up-to-date with a click!
Update - Week 04,  2018
Curated by Peter Lansberg,
a Dutch lipidologist and educator, and
reviewed by prof. Philip Barter, Past President of the
International Atherosclerosis Society.

The IAS Statin Newsletter will keep you up-to-date with all recent statin publications, using a curated approach to select relevant articles.

Key publications

Are Nutraceuticals the solution for SAMS?
Despite the evidence of statin safety, tolerability remains a pressing issue for patients and prescribers. Perceived side effects and genuine toxicity are difficult to properly separate and ultimately it is the patient’s perception and complaints that determines this diagnostic label. Ward and Watts present their findings and views on substituting statins for nutraceuticals to reduce LDL-c in patients with statin intolerance. The most commonly used substances; red yeast rice (RYR), policosanol, polyphenols (resveratrol, anthocyanins, curcumins and iso-flavones) are discussed and reviewed. One commercial available product Armolipid Plus, containing 6 compounds including RYR, berberine, and policosanol, is discussed as well as tested in a small clinical trial. Non-lipid lowering targets that potentially could neutralize the harmful effects of statin are presented and reviewed; e.g., Coenzyme Q10, Vitamin D and Curcumoids. These compounds are sometimes suggested to ameliorate statin associated muscle symptoms (SAMS), but the published evidence up until now is far from convincing partly because of the lack of studies (Vitamin D supplementation), poor quality of the studies and the very small number of well characterized participants. The authors emphasize the urgent need for properly designed and executed trials to properly manage patient presenting with SAMS and exploring the benefits of nutraceuticals.
Ward NC, Pang J, Ryan JDM, Watts GF. Nutraceuticals in the management of patients with statin-associated muscle symptoms, with a note on real-world experience. Clin Cardiol 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29363784
Intriguing effects of HDL-c on renal function in the TNT study
The renal effects of atorvastatin are examined this re-analysis of the TNT data. Data from 9542 participants with table CHD, using 10 or 80 mg of atorvastatin were included in the final analysis. HDL-c levels were divided into quintiles. Individuals (N=6 319) with normal eGFR (≥60mL/min per 1.73m2) plus higher HDL-c plasma levels, at 3 months, were at reduced risk for declining eGFR during follow-up. Compared to quintile 1, the quintiles 2,3,4 and 5 showed HR’s of 1.04, 0.88, 0.85 and 0.77 respectively. This was after adjusting the data for age, gender and treatment allocation, suggesting confounding effects of these variables. in the unadjusted model. No statistical significant impact of HDL-c levels was observed in the participants (N=3223) with reduced eGFR (≤60mL/min per 1.73m2); P for trend=0.27. Only when HDL-c was analyzed as a continuous variable borderline significance was noted (p=0.043). Acknowledging the protective effects of HDL-c levels on eGFR decline, in atorvastatin treated patients and with normal baseline renal function, the causal relationship between HDL and renal function remains a mystery.  In the discussion the authors noted that a recent Mendelian randomizations study suggested a causal relationship for HDL-c and renal function, while this was not observed for LDL-c and triglycerides. Several longitudinal observational studies such as the ARIC, and the Physicians Health Study Similar showed similar effects of HDL-c on renal function. Additional studies are needed to unravel the relationship of HDL and statins on renal function decline.
Ong KL, Waters DD, Fayyad R et al. Relationship of High-Density Lipoprotein Cholesterol With Renal Function in Patients Treated With Atorvastatin. J Am Heart Assoc 2018; 7. http://www.ncbi.nlm.nih.gov/pubmed/?term=29358194
Can statin reduce inflammation in RA patients?
Using statins in patients with rheumatoid arthritis (RA) is recognized as an important intervention to reduce their increased CVD risk. The potential anti-inflammatory effects of statins in RA patients have been reported but the information of the published studies were conflicting. The authors of this meta-analysis included 15 high quality RCT’s to examine the lipid changes as well as effects on hsCRP, Erythrocyte Sedimentation Rate (ESR) and RA activity score. In the majority of the included trials atorvastatin was used, in three trials atorvastatin was compared to simvastatin. In RA patients lipid parameters, including HDL-C, improved in the statin treated patients. Similar improvements of inflammatory markers were noted as well. Compared to simvastatin, atorvastatin showed superior effects on disease activity scores, anti-inflammatory and lipid lowering effects. The results of this meta-analysis confirm the importance of (atorva)statin use in RA patients not only to reduce their CVD risk but to improve RA related disease markers as well.
Li GM, Zhao J, Li B et al. The anti-inflammatory effects of statins on patients with rheumatoid arthritis: A systemic review and meta-analysis of 15 randomized controlled trials. Autoimmunity reviews 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29353098
Statins show promise in preventing and treating severe preeclampsia
Pregnancy related complication such as preeclampsia have remained a medical challenge despite novel insights in the cause and progression in the pregnant woman as well as the fetus. All three stages of preeclampsia are characterized by vascular changes that theoretically could benefit from pharmacological treatments targeting inflammation, cytokines and pro-thrombotic factors. Successful therapeutic interventions have been reported for low dose aspirin and low molecular weight heparin. Statins reduce CVD risk by lowering LDL-c but non-cholesterol lowering properties have been postulated as well. The potential protective effects of statins in pre-eclampsia have been tested in over numerous studies. Although the quality of the published trials is poor, no teratogenic effects of statins emerged and potential beneficial effects of preventing and treating severe pre-eclampsia complications as well as successful deliveries. Were observed. Pravastatin was the preferred statin in the majority of the trials because of reduced tissue penetrance and a favorable maternal/fetal pravastatin concentration ratio of 0.2. The authors stress the importance of conducing properly designed randomized prospective follow-up trial. Four studies are underway or have already been completed but no published. The observed safety of pravastatin, in terms of teratogenicity, should be of interest to physicians managing pregnant women with extremely high LDL-c plasma levels and manifest CAD.  Stopping statins for a prolonged time period might put these very high-risk women at peril.
Esteve-Valverde E, Ferrer-Oliveras R, Gil-Aliberas N et al. Pravastatin for Preventing and Treating Preeclampsia: A Systematic Review. Obstetrical & gynecological survey 2018; 73:40-55. http://www.ncbi.nlm.nih.gov/pubmed/?term=29368790
Only high dose high intensity statins improve vulnerable spotty calcium plaques
Determining plaque vulnerability, using IVUS and OTC imaging techniques, confirmed that lesions with a spotty pattern calcification, more often demonstrated unstable plaques features such as a thinner cap. Spotty calcification also predicted a higher risk of plaque rupture. And despite the use of medical therapies spotty calcifications were associated with accelerated disease progression as well.  The authors re-analyzed data from a randomized controlled trial comparing the effects of high and moderate dose, high intensity statins on lipid rich plaque progression. Of the 120 consecutive patients that entered the study, between September 2009 and March 2013, the data of 69 patients, with 96 lipid rich plaques were used for the final analysis. OCT analysis was performed at baseline, 6 and 12 months, and patients were divided into three groups: no calcifications (N=46), calcified (N=12) lesions and spotty calcification (N=38). Increased fibrous cap thickness was observed in all 3 groups comparing baseline to the changes at 6 and 12 months. Patients without calcifications FCT: 60.0 ±17.2, 125.5 ±62.1, and 161.0 ±80.5 𝜇m, respectively (P < .001). Calcified lesions FCT: 59.8 ±17.0, 93.4 ±51.4, and 155.2 ±61.7 𝜇m, respectively (P < .001). And spotty calcification FCT: 62.8 ±20.9, 126.4 ±84.9, and 169.2 ±81.6 𝜇m, respectively (P < .001). At 12 months greater increases in FCT were observed in patients using intensive statin and that had spotty calcification, P <0.034). That authors concluded that all patients in this study benefitted from using statins, but in the with spotty calcification pattern, the benefits from intensive statin therapy were superior to moderate intensity statin use. Larger studies with longer follow-up time are needed to confirm these findings.
Afolabi A, Mustafina I, Zhao L et al. Does spotty calcification attenuate the response of nonculprit plaque to statin therapy?: A serial optical coherence tomography study. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29359491 

Relevant publications
  1. Wang WT, Hellkamp A, Doll JA et al. Lipid Testing and Statin Dosing After Acute Myocardial Infarction. J Am Heart Assoc 2018; 7. http://www.ncbi.nlm.nih.gov/pubmed/?term=29371200
  2. Simes J, Robledo KP, White HD et al. D-dimer Predicts Long-Term Cause-Specific Mortality, Cardiovascular Events and Cancer in Stable Coronary Heart Disease Patients: The LIPID Study. Circulation 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29367425
  3. Ouyang XJ, Zhang YQ, Chen JH et al. Situational Analysis of Low-density Lipoprotein Cholesterol Control and the Use of Statin Therapy in Diabetes Patients Treated in Community Hospitals in Nanjing, China. Chinese medical journal 2018; 131:295-300. http://www.ncbi.nlm.nih.gov/pubmed/?term=29363644
  4. Okuyama H, Hamazaki T, Hama R et al. A Critical Review of the Consensus Statement from the European Atherosclerosis Society Consensus Panel 2017. Pharmacology 2018; 101:184-218. http://www.ncbi.nlm.nih.gov/pubmed/?term=29353277
  5. Ofori-Asenso R, Jakhu A, Curtis AJ et al. A Systematic Review and Meta-analysis of the Factors Associated With Nonadherence and Discontinuation of Statins Among People Aged >/=65 Years. J Gerontol A Biol Sci Med Sci 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29360935
  6. Kodera S, Morita H, Kiyosue A et al. Cost-Effectiveness of Statin Plus Eicosapentaenoic Acid Combination Therapy for Cardiovascular Disease Prevention in Japanese Patients With Hypercholesterolemia- An Analysis Based on the Japan Eicosapentaenoic Acid Lipid Intervention Study (JELIS). Circulation journal : official journal of the Japanese Circulation Society 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29367520
  7. Khouri C, Lepelley M, Mallaret M et al. [Muscle pain and statin, pharmacological or nocebo effect?]. Therapie 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=29366501
  8. Kasichayanula S, Grover A, Emery MG et al. Clinical Pharmacokinetics and Pharmacodynamics of Evolocumab, a PCSK9 Inhibitor. Clinical pharmacokinetics 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29353350
  9. Demasi MP. Statin wars: have we been misled about the evidence? A narrative review. British journal of sports medicine 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29353811
  10. Budoff M, Brent Muhlestein J, Le VT et al. Effect of Vascepa (icosapent ethyl) on progression of coronary atherosclerosis in patients with elevated triglycerides (200-499 mg/dL) on statin therapy: Rationale and design of the EVAPORATE study. Clin Cardiol 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365351
  11. Zodda D, Giammona R, Schifilliti S. Treatment Strategy for Dyslipidemia in Cardiovascular Disease Prevention: Focus on Old and New Drugs. Pharmacy (Basel, Switzerland) 2018; 6. http://www.ncbi.nlm.nih.gov/pubmed/?term=29361723
  12. Zhu B, Tang C. Atorvastatin upregulates expression of p16 and inhibits proliferation and migration of VSMCS via altered dna methylation. Atherosclerosis 2017; 263:e132. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365530
  13. Zandl M, Fanaee-Danesh E, Gali CC et al. Interactions of simvastatin and APOJ with amyloid processing in cerebrovascular endothelial cells. Atherosclerosis 2017; 263:e85-e86. http://www.ncbi.nlm.nih.gov/pubmed/?term=29366247
  14. Yasuda H, Fujiwara A, Komiya S, Haze T. Effects of rosuvastatin add-on treatment on hyperlipidemia in type 2 diabetic patients with chronic kidney disease receiving ethyl icosapentate. Atherosclerosis 2017; 263:e241-e242. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365927
  15. Waldmann E, Bamberger C, Parhofer KG. Statin intolerance is the main indication for PCSK9 inhibition in clinical practice. Atherosclerosis 2017; 263:e80. http://www.ncbi.nlm.nih.gov/pubmed/?term=29366231
  16. Vrablik M, Catapano A, Wiklund O et al. Clinician interview results about the experiences of their patients who report side effects with statin treatment. Atherosclerosis 2017; 263:e247. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365945
  17. Vladimirov S, Gojkovic T, Spasojevic-Kalimanovska V et al. Influence of LCAT and CETP activity on the reverse cholesterol transport and modification of HDL particles in statin-treated coronary artery disease patients and healthy subjects. Atherosclerosis 2017; 263:e217. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365842
  18. Uzokov J, Alyavi A, Alyavi B. Influence of combination therapy of rosuvastatin and telmisartan on vascular and metabolic profile in hypercholesterolemic patients with metabolic syndrome. Atherosclerosis 2017; 263:e241. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365928
  19. Tzani A, Doulamis I, Konstantopoulos P et al. Proteomics discovery of biomarkers in statin-treated patients with advanced coronary artery disease. Atherosclerosis 2017; 263:e241. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365926
  20. Toth PP, Bays H, Farnier M et al. A comparison of the attainment of guideline-recommended LDL-C lowering with statin and ezetimibe+statin therapies. Atherosclerosis 2017; 263:e240-e241. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365924
  21. Teramoto T, Kai T, Ozaki A et al. Treatment Patterns and Lipid Profile in Patients with Familial Hypercholesterolemia in Japan. J Atheroscler Thromb 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29353825
  22. Susekov A, Meshkov A, Scherbakova M. Fast regression of xanthomatosis in patient with homogous FH after intensive therapy with statin, ezetimibe and PCSK9 inhibitor evalocumab- the case. Atherosclerosis 2017; 263:e229-e230. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365883
  23. Stock JK. Update on SAMS: Statin-associated muscle symptoms. Atherosclerosis 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=29361270
  24. Singh D, Lippmann S. Can Statins Diminish Depression? The primary care companion for CNS disorders 2018; 20. http://www.ncbi.nlm.nih.gov/pubmed/?term=29372939
  25. Sarpong EM, Zuvekas SH. Trends in Statin Therapy among Adults (Age >/= 18), United States, 2000 to 2011. In: Statistical Brief (Medical Expenditure Panel Survey (US)). Rockville (MD): Agency for Healthcare Research and Quality (US); 2001. https://www.ncbi.nlm.nih.gov/pubmed/29360314
  26. Salami JA, Warraich HJ, Valero-Elizondo J et al. National Trends in Nonstatin Use and Expenditures Among the US Adult Population From 2002 to 2013: Insights From Medical Expenditure Panel Survey. J Am Heart Assoc 2018; 7. http://www.ncbi.nlm.nih.gov/pubmed/?term=29358195
  27. Reyes-Soffer G, Khavani M, Holleran S et al. Lipidomic and proteomic predictors of drastic reductions of HDL in the accord lipid trial. Atherosclerosis 2017; 263:e96. http://www.ncbi.nlm.nih.gov/pubmed/?term=29366287
  28. Reiner Z. PCSK9 inhibitors in clinical practice: Expectations and reality. Atherosclerosis 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29366497
  29. Putzu A, Ferrari E, Gallo M et al. Randomized Evidence on Perioperative Statin Therapy in Cardiac Surgery. The Annals of thoracic surgery 2018; 105:665-666. http://www.ncbi.nlm.nih.gov/pubmed/?term=29362180
  30. Pechlivanis S, Moebus S, Lehmann N et al. Pharmacogenetic association of blood-lipid related genetic variants with 5-year progression of coronary artery calcification following the treatment with statin in the Heinz Nixdorf Recall study. Atherosclerosis 2017; 263:e278. http://www.ncbi.nlm.nih.gov/pubmed/?term=29366052
  31. Ozerova I, Metelskaya V, Gavrilova N. Changes in subfractional distribution of apolipoprotein B-containing lipoproteins in patients with coronary atherosclerosis on statin therapy: Gender differences. Atherosclerosis 2017; 263:e190. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365737
  32. Nizomov A, Kenjaev S. Effect of high-dose atorvastatin on lipid spectrum and inflammation in acute myocardial infarction. Atherosclerosis 2017; 263:e245-e246. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365940
  33. Nikolic T, Zivkovic V, Jeremic N et al. Impact of atorvastatin and simvastatin on lipid and non-lipid biochemical risk factors in diet-induced hyperhomocisteinemia in wistar albino rats: A comparative study. Atherosclerosis 2017; 263:e136. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365545
  34. Nicholls SJ, Puri R, Ballantyne CM et al. MILANO-PILOT: will infusing HDL mimetics containing apoA-imilano continue to regress coronary atherosclerosis in the modern era of intensive statin therapy? Atherosclerosis 2017; 263:e11. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365456
  35. Morieri ML, Shah HS, Lovato L et al. Increase in apoliporotein-A2 Levels is associated with lower cardiovascular risk in the accord lipid trial. Atherosclerosis 2017; 263:e43. http://www.ncbi.nlm.nih.gov/pubmed/?term=29366108
  36. Meikle P, Barlow C, Nestel P et al. Decreases in plasma phosphatidylinositol species partially explain the reduction in cardiovascular events after pravastatin therapy in secondary prevention. Atherosclerosis 2017; 263:e239. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365917
  37. Mehrad H, Mokhtari-Dizaji M, Ghanaati H. Effect of high-dose atorvastatin therapy accompanied by discontinuation of cholesterol-rich diet on color-doppler ultrasonography parameters of atherosclerotic carotid artery. Atherosclerosis 2017; 263:e246. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365942
  38. Mehrad H, Farhoudi M, Foletti A. Confocal dual- pulse electrohydraulic shock wave therapy for advanced atherosclerosis regression accompanied by atorvastatin- loaded microbubbles administration. Atherosclerosis 2017; 263:e154. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365602
  39. Matsuo N, Takaishi A, Oonishi N et al. EPA/AA can be a predictive factor in the patients with coronary artery disease in the strong statin era. Atherosclerosis 2017; 263:e196-e197. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365757
  40. Mark L, Harangi M, Paragh G. [The labyrinth of residual risk: reduction of the remaining lipid and inflammation risk in the prevention of atherosclerosis]. Orvosi hetilap 2018; 159:124-130. http://www.ncbi.nlm.nih.gov/pubmed/?term=29353502
  41. Luginova Z, Tripoten M, Pogorelova O et al. Effect of short-term intensive rosuvastatin therapy on carotid plaque volume in very high cardiovascular risk patients: A three-dimensional ultrasound imaging study. Atherosclerosis 2017; 263:e40-e41. http://www.ncbi.nlm.nih.gov/pubmed/?term=29366103
  42. Kozlov S, Kchamchieva L, Tripoten M et al. Effect of intensive statin therapy on carotid plaque echogenicity in patients with nonobstructive asymptomatic carotid stenosis. Atherosclerosis 2017; 263:e147. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365582
  43. Klimushina M, Gumanova N, Gorshkov A et al. Marker of endothelial function, endothelin, is associated with gender-dependent response to statin therapy in patients with coronary atherosclerosis. Atherosclerosis 2017; 263:e281. http://www.ncbi.nlm.nih.gov/pubmed/?term=29366062
  44. Karlson BW, Jornten-Karlsson M, Xu Y et al. Rationale, design, and baseline characteristics of a randomised trial evaluating the effect of a smart phone based patient support tool on treatment duration in patients prescribed rosuvastatin in china (EHELP China). Atherosclerosis 2017; 263:e247-e248. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365946
  45. Huesch MD. Association of Baseline Statin Use Among Older Adults Without Clinical Cardiovascular Disease in the SPRINT Trial. JAMA Intern Med 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29356825
  46. Hong SJ, Choi SY, Han SH et al. Safety and tolerability of atorvastatin calcium anhydrous in Korean patients with dyslipidemia: An interim analysis from the lamp study. Atherosclerosis 2017; 263:e236. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365909
  47. Hoeke G, Wang Y, Van Dam A et al. Statin treatment potentiates the lipid-lowering and anti-atherogenic effect of bat activation by accelerating lipoprotein remnant clearance. Atherosclerosis 2017; 263:e212. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365823
  48. Hamada T, Khalaf N, Yuan C et al. Statin use and pancreatic cancer risk in two prospective cohort studies. Journal of gastroenterology 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29362938
  49. Greve AM, Bang CN, Boman K et al. Effect Modifications of Lipid-Lowering Therapy on Progression of Aortic Stenosis (from the Simvastatin and Ezetimibe in Aortic Stenosis [SEAS] Study). Am J Cardiol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=29361285
  50. Gorzelak-Pabis P, Durma A, Trambowicz K et al. The association between atorvastatin and rosuvastatin use and sleep disturbance. Atherosclerosis 2017; 263:e238. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365915
  51. Gojkovic T, Vladimirov S, Spasojevic-Kalimanovska V et al. Association of LDL phenotypes with cholesterol synthesis and HDL subclasses in statin-treated coronary artery disease patients and healthy subjects. Atherosclerosis 2017; 263:e205. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365796
  52. Gocmen AY, Gumuslu S. Atorvastatin influences oxidative stress markers in hypercholesterolemic rats. Atherosclerosis 2017; 263:e162. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365633
  53. Filatova A, Kuznetsova G, Shchinova A et al. Influence of short-term intensive atorvastatin therapy on lymphocyte and monocyte subpopulations and CCR2, CCR5, CX3CR1 and TLR4 expression in blood of patients with stable angina. Atherosclerosis 2017; 263:e112-e113. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365463
  54. Chua NYC, Chong PF, Najme Khir R et al. Statin naive patients during acute coronary syndrome in Malaysia. Atherosclerosis 2017; 263:e184. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365712
  55. Cea-Soriano L, Fowkes FGR, Johansson S et al. Time trends in peripheral artery disease incidence, prevalence and secondary preventive therapy: a cohort study in The Health Improvement Network in the UK. BMJ Open 2018; 8:e018184. http://www.ncbi.nlm.nih.gov/pubmed/?term=29358428
  56. Casula M, Mozzanica F, Scotti L et al. Statin use and risk of new-onset diabetes: a meta-analysis of observational studies. Atherosclerosis 2017; 263:e262-e263. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365998
  57. Benczur B, Herczeg B. Safety of long-term statin therapy: Data from real-world observation in subjects at very high risk. Atherosclerosis 2017; 263:e246. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365943
  58. Barkas F, Elisaf M, Liberopoulos E et al. Metabolic markers to predict incident diabetes in statin-treated individuals. Atherosclerosis 2017; 263:e259. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365987
  59. Bakar NS, Neely D, Avery P et al. Patient specific genetic and clinical factors are associated with statin-related myotoxicity of moderate severity: A case-control study. Atherosclerosis 2017; 263:e243. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365932
  60. Aziz N, Sirojiddin K, Majid K. Influence of high doses of atorvastatin on myocardial stanning in acute myocardial infarction. Atherosclerosis 2017; 263:e245. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365939
  61. Askri I, Kelbousi S, Sakly M, Attia N. Atorvastatin effect on phospholipid profile and distribution between lipoprotein fractions in type 2 diabetic patients with and without CAD. Atherosclerosis 2017; 263:e246. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365941
  62. Alyavi A, Alyavi B, Uzokov J. Efficiency and safety of rosuvastatin in patients with metabolic syndrome. Atherosclerosis 2017; 263:e245. http://www.ncbi.nlm.nih.gov/pubmed/?term=29365938

Miscellaneous publications
  1. Wu F, Luo T, Mei Y et al. Simvastatin alters M1/M2 polarization of murine BV2 microglia via Notch signaling. Journal of neuroimmunology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=29361314
  2. Uchiyama H, Tsujimoto M, Shimada N et al. Evaluation of Trace Elements in Augmentation of Statin-Induced Cytotoxicity in Uremic Serum-Exposed Human Rhabdomyosarcoma Cells. Toxins 2018; 10. http://www.ncbi.nlm.nih.gov/pubmed/?term=29370118
  3. Singh P, Zhang Y, Sharma P et al. Statins decrease leptin expression in human white adipocytes. Physiological reports 2018; 6. http://www.ncbi.nlm.nih.gov/pubmed/?term=29372612
  4. Shahrezaee M, Oryan A, Bastami F et al. Comparative impact of systemic delivery of atorvastatin, simvastatin, and lovastatin on bone mineral density of the ovariectomized rats. Endocrine 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29372484
  5. Feng WW, Kuang SY, Tu C et al. Natural products berberine and curcumin exhibited better ameliorative effects on rats with non-alcohol fatty liver disease than lovastatin. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2018; 99:325-333. http://www.ncbi.nlm.nih.gov/pubmed/?term=29353208
  6. Defilippi C, Lo J, Christenson R et al. Novel mediators of statin effects on plaque in HIV: a proteomics approach. Aids 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29369166
  7. Cheng Y, Zheng H, Wang B et al. Sorafenib and fluvastatin synergistically alleviate hepatic fibrosis via inhibiting the TGFbeta1/Smad3 pathway. Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=29373239
  8. Bao JW, Sun B, Ma PP et al. Rosuvastatin inhibits inflammatory response and resists fibrosis after myocardial infarction. Eur Rev Med Pharmacol Sci 2018; 22:238-245. http://www.ncbi.nlm.nih.gov/pubmed/?term=29364492
  9. Verma AK, Laha B, Pandey M et al. Cholesterol-lowering drug, in combination with chromium chloride, induces early apoptotic signals in intracellular L. donovani amastigotes, leading to death. Journal of biosciences 2017; 42:427-438. http://www.ncbi.nlm.nih.gov/pubmed/?term=29358556
  10. Misaka S, Abe O, Sato H et al. Lack of pharmacokinetic interaction between fluvastatin and green tea in healthy volunteers. Eur J Clin Pharmacol 2018. http://www.ncbi.nlm.nih.gov/pubmed/?term=29368187

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