Lloyd-Jones D, Sibley CT, Mora S. High-density lipoprotein cholesterol and particle concentrations, carotid atherosclerosis, and coronary events: MESA (Multi-Ethnic Study of Atherosclerosis). J. Am. Coll. Cardiol. 60(6), 508–516 (2012). ▪▪ Describes, for the first time, the significant inverse relationship between HDL particles and cardiovascular risk, independent of atherogenic lipoproteins including HDL-C.
  • Jafri H, Alsheikh-Ali AA, Mooney P, Kimmelstiel CD, Karas RH, Kuvin JT. Extended-release niacin reduces LDL particle number without changing total LDL cholesterol in patients with stable CAD. J. Clin. Lipidol. 3(1), 45–50 (2009).
  • Rashedi N, Brennan D, Kastelein JJ, Nissen SE, Nicholls S. Impact of cholesteryl ester transfer protein inhibition on nuclear magnetic resonance derived lipoprotein particle parameters. Atheroscler. Suppl. 12, 48 (2011).
  • Zhang Y, Zanotti I, Reilly MP, Glick JM, Rothblat GH, Rader DJ. Overexpression of apolipoprotein A-I promotes reverse transport of cholesterol from macrophages to feces in vivo. Circulation 108(6), 661–663 (2003).
  • Nissen SE, Tsunoda T, Tuzcu EM et al. Effect of recombinant apoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial. JAMA 290(17), 2292–2300 (2003).
  • Khera AV, Cuchel M, de la Llera-Moya M et al. Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis. N. Engl. J. Med. 364(2), 127–135 (2011). ▪▪ Cholesterol efflux capacity is a better quantitative measure of HDL.
  • Zhang LH, Kamanna VS, Ganji SH et al. Pioglitazone increases apolipoprotein A-I production by directly enhancing PPREdependent transcription in HepG2 cells. J. Lipid. Res. 51, 2211–2222 (2010).
  • Kishida K, Funahashi T, Shimomura I. Molecular mechanisms of diabetes and atherosclerosis: role of adiponectin. Endocr. Metab. Immune Disord. Drug Targets 12(2), 118–131 (2012).
  • Ryo M, Nakamura T, Kihara S et al. Adiponectin as a biomarker of the metabolic syndrome. Circ. J. 68(11), 975–981 (2004).
  • Matsuura F, Oku H, Koseki M et al. Adiponectin accelerates reverse cholesterol transport by increasing high density lipoprotein assembly in the liver. Biochem. Biophys. Res. Commun. 358(4), 1091–1095 (2007).
  • Oku H, Matsuura F, Koseki M et al. Adiponectin deficiency suppresses ABCA1 expression and apoA-I synthesis in the liver. FEBS Lett. 581(26), 5029–5033 (2007).
  • Tsubakio-Yamamoto K, Matsuura F, Koseki M et al. Adiponectin prevents atherosclerosis by increasing cholesterol efflux from macrophages. Biochem. Biophys. Res. Commun. 375(3), 390–394 (2008).
  • Hirano K, Yamashita S, Matsuzawa Y. Pros and cons of inhibiting cholesteryl ester transfer protein. Curr. Opin. Lipidol. 11(6), 589–596 (2000).
  • Khera AV, Wolfe ML, Cannon CP, Qin J, Rader DJ. On-statin cholesteryl ester transfer protein mass and risk of recurrent coronary events (from the pravastatin or atorvastatin evaluation and infection therapy-thrombolysis in myocardial infarction 22 [PROVE IT-TIMI 22] study). Am. J. Cardiol. 106(4), 451–456 (2010). ▪▪ Describes, for the first time, the inverse correlation between decreasing CETP mass and coronary outcome during statin treatment.
  • Maejima T, Yamazaki H, Aoki T et al. Effect of pitavastatin on apolipoprotein A-I production in HepG2 cell. Biochem. Biophys. Res. Commun. 324(2), 835–839 (2004). ▪ In vitro study demonstrating higher production of apoA-I by pitavastatin compared with other statins.
  • Qin S, Koga T, Ganji SH, Kamanna VS, Kashyap ML. Rosuvastatin selectively stimulates apolipoprotein A-I but not apolipoprotein A-II synthesis in Hep G2 cells. Metabolism 57(7), 973–979 (2008).
  • Kobayashi M, Gouda K, Chisaki I, Ochiai M, Itagaki S, Iseki K. Regulation mechanism of ABCA1 expression by statins in hepatocytes. Eur. J. Pharmacol. 662(1–3), 9–14 (2011).
  • Nomura S, Shouzu A, Omoto S et al. Effects of pitavastatin on monocyte chemoattractant protein-1 in hyperlipidemic patients. Blood Coagul. Fibrinolysis 20(6), 440–447 (2009).
  • Matsubara T, Naruse K, Arakawa T et al. Impact of pitavastatin on high-sensitivity C-reactive protein and adiponectin in hypercholesterolemic patients with the metabolic syndrome: the PREMIUM study. J. Cardiol. 60(5), 389–394 (2012).
  • Kawano M, Nagasaka S, Yagyu H, Ishibashi S. Pitavastatin decreases plasma prebeta1-HDL concentration and might promote its disappearance rate in hypercholesterolemic patients. J. Atheroscler. Thromb. 15(1), 41–46 (2008).
  • Tani S, Nagao K, Hirayama A. Association of cholesteryl ester transfer protein mass with peripheral leukocyte count following statin therapy; a pilot study. Am. J. Cardiovasc. Drugs 12(5), 349–354 (2012). ▪ Comparative study demonstrating a higher rise in circulating HDL-C and production of apoA-I, and lower inhibitory action for CETP following treatment with pitavastatin compared with atorvastatin.
  • Watts GF, Barrett PH, Ji J et al. Differential regulation of lipoprotein kinetics by atorvastatin and fenofibrate in subjects with the metabolic syndrome. Diabetes 52(3), 803–811 (2003).
  • Vergès B, Florentin E, Baillot-Rudoni S et al. Rosuvastatin 20 mg restores normal HDLapoA-I kinetics in Type 2 diabetes. J. Lipid Res. 50(6), 1209–1215 (2009).
  • Kishida K, Funahashi T, Shimomura I. Importance of assessing the effect of statins on the function of high-density lipoproteins on coronary plaque. Cardiovasc. Hematol. Disord. Drug Targets 12(1), 28–34 (2012). ▪ The largest coronary plaque regression index associated with elevation in HDL-C (PH index) was noted following treatment with pitavastatin compared with atorvastatin, pravastatin, simvastatin and rosuvastatin.
  • Sponseller C, Morgan R et al. Pitavastatin 4 mg significantly reduces LDL-P and increases HDL size compared with pravastatin 40 mg: results from PREVAIL US. J. Clin. Lipid. 6(3), 288–289 (2012).
  • Camont L, Chapman MJ, Kontush A. Biological activities of HDL subpopulations and their relevance to cardiovascular disease. Trends Mol. Med. 17(10), 594–603 (2011).
  • Vaisar T, Shao B, Green PS, Oda MN, Oram JF, Heinecke JW. Myeloperoxidase and inflammatory proteins: pathways for generating dysfunctional high-density lipoprotein in humans. Curr. Atheroscler. Rep. 9(5), 417–424 (2007).
  • Vaisar T, Pennathur S, Green PS et al. Shotgun proteomics implicates protease inhibition and complement activation in the antiinflammatory properties of HDL. J. Clin. Invest. 117(3), 746–756 (2007).
  • Fournier N, Paul JL, Atger V et al. HDL phospholipid content and composition as a major factor determining cholesterol efflux capacity from Fu5AH cells to human serum. Arterioscler. Thromb. Vasc. Biol. 17(11), 2685–2691 (1997).
  • Arii K, Suehiro T, Ota K et al. Pitavastatin induces PON1 expression through p44/42 mitogen-activated protein kinase signaling cascade in Huh7 cells. Atherosclerosis 202(2), 439–445 (2009).
  • Ota K, Suehiro T, Arii K et al. Effect of pitavastatin on transactivation of human serum paraoxonase 1 gene. Clin. Biochem. 30(7), 517–525 (1997).
  • Kojima Y, Ishida T, Sun L et al. Pitavastatin decreases the expression of endothelial lipase both in vitro and in vivo. Cardiovasc Res. 87(2), 385–393 (2010).
  • Paradis ME, Badellino KO, Rader DJ et al. Endothelial lipase is associated with inflammation in humans. J. Lipid. Res. 47(12), 2808–2813 (2006).
  • Stender S, Budinski D, Gosho M, Hounslow N. Pitavastatin shows greater lipid-lowering efficacy over 12 weeks than pravastatin in elderly patients with primary hypercholesterolaemia or combined (mixed) dyslipidaemia. Eur. J. Prev. Cardiol. 20(1), 40–53 (2013).
  • Sansanayudh N, Wongwiwatthananukit S, Putwai P, Dhumma-Upakorn R. Comparative efficacy and safety of low-dose pitavastatin versus atorvastatin in patients with hypercholesterolemia. Ann. Pharmacother. 44(3), 415–423 (2010).
  • Ikeda K, Takahashi T, Yamada H et al. Effect of intensive statin therapy on regression of carotid intima-media thickness in patients with subclinical carotid atherosclerosis (a prospective, randomized trial: PEACE (Pitavastatin Evaluation of Atherosclerosis Regression by Intensive Cholesterol-lowering Therapy) study. Eur. J. Prev. Cardiol. (2012) (In Press).
  • Ose L, Budinski D, Hounslow N, Arneson V. Comparison of pitavastatin with simvastatin in primary hypercholesterolaemia or combined dyslipidaemia. Curr. Med. Res. Opin. 25(11), 2755–2764 (2009).
  • Budinski D, Arneson V, Hounslow N, Gratsiansky N. Pitavastatin compared with atorvastatin in primary hypercholesterolemia or combined dyslipidemia. Clin. Lipidol. 4(3), 291–302 (2009).
  • Saito Y, Yamada N, Teramoto T et al. A randomized, double-blind trial comparing the efficacy and safety of pitavastatin versus pravastatin in patients with primary hypercholesterolemia. Atherosclerosis 162(2), 373–379 (2002).
  • Yokote K, Bujo H, Hanaoka H et al. Multicenter collaborative randomized parallel group comparative study of pitavastatin and atorvastatin in Japanese hypercholesterolemic patients: collaborative study on hypercholesterolemia drug intervention and their benefits for atherosclerosis prevention (CHIBA study). Atherosclerosis 201(2), 345–352 (2008).
  • Yoshida H, Shoda T, Yanai H et al. Effects of pitavastatin and atorvastatin on lipoprotein oxidation biomarkers in patients with dyslipidemia. Atherosclerosis 226(1), 161–164 (2013).
  • Toi T, Taguchi I, Yoneda S et al. Early effect of lipid-lowering therapy with pitavastatin on regression of coronary atherosclerotic plaque. Comparison with atorvastatin. Circ. J. 73(8), 1466–1472 (2009).
  • Kimura S, Inoguchi T, Yokomizo H, Maeda Y, Sonoda N, Takayanagi R. Randomized comparison of pitavastatin and pravastatin treatment on the reduction of urinary albumin in patients with Type 2 diabetic nephropathy. Diabetes Obes. Metab. 14(7), 666–669 (2012).
  • Saku K, Zhang B, Noda K; PATROL Trial Investigators. Randomized head-to-head comparison of pitavastatin, atorvastatin, and rosuvastatin for safety and efficacy (quantity and quality of LDL): the PATROL trial. Circ. J. 75(6), 1493–1505 (2011).
  • Shimabukuro M, Higa M, Tanaka H, Shimabukuro T, Yamakawa K, Masuzaki H. Distinct effects of pitavastatin and atorvastatin on lipoprotein subclasses in patients with Type 2 diabetes mellitus. Diabet. Med. 28(7), 856–864 (2011).
  • Yanagi K, Monden T, Ikeda S, Matsumura M, Kasai K. A crossover study of rosuvastatin and pitavastatin in patients with Type 2 diabetes. Adv. Ther. 28(2), 160–171 (2011).
  • Nozue T, Yamamoto S, Tohyama S et al. Statin treatment for coronary artery plaque composition based on intravascular ultrasound radiofrequency data analysis. Am. Heart J. 163(2), 191.e1–199.e1 (2012).
  • Hiro T, Kimura T, Morimoto T et al. Effect of intensive statin therapy on regression of coronary atherosclerosis in patients with acute coronary syndrome: a multicenter randomized trial evaluated by volumetric intravascular ultrasound using pitavastatin versus atorvastatin (JAPAN-ACS [Japan assessment of pitavastatin and atorvastatin in acute coronary syndrome] study). J. Am. Coll. Cardiol. 54(4), 293–302 (2009).
  • Eriksson M, Budinski D, Hounslow N. Comparative efficacy of pitavastatin and simvastatin in high-risk patients: a randomized controlled trial. Adv. Ther. 28(9), 811–823 (2011).
  • Eriksson M, Budinski D, Hounslow N. Long-term efficacy of pitavastatin versus simvastatin. Adv. Ther. 28(9), 799–810 (2011).
  • Martin G, Duez H, Blanquart C et al. Statin-induced inhibition of the Rhosignaling pathway activates PPARalpha and induces HDL apoA-I. J. Clin. Invest. 107(11), 1423–1432 (2001).
  • Fan P, Zhang B, Kuroki S, Saku K. Pitavastatin, a potent hydroxymethylglutaryl coenzyme a reductase inhibitor, increases cholesterol 7 alpha-hydroxylase gene expression in HepG2 cells. Circ. J. 68(11), 1061–1066 (2004).
  • Marchesi M, Parolini C, Caligari S et al. Rosuvastatin does not affect human apolipoprotein A-I expression in genetically modified mice: a clue to the disputed effect of statins on HDL. Br. J. Pharmacol. 164(5), 1460–1468, (2011).
  • Maejima T, Sugano T, Yamazaki H et al. Pitavastatin increases ABCA1 expression by dual mechanisms: SREBP2-driven transcriptional activation and PPARadependent protein stabilization but without activating LXR in rat hepatoma McARH7777 cells. J. Pharmacol. Sci. 116(1), 107–115 (2011).
  • Fukutomi T, Takeda Y, Suzuki S, Ito T, Joh T, Itoh M. High density lipoprotein cholesterol and apolipoprotein A-I are persistently elevated during long-term treatment with pitavastatin, a new HMG-CoA reductase inhibitor. Int. J. Cardiol. 141(3), 320–322 (2010).
  • Kawashiri MA, Nohara A, Tada H et al. Comparison of effects of pitavastatin and atorvastatin on plasma coenzyme Q10 in heterozygous familial hypercholesterolemia: results from a crossover study. Clin. Pharmacol. Ther. 83(5), 731–739 (2008).
  • Ishihara Y, Ohmori K, Mizukawa M, Hasan AU, Noma T, Kohno M. Beneficial direct adipotropic actions of pitavastatin in vitro and their manifestations in obese mice. Atherosclerosis 212(1), 131–138 (2010).
  • Abe M, Matsuda M, Kobayashi H et al. Effects of statins on adipose tissue inflammation: their inhibitory effect on MyD88-independent IRF3/IFN-beta pathway in macrophages. Arterioscler. Thromb. Vasc. Biol. 28(5), 871–877 (2008).
  • Yasuda Y, Shimizu M, Shirakami Y et al. Pitavastatin inhibits azoxymethane-induced colonic preneoplastic lesions in C57BL/KsJdb/db obese mice. Cancer Sci. 101(7), 1701–1707 (2010).
  • Shimizu M, Yasuda Y, Sakai H et al. Pitavastatin suppresses diethylnitrosamineinduced liver preneoplasms in male C57BL/ KsJ-db/db obese mice. BMC Cancer 28(11), 281 (2011).
  • Nakagawa H, Tsunooka N, Yamamoto Y, Yoshida M, Nakata T, Kawachi K. Pitavastatin prevents intestinal ischemia/ reperfusion-induced bacterial translocation and lung injury in atherosclerotic rats with hypoadiponectinemia. Surgery 145(5), 542–549 (2009).
  • Nomura S, Shouzu A, Omoto S et al. Correlation between adiponectin and reduction of cell adhesion molecules after pitavastatin treatment in hyperlipidemic patients with Type 2 diabetes mellitus. Thromb. Res. 122(1), 39–45 (2008).
  • Inami N, Nomura S, Shouzu A et al. Effects of pitavastatin on adiponectin in patients with hyperlipidemia. Pathophysiol. Haemost. Thromb. 36(1), 1–8 (2007).
  • Nomura S, Inami N, Shouzu A et al. The effects of pitavastatin, eicosapentaenoic acid and combined therapy on platelet-derived microparticles and adiponectin in hyperlipidemic, diabetic patients. Platelets 20(1), 16–22 (2009).
  • Yoshioka K, Murakami Y, Ego K, Nakajima Y. Effect of pitavastatin on serum high-molecular weight (HMW) adiponectin to total adiponectin ratio in Type 2 diabetic patients. Clin. Res. Rev. 4, 95–96 (2010).
  • Nomura S, Taniura T, Shouzu A et al. Effects of pitavastatin on plasminogen activator inhibitor-1 in hyperlipidemic patients. Int. J. Gen. Med. 5, 535–540 (2012).
  • Arao K, Yasu T, Umemoto T et al. Effects of pitavastatin on fasting and postprandial endothelial function and blood rheology in patients with stable coronary artery disease. Circ. J. 73(8), 1523–1530 (2009).
  • Ohashi T, Shibata R, Morimoto T et al. Correlation between circulating adiponectin levels and coronary plaque regression during aggressive lipid-lowering therapy in patients with acute coronary syndrome: subgroup analysis of JAPAN-ACS study. Atherosclerosis 212(1), 237–242 (2010).
  • Ohbayashi H. Pitavastatin improves serum resistin levels in patients with hypercholesterolemia. J. Atheroscler. Thromb. 15(2), 87–93 (2008).
  • Wong J, Quinn CM, Gelissen IC, Jessup W, Brown AJ. The effect of statins on ABCA1 and ABCG1 expression in human macrophages is influenced by cellular cholesterol levels and extent of differentiation. Atherosclerosis 196(1), 180–189 (2008).
  • Zanotti I, Potì F, Favari E, Steffensen KR, Gustafsson JA, Bernini F. Pitavastatin effect on ATP binding cassette A1-mediated lipid efflux from macrophages: evidence for liver X receptor (LXR)-dependent and LXRindependent mechanisms of activation by cAMP. J. Pharmacol. Exp. Ther. 317(1), 395–401 (2006).
  • Akisato Y, Ishii I, Kitahara M, Tamaki T, Saito Y, Kitada M. [Effect of pitavastatin on macrophage cholesterol metabolism]. Yakugaku Zasshi 128(3), 357–363 (2008).
  • Ando H, Tsuruoka S, Yamamoto H, Takamura T, Kaneko S, Fujimura A. Effects of pravastatin on the expression of ATP-binding cassette transporter A1. J. Pharmacol. Exp. Ther. 311(1), 420–425 (2004).
  • Navab M, Anantharamaiah GM, Hama S et al. D-4F and statins synergize to render HDL antiinflammatory in mice and monkeys and cause lesion regression in old apolipoprotein E-null mice. Arterioscler. Thromb. Vasc. Biol. 25(7), 1426–1432 (2005).
  • Schweitzer M, Tessier D, Vlahos WD et al. A comparison of pravastatin and gemfibrozil in the treatment of dyslipoproteinemia in patients with non-insulin-dependent diabetes mellitus. Atherosclerosis 162(1), 201–210 (2002).
  • Tani S, Nagao K, Anazawa T et al. Relation of change in apolipoprotein B/apolipoprotein A-I ratio to coronary plaque regression after pravastatin treatment in patients with coronary artery disease. Am. J. Cardiol. 105(2), 144–148 (2010).
  • Cheung MC, Austin MA, Moulin P, Wolf AC, Cryer D, Knopp RH. Effects of pravastatin on apolipoprotein-specific high density lipoprotein subpopulations and low density lipoprotein subclass phenotypes in patients with primary hypercholesterolemia. Atherosclerosis 102(1), 107–119 (1993).
  • Blom DJ, Marais AD, Retterstøl K et al. Rosuvastatin reduces non-high-density lipoprotein cholesterol and lipoprotein remnants in patients with dysbetalipoproteinemia (Fredrickson type III hyperlipoproteinemia). J. Clin. Lipidol. 2(6), 418–425 (2008).
  • Napoli C, Leccese M, Palumbo G et al. Effects of vitamin E and HMG-CoA reductase inhibition on cholesteryl ester transfer protein and lecithin-cholesterol acyltransferase in hypercholesterolemia. Coron. Artery Dis. 9(5), 257–264 (1998).
  • Inazu A, Koizumi J, Kajinami K, Kiyohar T, Chichibu K, Mabuchi H. Opposite effects on serum cholesteryl ester transfer protein levels between long-term treatments with pravastatin and probucol in patients with primary hypercholesterolemia and xanthoma. Atherosclerosis 145(2), 405–413 (1999).
  • Doncheva NI, Nikolov KV, Vassileva DP. Lipid-modifying and pleiotropic effects of gemfibrozil, simvastatin and pravastatin in patients with dyslipidemia. Folia Med. (Plovdiv) 48(3–4), 56–61 (2006).
  • Takagi T, Matsuda M, Abe M et al. Effect of pravastatin on the development of diabetes and adiponectin production. Atherosclerosis 196(1), 114–121 (2008).
  • Chen Y, Ohmori K, Mizukawa M et al. Differential impact of atorvastatin vs pravastatin on progressive insulin resistance and left ventricular diastolic dysfunction in a rat model of Type II diabetes. Circ. J. 71(1), 144–152 (2007).
  • Beltowski J, Atanassova P, Chaldakov GN, Jamroz-Wisniewska A, Kula W, Rusek M. Opposite effects of pravastatin and atorvastatin on insulin sensitivity in the rat: role of vitamin D metabolites. Atherosclerosis 219(2), 526–531 (2011).
  • Saito S, Fujiwara T, Matsunaga T et al. Increased adiponectin synthesis in the visceral adipose tissue in men with coronary artery disease treated with pravastatin: a role of the attenuation of oxidative stress. Atherosclerosis 199(2), 378–383 (2008).
  • Yokoyama H, Saito S, Daitoku K et al. Effects of pravastatin and rosuvastatin on the generation of adiponectin in the visceral adipose tissue in patients with coronary artery disease. Fundam. Clin. Pharmacol. 25(3), 378–387 (2011).
  • Koh KK, Quon MJ, Sakuma I et al. Differential metabolic effects of rosuvastatin and pravastatin in hypercholesterolemic patients. Int. J. Cardiol. doi: 10.1016/j.ijcard.2011.11.028">10.1016/j.ijcard.2011.11.028 (2011) (Epub ahead of print).
  • Gannagé-Yared MH, Azar RR, Amm-Azar M et al. Pravastatin does not affect insulin sensitivity and adipocytokines levels in healthy nondiabetic patients. Metabolism 54(7), 947–951 (2005).
  • Tanaka N, Abe-Dohmae S, Iwamoto N, Fitzgerald ML, Yokoyama S. HMG-CoA reductase inhibitors enhance phagocytosis by upregulating ATP-binding cassette transporter A7. Atherosclerosis 217(2), 407–414 (2011).
  • Genvigir FD, Rodrigues AC, Cerda A et al. Effects of lipid-lowering drugs on reverse cholesterol transport gene expressions in peripheral blood mononuclear and HepG2 cells. Pharmacogenomics 11(9), 1235–1246 (2010).
  • Song G, Liu J, Zhao Z et al. Simvastatin reduces atherogenesis and promotes the expression of hepatic genes associated with reverse cholesterol transport in apoE-knockout mice fed high-fat diet. Lipids Health Dis. 10, 8 (2011).
  • Quinet EM, Basso MD, Halpern AR et al. LXR ligand lowers LDL cholesterol in primates, is lipid neutral in hamster, and reduces atherosclerosis in mouse. J. Lipid Res. 50(12), 2358–2370 (2009).
  • Homma Y, Ozawa H, Kobayashi T, Yamaguchi H, Sakane H, Nakamura H. Effects of simvastatin on plasma lipoprotein subfractions, cholesterol esterification rate, and cholesteryl ester transfer protein in type II hyperlipoproteinemia. Atherosclerosis 114(2), 223–234 (1995).
  • Guan JZ, Tamasawa N, Murakami H et al. HMG-CoA reductase inhibitor, simvastatin improves reverse cholesterol transport in Type 2 diabetic patients with hyperlipidemia. J. Atheroscler. Thromb. 15(1), 20–25 (2008).
  • Franceschini G, Calabresi L, Colombo C, Favari E, Bernini F, Sirtori CR. Effects of fenofibrate and simvastatin on HDL-related biomarkers in low-HDL patients. Atherosclerosis 195(2), 385–391 (2007).
  • Hajer GR, Dallinga-Thie GM, van Vark-van der Zee LC, Olijhoek JK, Visseren FL. Lipid-lowering therapy does not affect the postprandial drop in high density lipoproteincholesterol (HDL-C) plasma levels in obese men with metabolic syndrome: a randomized double blind crossover trial. Clin. Endocrinol. (Oxf.) 69(6), 870–877 (2008).
  • Yin X, Tu L, Yang H. Effect of simvastatin on IL-6 and adiponectin secretion and mRNA expression in 3T3-L1 adipocytes. J. Huazhong Univ. Sci. Technol. Med. Sci. 27(3), 248–251 (2007).
  • Sakamoto K, Osaki M, Hozumi A et al. Simvastatin suppresses dexamethasoneinduced secretion of plasminogen activator inhibitor-1 in human bone marrow adipocytes. BMC Musculoskelet. Disord. 12(1), 82 (2011).
  • Hu Y, Tong G, Xu W et al. Anti-inflammatory effects of simvastatin on adipokines in Type 2 diabetic patients with carotid atherosclerosis. Diab. Vasc. Dis. Res. 6(4), 262–268 (2009).
  • Tsutamoto T, Yamaji M, Kawahara C et al. Effect of simvastatin vs. rosuvastatin on adiponectin and haemoglobin A1c levels in patients with non-ischaemic chronic heart failure. Eur. J. Heart Fail. 11(12), 1195–1201 (2009).
  • Devaraj S, Siegel D, Jialal I. Simvastatin (40 mg/day), adiponectin levels, and insulin sensitivity in subjects with the metabolic syndrome. Am. J. Cardiol. 100(9), 1397–1399 (2007).
  • Koh KK, Quon MJ, Han SH et al. Simvastatin improves flow-mediated dilation but reduces adiponectin levels and insulin sensitivity in hypercholesterolemic patients. Diabetes Care 31(4), 776–782 (2008).
  • Pfützner A, Hanefeld M, Lübben G et al. Visfatin: a putative biomarker for metabolic syndrome is not influenced by pioglitazone or simvastatin treatment in nondiabetic patients at cardiovascular risk – results from the PIOSTAT study. Horm. Metab. Res. 39(10), 764–768 (2007).
  • Sone H, Shimano H, Shu M et al. Statins downregulate ATP-binding-cassette transporter A1 gene expression in macrophages. Biochem. Biophys. Res. Commun. 316(3), 790–794 (2004).
  • Schmidt WM, Spiel AO, Jilma B, Wolzt M, Müller M. In-vivo effects of simvastatin and rosuvastatin on global gene expression in peripheral blood leucocytes in a human inflammation model. Pharmacogenet. Genomics 18(2), 109–120 (2008).
  • Dallongeville J, Fruchart JC, Pfister P, Bard JM. Fluvastatin reduces levels of plasma apo B-containing particles and increases those of LpA-I. European Fluvastatin Study Group. Am. J. Med. 96(6A), S32–S36 (1994).
  • Broyles FE, Walden CE, Hunninghake DB, Hill-Williams D, Knopp RH. Effect of fluvastatin on intermediate density lipoprotein (remnants) and other lipoprotein levels in hypercholesterolemia. Am. J. Cardiol. 76(2), A129–A135 (1995).
  • Sonmez A, Dogru T, Tasci I et al. The effect of fluvastatin on plasma adiponectin levels in dyslipidaemia. Clin. Endocrinol. (Oxf.) 64(5), 567–572 (2006).
  • de Haan W, van der Hoogt CC, Westerterp M et al. Atorvastatin increases HDL cholesterol by reducing CETP expression in cholesterolfed APOE*3-Leiden.CETP mice. Atherosclerosis 197(1), 57–63 (2008).
  • Rashid S, Uffelman KD, Barrett PH, Lewis GF. Effect of atorvastatin on high-density lipoprotein apolipoprotein A-I production and clearance in the New Zealand white rabbit. Circulation 106(23), 2955–2960 (2002).
  • Ooi TC, Heinonen T, Alaupovic P et al. Efficacy and safety of a new hydroxymethylglutaryl-coenzyme A reductase inhibitor, atorvastatin, in patients with combined hyperlipidemia: comparison with fenofibrate. Arterioscler. Thromb. Vasc. Biol. 17(9), 1793–1799 (1997).
  • Koh KK, Quon MJ, Han SH et al. Additive beneficial effects of fenofibrate combined with atorvastatin in the treatment of combined hyperlipidemia. J. Am. Coll. Cardiol. 45(10), 1649–1653 (2005).
  • Harangi M, Mirdamadi HZ, Seres I et al. Atorvastatin effect on the distribution of high-density lipoprotein subfractions and human paraoxonase activity. Transl. Res. 153(4), 190–198 (2009).
  • Guerin M, Lassel TS, Le Goff W, Farnier M, Chapman MJ. Action of atorvastatin in combined hyperlipidemia : preferential reduction of cholesteryl ester transfer from HDL to VLDL1 particles. Arterioscler. Thromb. Vasc. Biol. 20(1), 189–197 (2000).
  • Qu HY, Xiao YW, Jiang GH, Wang ZY, Zhang Y, Zhang M. Effect of atorvastatin versus rosuvastatin on levels of serum lipids, inflammatory markers and adiponectin in patients with hypercholesterolemia. Pharm. Res. 26(4), 958–964 (2009).
  • Karalis IK, Bergheanu SC, Wolterbeek R et al. Effect of increasing doses of Rosuvastatin and atorvastatin on apolipoproteins, enzymes and lipid transfer proteins involved in lipoprotein metabolism and inflammatory parameters. Curr. Med. Res. Opin. 26(10), 2301–2313 (2010).
  • van Hoek M, van Tol A, van Vark-van der Zee LC et al. Role of plasma adiponectin on the HDL-Cholesterol raising effect of atorvastatin in patients with Type 2 diabetes. Curr. Med. Res. Opin. 25(1), 93–101 (2009).
  • Labuzek K, Buldak L, Dulawa-Buldak A et al. Atorvastatin and fenofibric acid differentially affect the release of adipokines in the visceral and subcutaneous cultures of adipocytes that were obtained from patients with and without mixed dyslipidemia. Pharmacol. Rep. 63(5), 1124–1136 (2011).
  • Mäuser W, Perwitz N, Meier B, Fasshauer M, Klein J. Direct adipotropic actions of atorvastatin: differentiation state-dependent induction of apoptosis, modulation of endocrine function, and inhibition of glucose uptake. Eur. J. Pharmacol. 564(1–3), 37–46 (2007).
  • Matafome P, Monteiro P, Nunes E et al. Therapeutic association of atorvastatin and insulin in cardiac ischemia: study in a model of Type 2 diabetes with hyperlipidemia. Pharmacol. Res. 58(3–4), 208–214 (2008).
  • Miyagishima K, Hiramitsu S, Kato S et al. Efficacy of atorvastatin therapy in ischaemic heart disease – effects on oxidized low-density lipoprotein and adiponectin. J. Int. Med. Res. 35(4), 534–539 (2007).
  • Chu CS, Lee KT, Lee MY et al. Effects of atorvastatin and atorvastatin withdrawal on soluble CD40L and adipocytokines in patients with hypercholesterolaemia. Acta Cardiol. 61(3), 263–269 (2006).
  • Chan KC, Chou HH, Huang CN, Chou MC. Atorvastatin administration after percutaneous coronary intervention in patients with coronary artery disease and normal lipid profiles: impact on plasma adiponectin level. Clin. Cardiol. 31(6), 253–258 (2008).
  • de Haan W, de Vries-van der Weij J, van der Hoorn JW et al. Torcetrapib does not reduce atherosclerosis beyond atorvastatin and induces more proinflammatory lesions than atorvastatin. Circulation 117(19), 2515–2522 (2008).
  • Argmann CA, Edwards JY, Sawyez CG et al. Regulation of macrophage cholesterol efflux through hydroxymethylglutaryl-CoA reductase inhibition: a role for RhoA in ABCA1-mediated cholesterol efflux. J. Biol. Chem. 280(23), 22212–22221 (2005).
  • Qiu G, Hill JS. Atorvastatin inhibits ABCA1 expression and cholesterol efflux in THP-1 macrophages by an LXR-dependent pathway. J. Cardiovasc. Pharmacol. 51(4), 388–395 (2008).
  • Ishibashi Y, Matsui T, Takeuchi M, Yamagishi S. Rosuvastatin blocks advanced glycation end products-elicited reduction of macrophage cholesterol efflux by suppressing NADPH oxidase activity via inhibition of geranylgeranylation of Rac-1. Horm. Metab. Res. 43(9), 619–624 (2011).
  • Nissen SE, Tuzcu EM, Schoenhagen P et al. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. JAMA 291(9), 1071–1080 (2004).
  • Hong MK, Park DW, Lee CW et al. Effects of statin treatments on coronary plaques assessed by volumetric virtual histology intravascular ultrasound analysis. JACC Cardiovasc. Interv. 2(7), 679–688 (2009).
  • Nissen SE, Nicholls SJ, Sipahi I et al. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. JAMA 295(13), 1556–1565 (2006).
  • Takashima H, Ozaki Y, Yasukawa T et al. Impact of lipid-lowering therapy with pitavastatin, a new HMG-CoA reductase inhibitor, on regression of coronary atherosclerotic plaque. Circ. J. 71(11), 1678–1684 (2007).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.