up-to-date with a click!
Update - Issue 9-10, 2017
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

Issue 9

Hepatitis C patients benefit from statin co-administration
This meta-analysis based on 23 studies, evaluated the effects of statins as adjuvant to anti-viral therapy, 18 studies were analyzed; for prognosis/survival 8 studies. Chronic hepatitis C (CHC) patients using statins had reduced hepatitis C virus (HCV) viral load due to an improved response to the treatment with interferon-α plus ribavirin. RR=1.31 (95% CI: 1.23–1.39; P< 0.001). This was not observed in the 3 studies where direct anti-viral agents were used. This was not possible due to heterogeneity of these studies and the >90% sustained viral load response (SVR) rate of these new agents. Statins add-on improved the prognosis of HCC, cirrhosis, and death in CHC patients as well. This effect was stratified for HCV genotype and suggested that the beneficial effects were exaggerated in HCV type 1 patients; RR= 1.51; (95% CI:1.26–1.80; P<0.001) and lost significance in HCV type 2 and HCV type 3 patients, however most studies were performed in type 1 patients (12/16), and there was considerable heterogeneity across the studies. CHC is considered a risk factor for the development of cirrhosis and hepatocellular carcinoma (HCC). These serious complications were less frequently observed in patients using statins; HCC: RR=0.46 and cirrhosis: RR=0.47. The authors cautioned that due the small number and heterogeneity of the studies, bias and confounding could not be ruled out. Properly designed prospective and randomized studies are needed for more reliable conclusions.
Zheng YX, Zhou PC, Zhou RR, Fan XG. The benefit of statins in chronic hepatitis C patients: a systematic review and meta-analysis. European journal of gastroenterology & hepatology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28240613
Combined dyslipidemia: simvastatin + fenofibrate?
Review presenting an overview of trials where simvastatin and fenofibrate were combined in a fixed dose combination or in dose escalating studies. The ACCORD, LIPID and EYE study showed trends in improved clinical outcomes, but non-were statistical significant, except for less vision loss and retinopathy. In the smaller phase 3 studies, efficacy improved when a combination therapy was used. Higher baseline lipid levels resulted in better reductions of cholesterol and triglycerides. No serious safety signals emerged, but the authors do advise to monitor high risk patients more frequently and in patients with gall bladder disease fenofibrate is contraindicated. Specific patients and conditions are addressed in more detail e.g. diabetes/metabolic syndrome, chronic kidney disease, hypothyroidism, HIV and children with combined dyslipidemia.  Although LDL-cholesterol remains the major guideline dictated target, in patients with a refractory combined dyslipidemia, simvastatin + fenofibrate are an attractive alternative. Moderate clinical benefits are realistic and toxicity seems a marginal problem; however careful monitoring is advised in patients where older age and/or co-morbidities are present.
Tarantino N, Santoro F, De Gennaro L et al. Fenofibrate/simvastatin fixed-dose combination in the treatment of mixed dyslipidemia: safety, efficacy, and place in therapy. Vasc Health Risk Manag 2017; 13:29-41. http://www.ncbi.nlm.nih.gov/pubmed/?term=28243111
Updated Taiwan Guidelines for Lipid Management 2017
The updated Taiwanese Lipids Guidelines are the most recently released National Guidelines. They included the most recent published trial data and thus enable Taiwanese doctors to incorporate this evidence when caring for their high-risk patients. In contrast with the 2013 ACC/AHA guidelines, LDL-targets are emphasized and add on treatment considered as valuable expansions of their lipid lowering drug portfolio. This is the first National guideline were LDL-c Targets of <55 mg/dl are incorporated for very high risk diabetic ACS patients The American Association of Clinical endocrinologist embraced an LDL-C <55mg/dl in their most recent updated guidelines as well. Familial Hypercholesterolemia is discussed in depth, for refractory FH patients, especially homozygous FH, LDL-apheresis and new pharmacological therapies are indicated if treatment targets are not reached: LDL< 100 mg/dl for FH patient without atherothrombotic manifestations and < 70mg/dl in secondary prevention. PCSK9ab, MTP-inhibitors and anti-sense mRNA are to be considered for high risk patients, unable to reach LDL-C targets because of statin intolerance or inadequate LDL-C reduction. PCSK9ab can be considered as an ad-on treatment or mono therapy. The Taiwanese guidelines promote, at this point, the most progressive and aggressive recommendations. Not only incorporating very low LDL-targets in very high risk patients but putting strong emphasis on FH diagnosis and treatment as well. Including novel pharmacological approaches that could be lifesaving for a significant number of these very high risk patients     
Li YH, Ueng KC, Jeng JS et al. 2017 Taiwan lipid guidelines for high risk patients. Journal of the Formosan Medical Association = Taiwan yi zhi 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28242176
Adoption of ACC/AHA 2013 Guidelines disappointing
Evaluation of 161 US cardiology practices, including 1 105 356 pre-guideline patients (2 431 192 patient encounters) compared to 1 116 472 post-guideline patients (2 377 219 patient encounters), in the cohorts 97% of the patients were ASCVD patients. The following cohort were compared: the overall cohort; ASCVD patients, high LDL-c (≥190 mg/dl), diabetic patients and patients with a 10 year ASCVD risk ≥7.5%. The percentage use of moderate/high intensity statins were respectively: 62.1%/66.1%; 62.7%/67.0%; 50.6%/52.3%; 52.4%/55.2%; and 41.9%/46.9%.
Moderate-intensity to high-intensity statins increased only in the overall cohort (4.8%) and in the ASCVD cohort (4.3%) (P < .01 for slope for both). No significant change in the other risk
cohorts. Non-statin lipid lowering treatment remained unchanged in all cohorts. The authors concluded that interventions are urgently needed to improve guideline dictated cardiology practice
.Pokharel Y, Tang F, Jones PG et al. Adoption of the 2013 American College of Cardiology/American Heart Association Cholesterol Management Guideline in Cardiology Practices Nationwide. JAMA cardiology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28249067
Blumenthal RS, Gluckman TJ, Martin SS. Trends in the Use of Moderate-Intensity to High-Intensity Statin and Nonstatin Lipid-Lowering Therapy: Turning Off the Faucet Is Much More Valuable Than Mopping Up the Floor. JAMA cardiology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28249079
In patients on Dabigatran, should simvastatin and lovastatin be avoided?
In a Canadian cohort of 45 991 elderly patients, the effects of statins on Dabigatran pharmacokinetics were evaluated. Dabigatran is removed from the plasma by a P-glycoprotein that promotes its intestinal efflux. Both Lovastatin and simvastatin uniquely inhibit this pathway and potentially increase concentrations of this anti-coagulant pro-drug. This was a retrospective nested case-control study. Four controls were matched to one case with atherothrombotic stroke/TIA (N=397) or one case with hemorrhagic stroke (N=1117).  Simvastatin and Lovastatin were compared with other statins (Atorvastatin, Rosuvastatin, Fluvastatin, Pravastatin and Pitavastatin). The period evaluated was from May 1st, 2012 – March 31st 2014. The risk for ischemic stroke was not significantly different (adjusted OR 1.33, 95% CI 0.88 to 2.01). However the risk for hemorrhagic stroke was higher in the Lovastatin and Simvastatin users (adjusted OR 1.46, 95% CI 1.17 to 1.82). A letter from the Dabigatran manufactures disputing the validity of the study was refuted by a letter from the authors. The authors recommendation is to preferentially use other statins than Lovastatin or Simvastatin in patients on Dabigatran
Antoniou T, Macdonald EM, Yao Z et al. Association between statin use and ischemic stroke or major hemorrhage in patients taking dabigatran for atrial fibrillation. CMAJ: Canadian Medical Association journal = journal de l'Association medicale canadienne 2017; 189:E4-e10. http://www.ncbi.nlm.nih.gov/pubmed/?term=28246253
Canadian Medical Association journal = journal de l'Association medicale canadienne 2017; 189:E326. http://www.ncbi.nlm.nih.gov/pubmed/?term=28246232
Haertter S, Huang F, Franca LR. Association between statin use and ischemic stroke or major hemorrhage in patients taking dabigatran for atrial fibrillation. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne 2017; 189:E325. http://www.ncbi.nlm.nih.gov/pubmed/?term=28246231
Antoniou T, Mamdani M, Juurlink D. Response to "Association between statin use and ischemic stroke or major hemorrhage in patients taking dabigatran for atrial fibrillation". CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne 2017; 189:E326. http://www.ncbi.nlm.nih.gov/pubmed/?term=28246232

Issue 10

Review supporting the benefits of statins in chronic hepatic disease

In this comprehensive review, the potential role of statins in managing patients with chronic liver disease are discussed. Statins major indication is reducing CVD risk, not an uncommon additional problem in patients with NAFLD or NASH. More and more evidence is emerging that statins preserve liver function in several chronic liver diseases. These healing effect are triggered by statins pleiotropic effects, as well as decreased cholesterol synthesis. Statins impede cholesterol synthesis by interfering with the transformation of HMG-CoA to mevalonate. Consequently, several intermediate steps in cholesterol synthesis are curbed as well. Prenylation of small GTP-ases and their downstream products such as RhoA and Ras are diminished and this is linked to reduced inflammation, beta-oxidation and increased NO production. These metabolic changes protect liver cell damage and promote recovery. The authors conclude that the benefits clearly outweigh the miniscule risks of toxic liver damage and that statins should get a more prominent role in managing patients with chronic liver disease
Schierwagen R, Uschner FE, Magdaleno F et al. Rationale for the use of statins in liver disease. American journal of physiology. Gastrointestinal and liver physiology 2017:ajpgi.00441.02016. http://www.ncbi.nlm.nih.gov/pubmed/?term=28280144
CVD risk in FH patients depends on classic risk factors
The Spanish FH registry, SAFEHEART, was used to estimate the risk of CV events patients already at very high risk. The registry collected prospective data on 2404 FH patients. Participants were followed-up for a mean period 5.5 years (SD 3.2), during which 12 (0.5%) and 122 (5.1%) suffered fatal and non-fatal CVD events. The classic risk predictors: age, male gender, history of CVD, hypertension, BMI, smoking, LDL-C and Lp(a) levels were independent predictors of CVD events and based on these risk factors a SAFEHEART risk equation (SHRE) was developed. The authors suggest that this score could be used to guide treatment decisions, especially when new, costly treatment strategies are considered. Statistical evaluations were convincing and the SHRE was significantly superior to the Pooled Cohort Risk Equation and modified Framingham’s Risk Equation. What must be considered is that the evaluation was conducted in a ethnic Spanish population, living in Spain. Extrapolation to other populations with different ethnic and culture background remains challenging. The number of events and years follow-up is limited as well. Despite these shortcomings this initiative is a valuable contribution to generate a better understanding of FH and the associated risk as well as optimal management this increasing number of very high risk patients.
Perez de Isla L, Alonso R, Mata N et al. Predicting Cardiovascular Events in Familial Hypercholesterolemia: The SAFEHEART Registry. Circulation 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28275165
Severe statin related necrotizing myositis
In this review, the authors collected case reports, case series and systematic reviews of publications on patients with on statin associated autoimmune myopathy. A total of 16 articles containing 100 cases of this rare complication (2:1 000 000 000) were evaluated and reviewed.
Average age 64.72 years and no difference in gender. There was a preponderance of increased genetic allele frequency of DRB1*11:01. Duration of statin use was an average of 40 months before symptomatology developed and the most common clinical presentation was symmetrical proximal muscle weakness. In most cases symptoms persisted despite statin discontinuations and immunosuppressive treatment. Mean CK levels were 45 times elevated and biopsies showed muscle cell necrosis in all cases. Treatment consisted of statin discontinuation and majority of patients (83.82%) needed at least 2 immunosuppressant’s. Response to treatment was observed in 90% of the patients. Statin re-challenge was unsuccessful in all patients, with worsening of complaints as well. Recognizing these unique symptoms makes complete recovery of these serious and debilitating complications more likely.  
Nazir S, Lohani S, Tachamo N et al. Statin-Associated Autoimmune Myopathy: A Systematic Review of 100 Cases. Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28277343
Statins “on board” reduces stroke severity
Patients suffering an ischemic stroke triggered by atrial fibrillation were identified in three academic hospitals Boston Medical Center, Geisinger Health System, and the University of Alabama. Over a 5-year (2006 -2010) period 1030 patients were included in this analysis, 69% (n=711) sustained severe neurological deficits (mRS ≥4); 21% (n =216) died within 30 days. At the time of stroke, 39% (n = 400) of patients was taking a statin. Pre-stroke statin use was associated with a 32% reduction in frequency of severe stroke; OR: 0.68; (95% CI 0.50-0.92). Severity of stroke was associated with older age, female sex, non-White race, diabetes
mellitus, prior ischemic stroke, prior venous thromboembolism and dementia. Statin use at time of stroke was the only modifiable risk factor independently associated with less severe stroke in this study, statin therapy at the time of stroke. The observational nature of this study cannot exclude potential confounding and randomized controlled trials are needed to ultimately confirm this protective effect of statins.
Ko D, Thigpen JL, Otis JA et al. Influence of statin therapy at time of stroke onset on functional outcome among patients with atrial fibrillation. Int J Cardiol 2017; 227:808-812. http://www.ncbi.nlm.nih.gov/pubmed/?term=28273786

Guidance on how to manage statins prescription in patients at risk for diabetes
Development of new onset diabetes (NOD) is considered a recognized statin side effect. This updated review discusses the trials, pathophysiology, genetics and management advice. Overall incidence of NOD was a modest 3.8-8.8% compared to placebo in combined meta-analyses and prospective population based cohort studies. Exceptions were the Jupiter study (28%) and the UK prospective study (43.5%). the pathophysiologic mechanisms responsible for this effect are complex and not clearly delineated. Predisposing factors that increased the risk of developing NOD were, prediabetes, obesity, the metabolic syndrome, older age, Asian ethnicity, CVD, hyperlipidemia and hypertension. The authors emphasized the importance of (high dose) statin  for these patients with predisposing risk factors and at risk for CVD and suggested simple strategies to monitor and manage patients that could or have developed NOD. Such as periodic assessment of glucose and HbA1C, reduction of dose, interval dosing or switching to statins with a lower risk of NOD e.g Pitavastatin and Atorvastatin.
Chrysant SG. New onset diabetes mellitus induced by statins: current evidence. Postgraduate medicine 2017:1-6. http://www.ncbi.nlm.nih.gov/pubmed/?term=28276790
Statin Escape phenomenon?
The LDL-C lowering efficacy of statins has been reported to decrease over time in small subgroups of patients. This retrospective analysis of 1240 hyperlipidemic patients that were followed for ≥ 3 years statin escape phenomenon (SEP) was studied. SEP was defined as an increase in LDL-CL-C) levels at the most recent visit by > 10% compared with the value at 6 month following initiation of statin treatment. SEP was observed in 181 patients (31%). SEP patients achieved lower LDL-C levels after 6 months of treatment: 88 (78-97) mg/dL vs
109 (91-129) mg/dL, P < 0.05]. However, LDL levels were higher at their latest visit: 103 (96-118) mg/dL vs 94 (79-114) mg/dL, P < 0.05. No predictive factors could be determined. Patients were not significantly different in terms of BMI change, glycemic control and kidney function. The authors note that not all confounding factors could be thoroughly evaluated, they suggested that non-lipid lowering medication changes, temporary reduced adherence could be responsible for the observed reduced efficacy. Alternatively, a prolonged exposure to statins could increase the concentration of HMG-CoA reductase or PCSK9. Statin ESP is not an uncommon finding as confirmed in this retrospective analysis. The clinical significance of this phenomenon needs to be determined but regular monitoring of patients using statins is recommended.
Barkas F, Elisaf M, Klouras E et al. Statin escape phenomenon: Fact or fiction? World journal of experimental medicine 2017; 7:25-30. http://www.ncbi.nlm.nih.gov/pubmed/?term=28261552
Relevant publications
Issue 9
  1. Xiong B, Nie D, Cao Y et al. Preoperative Statin Treatment for the Prevention of Acute Kidney Injury in Patients Undergoing Cardiac Surgery: A Meta-Analysis of Randomised Controlled Trials. Heart, lung & circulation 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28242291
  2. Whayne TF. Low-Density Lipoprotein Cholesterol (LDL-C): How Low? Current vascular pharmacology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28245773
  3. Toribio M, Fitch KV, Sanchez L et al. Effects of pitavastatin and pravastatin on markers of immune activation and arterial inflammation in intrepid: a randomized trial in HIV. Aids 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28252528
  4. Rumyantsev NA, Kukes VG, Kazakov RE et al. [Use of pharmacogenetic testing to prevent adverse drug reactions during statin therapy]. Ter Arkh 2017; 89:82-88. http://www.ncbi.nlm.nih.gov/pubmed/?term=28252633
  5. Lopes Nunes JP. Statins in primary prevention, impact on mortality. A meta-analysis study. Minerva cardioangiologica 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28249380
  6. Lee CJ, Choi S, Cheon DH et al. Effect of two lipid-lowering strategies on high-density lipoprotein function and some HDL-related proteins: a randomized clinical trial. Lipids Health Dis 2017; 16:49. http://www.ncbi.nlm.nih.gov/pubmed/?term=28245873
  7. Kim HS, Kim H, Jeong YJ et al. Development of Clinical Data Mart of HMG-CoA Reductase Inhibitor for Varied Clinical Research. Endocrinol Metab (Seoul) 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28256114
  8. Kadohira T, Mintz GS, Souza CF et al. Impact of chronic statin therapy on clinical presentation and underlying lesion morphology in patients undergoing percutaneous intervention: an ADAPT-DES IVUS substudy. Coronary artery disease 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28240675
  9. Jeong YJ, Kim H, Baik SJ et al. Analysis and comparison of the cost-effectiveness of statins according to the baseline low-density lipoprotein cholesterol level in Korea. Journal of clinical pharmacy and therapeutics 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28251662
  10. Sreter KB, Barisic B, Popovic-Grle S. Pharmacogenomics and tailored polypharmacy: an 80-year-old lady with rosuvastatin-associated rhabdomyolysis and maprotiline-related Ogilvie's syndrome. International journal of clinical pharmacology and therapeutics 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28257284
  11. Seckl MJ, Ottensmeier CH, Cullen M et al. Multicenter, Phase III, Randomized, Double-Blind, Placebo-Controlled Trial of Pravastatin Added to First-Line Standard Chemotherapy in Small-Cell Lung Cancer (LUNGSTAR). Journal of clinical oncology : official journal of the American Society of Clinical Oncology 2017:Jco2016697391. http://www.ncbi.nlm.nih.gov/pubmed/?term=28240967
  12. Oztas M, Ugurlu S, Aydin O. Atorvastatin-induced dermatomyositis. Rheumatology international 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28238074
  13. Nguyen T, Karl M, Santini A. Red Yeast Rice. Foods (Basel, Switzerland) 2017; 6. http://www.ncbi.nlm.nih.gov/pubmed/?term=28257063
  14. Mikashinovich ZI, Belousova ES, Sarkisyan OG. Impairment of Energy-Dependent Processes in the Muscle Tissue as a Pathogenetic Mechanism of Statin-Induced Myopathy. Bulletin of experimental biology and medicine 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28239789
  15. Liu X, Li J, Schild SE et al. Statins and Metformin Use Is Associated with Lower PSA Levels in Prostate Cancer Patients Presenting for Radiation Therapy. Journal of cancer therapy 2017; 8:73-85. http://www.ncbi.nlm.nih.gov/pubmed/?term=28239505
  16. Kataoka Y, Andrews J, Puri R et al. Lipid Lowering Therapy to Modify Plaque Microstructures. J Atheroscler Thromb 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28239070
  17. Falk E. Appropriate use of cholesterol-lowering therapy. Atherosclerosis 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28236436
  18. Drechsler H, Ayers C, Cutrell J et al. Current use of statins reduces risk of HIV rebound on suppressive HAART. PLoS One 2017; 12:e0172175. http://www.ncbi.nlm.nih.gov/pubmed/?term=28249009
  19. Chen J. [Non-statin therapies for dylipidemia]. Zhonghua nei ke za zhi 2017; 56:176-178. http://www.ncbi.nlm.nih.gov/pubmed/?term=28253596
  20. Bischoff-Ferrari HA, Fischer K, Orav EJ et al. Statin Use and 25-Hydroxyvitamin D Blood Level Response to Vitamin D Treatment of Older Adults. J Am Geriatr Soc 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28240766
  21. Asping M, Stride N, Sogaard D et al. The effects of 2 weeks of statin treatment on mitochondrial respiratory capacity in middle-aged males: the LIFESTAT study. Eur J Clin Pharmacol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28246888

Issue 10
  1. Yang J, Wang Y, Zhou T et al. Generation of Human Liver Chimeric Mice with Hepatocytes from Familial Hypercholesterolemia Induced Pluripotent Stem Cells. Stem cell reports 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28262545
  2. Tomlinson B, Hu M, Zhang Y et al. Alirocumab for the treatment of hypercholesterolaemia. Expert opinion on biological therapy 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28277798
  3. Rossi A, Inciardi RM, Rossi A et al. Prognostic effects of rosuvastatin in patients with co-existing chronic obstructive pulmonary disease and chronic heart failure: A sub-analysis of GISSI-HF trial. Pulmonary pharmacology & therapeutics 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28263812
  4. Nezarat N, Kim M, Budoff M. Role of Coronary Calcium for Risk Stratification and Prognostication. Current treatment options in cardiovascular medicine 2017; 19:8. http://www.ncbi.nlm.nih.gov/pubmed/?term=28275938
  5. Hou T, Li Y, Chen W et al. Histopathologic and Biochemical Evidence for Mitochondrial Disease Among 279 Patients with Severe Statin Myopathy. Journal of neuromuscular diseases 2017; 4:77-87. http://www.ncbi.nlm.nih.gov/pubmed/?term=28269789
  6. He X, Yang J, Li L et al. Atorvastatin protects against contrast-induced nephropathy via anti-apoptosis by the upregulation of Hsp27 in vivo and in vitro. Mol Med Rep 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28260077
  7. Barstow C, McDivitt JD. Cardiovascular Disease Update: Care of Patients After Coronary Artery Bypass Graft. FP essentials 2017; 454:29-33. http://www.ncbi.nlm.nih.gov/pubmed/?term=28266826
  8. Arbel R, Greenberg D. Using Lower Cost Statins Improves Outcomes for Normal Cholesterol Non-diabetic Patients. Expert review of pharmacoeconomics & outcomes research 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28277855
  9. Wani ZA, Mohapatra S, Khan AA et al. Addition of simvastatin to carvedilol non responders: A new pharmacological therapy for treatment of portal hypertension. World J Hepatol 2017; 9:270-277. http://www.ncbi.nlm.nih.gov/pubmed/?term=28261384
  10. Sun J, Zhao XQ, Balu N et al. Carotid Plaque Lipid Content and Fibrous Cap Status Predict Systemic CV Outcomes: The MRI Substudy in AIM-HIGH. JACC. Cardiovascular imaging 2017; 10:241-249. http://www.ncbi.nlm.nih.gov/pubmed/?term=28279371
  11. Ravnskov U. Comment on 'Statin use and all-cancer survival: prospective results from the Women's Health Initiative'. Br J Cancer 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28278516
  12. Punekar RS, Fox KM, Paoli CJ et al. Lipid-lowering treatment modifications among patients with hyperlipidemia and a prior cardiovascular event: a US retrospective cohort study. Current medical research and opinion 2017:1-8. http://www.ncbi.nlm.nih.gov/pubmed/?term=28276256
  13. Philibert C, Bres V, Jean-Pastor MJ et al. [Red yeast-rice-induced muscular injuries: Analysis of French pharmacovigilance database and literature review]. Therapie 2016. http://www.ncbi.nlm.nih.gov/pubmed/?term=28277227
  14. Ofori-Asenso R, Zomer E, Curtis A et al. Patterns and Predictors of Adherence to Statin Therapy Among Older Patients: Protocol for a Systematic Review. JMIR research protocols 2017; 6:e39. http://www.ncbi.nlm.nih.gov/pubmed/?term=28270383
  15. Mansi IA, Frei CR, Halm EA, Mortensen EM. Association of statins with aortic, peripheral, and visceral artery aneurysm development. Vascular 2016:1708538116684942. http://www.ncbi.nlm.nih.gov/pubmed/?term=28264180
  16. Lin X, Racette SB, Ma L et al. Ezetimibe Increases Endogenous Cholesterol Excretion in Humans. Arterioscler Thromb Vasc Biol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28279967
  17. Liao KF, Cheng KC, Lin CL, Lai SW. Statin Use Correlates with Reduced Risk of Pyogenic Liver Abscess: A Population-based Case-Control Study. Basic & clinical pharmacology & toxicology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28273396
  18. Li J, Zhao SP. [Renewed evaluation on statin-associated side effects]. Zhonghua xin xue guan bing za zhi 2017; 45:102-103. http://www.ncbi.nlm.nih.gov/pubmed/?term=28260313
  19. Kim CO, Oh ES, Kim H, Park MS. Pharmacokinetic interactions between glimepiride and rosuvastatin in healthy Korean subjects: does the SLCO1B1 or CYP2C9 genetic polymorphism affect these drug interactions? Drug design, development and therapy 2017; 11:503-512. http://www.ncbi.nlm.nih.gov/pubmed/?term=28260863
  20. Keser T, Vuckovic F, Barrios C et al. Effects of statins on the immunoglobulin G glycome. Biochim Biophys Acta 2017; 1861:1152-1158. http://www.ncbi.nlm.nih.gov/pubmed/?term=28263871
  21. Gui Q, Yang Y, Zhang J. Effects of statins on the development of sepsis and organ dysfunction in hospitalized older patients in China. Braz J Infect Dis 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28282509
  22. Eliasson P, Svensson RB, Giannopoulos A et al. Simvastatin and atorvastatin reduce the mechanical properties of tendon constructs in vitro and introduce catabolic changes in the gene expression pattern. PLoS One 2017; 12:e0172797. http://www.ncbi.nlm.nih.gov/pubmed/?term=28264197
  23. El-Hamamsy M, Elwakil H, Saad AS, Shawki MA. A Randomized Controlled Open-Label Pilot Study of Simvastatin Addition to Whole-Brain Radiation Therapy in Patients With Brain Metastases. Oncology research 2016; 24:521-528. http://www.ncbi.nlm.nih.gov/pubmed/?term=28281972
  24. Chang YH, Hwu DW, Kao WP, Lee YJ. Benefits of Rosuvastatin in Cardiovascular Protection Remain Unclear After HOPE-3. The review of diabetic studies : RDS 2016; 13:212-214. http://www.ncbi.nlm.nih.gov/pubmed/?term=28278306
  25. Blackburn R, Osborn D, Walters K et al. Statin prescribing for people with severe mental illnesses: a staggered cohort study of 'real-world' impacts. BMJ Open 2017; 7:e013154. http://www.ncbi.nlm.nih.gov/pubmed/?term=28270387
  26. Bianconi V, Sahebkar A, Banach M, Pirro M. Statins, haemostatic factors and thrombotic risk. Current opinion in cardiology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28266936
  27. Alexandropoulos D, Bazigos GV, Doulamis IP et al. Protective effects of N-acetylcystein and atorvastatin against renal and hepatic injury in a rat model of intestinal ischemia-reperfusion. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2017; 89:673-680. http://www.ncbi.nlm.nih.gov/pubmed/?term=28273631
  28. Abd El-Hakeem EE, Kaki AM, Almazlom SA, Alsayyad AJ. Laparoscopic partial nephrectomy in a patient on simvastatin : Delayed recovery from neuromuscular blockade. Der Anaesthesist 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28265685
Miscellaneous publications
Issue 9
  1. Zhou HX, Gao LH, Meng LL et al. Preventive and therapeutic effect of simvastatin on secondary inflammatory damage of rats with cerebral hemorrhage. Asian Pac J Trop Med 2017; 10:152-156. http://www.ncbi.nlm.nih.gov/pubmed/?term=28237480
  2. Wang XL, Zhang T, Hu LH et al. Comparison of Effects of Different Statins on Contrast-Induced Acute Kidney Injury in Rats: Histopathological and Biochemical Findings. Oxidative medicine and cellular longevity 2017; 2017:6282486. http://www.ncbi.nlm.nih.gov/pubmed/?term=28243357
  3. Sohn HM, Hwang JY, Ryu JH et al. Simvastatin protects ischemic spinal cord injury from cell death and cytotoxicity through decreasing oxidative stress: in vitro primary cultured rat spinal cord model under oxygen and glucose deprivation-reoxygenation conditions. Journal of orthopaedic surgery and research 2017; 12:36. http://www.ncbi.nlm.nih.gov/pubmed/?term=28241838
  4. Roever L. Erratum to "Pitavastatin vs Pravastatin in Reduction of Remnant Lipoprotein Cholesterol in Patients with Dyslipidemias" Clin Ther. 2016;39:1250--1251. Clinical therapeutics 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28237671
  5. Pinho-Ribeiro V, Melo AC, Kennedy-Feitosa E et al. Atorvastatin and Simvastatin Promoted Mouse Lung Repair After Cigarette Smoke-Induced Emphysema. Inflammation 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28251446
  6. Park J, Kwon OS, Cho SY et al. Chronic administration of atorvastatin could partially ameliorate erectile function in streptozotocin-induced diabetic rats. PLoS One 2017; 12:e0172751. http://www.ncbi.nlm.nih.gov/pubmed/?term=28245261
  7. Ouweneel AB, van der Sluis RJ, Nahon JE et al. Simvastatin treatment aggravates the glucocorticoid insufficiency associated with hypocholesterolemia in mice. Atherosclerosis 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28242047
  8. Messora MR, Apolinario Vieira GH, Vanderlei JM et al. Rosuvastatin promotes benefits on induced periodontitis in hypertensive rats. Journal of periodontal research 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28256038
  9. Elahi MM, Matata BM. Effects of maternal high-fat diet and statin treatment on bone marrow endothelial progenitor cells and cardiovascular risk factors in female mice offspring fed a similar diet. Nutrition 2017; 35:6-13. http://www.ncbi.nlm.nih.gov/pubmed/?term=28241992
  10. Zang YY, Li YM, Yin Y et al. Discovery and quantitative structure-activity relationship study of lepidopteran HMG-CoA reductase inhibitors as selective insecticides. Pest management science 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28247468
  11. Elkadi S, Elsamaligy S, Al-Suwayeh S, Mahmoud H. The Development of Self-nanoemulsifying Liquisolid Tablets to Improve the Dissolution of Simvastatin. AAPS PharmSciTech 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28236269

Issue 10
  1. Yu H, Sun SQ, Gu XB et al. Atorvastatin prolongs the lifespan of radiationinduced reactive oxygen species in PC-3 prostate cancer cells to enhance the cell killing effect. Oncology reports 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28260074
  2. Sun J, Bao J, Shi Y et al. Effect of simvastatin on MMPs and TIMPs in cigarette smoke-induced rat COPD model. International journal of chronic obstructive pulmonary disease 2017; 12:717-724. http://www.ncbi.nlm.nih.gov/pubmed/?term=28260878
  3. Rivero J, Henriquez-Hernandez LA, L DB et al. Simvastatin down-regulates differential genetic profiles produced by organochlorine mixtures in primary breast cell (HMEC). Chemico-biological interactions 2017; 268:85-92. http://www.ncbi.nlm.nih.gov/pubmed/?term=28263720
  4. Gbelcova H, Rimpelova S, Ruml T et al. Variability in statin-induced changes in gene expression profiles of pancreatic cancer. Scientific reports 2017; 7:44219. http://www.ncbi.nlm.nih.gov/pubmed/?term=28276528
  5. Zhao BJ, Xu Y, Liu YH. [Drug release from electrospun simvastatin/polycaprolactone fibrous membranes]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 2016; 25:673-677. http://www.ncbi.nlm.nih.gov/pubmed/?term=28275788
  6. Selvasudha N, Koumaravelou K. The multifunctional synergistic effect of chitosan on simvastatin loaded nanoparticulate drug delivery system. Carbohydrate polymers 2017; 163:70-80. http://www.ncbi.nlm.nih.gov/pubmed/?term=28267520
  7. Safwat S, Ishak RA, Hathout RM, Mortada ND. Nanostructured lipid carriers loaded with simvastatin: effect of PEG/glycerides on characterization, stability, cellular uptake efficiency and in vitro cytotoxicity. Drug development and industrial pharmacy 2017:1-14. http://www.ncbi.nlm.nih.gov/pubmed/?term=28276784
  8. Poksay KS, Sheffler DJ, Spilman P et al. Screening for Small Molecule Inhibitors of Statin-Induced APP C-terminal Toxic Fragment Production. Frontiers in pharmacology 2017; 8:46. http://www.ncbi.nlm.nih.gov/pubmed/?term=28261092
  9. Dolci GS, Portela LV, Onofre de Souza D, Medeiros Fossati AC. Atorvastatin-induced osteoclast inhibition reduces orthodontic relapse. American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics 2017; 151:528-538. http://www.ncbi.nlm.nih.gov/pubmed/?term=28257738
  10. Bilski P, Druzbicki K, Jenczyk J et al. Molecular and Vibrational Dynamics in a Cholesterol-Lowering Agent Lovastatin: Solid-State NMR, Inelastic Neutron Scattering and Periodic DFT Study. The journal of physical chemistry. B 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28282493  
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