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up-to-date with a click!
Update - Issue 7-8, 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 7

Stating the right statin and adherence remains a challenge in secondary prevention
In this retrospective study conducted in South Wales 2248 Patients admitted with ACS were selected for a 3-year retrospective longitudinal analysis. Over 80% of the patients were discharged with a statin. Simvastatin was prescribed in 53.6% of al patients. Only 38% were prescribed then NICE guideline recommended high intensity/high dosage statin. Cholesterol levels were virtually unchanged with discontinuation rates of 53.7% and 84.3% respectively at 1 and 3 years! Total cholesterol increased by 4% at 1 year and decreased by 3% after 3 years. This study reflects the real life practice of secondary prevention. It highlights the challenges in providing patients with optimal stain treatment and at the same time preventing early discontinuation of this essential medication for patients that suffered an Acute MI
Protty MB, Lacey A, Hayes J, Freeman P. Statins for secondary prevention: clinical use in patients with acute coronary syndrome in Wales. Future cardiology 2017; 13:137-141. http://www.ncbi.nlm.nih.gov/pubmed/?term=28185473
 
Statin prescription based on harm prevented or benefit gained?
Based on US ENHANES data the authors compared guiding statin prescription by calculating a person’s estimated 10-year risk of ASCVD events risk, according to the 2013 ACC/AHA guidelines of 7.5% threshold, or Benefit. Statin benefit was calculated by absolute reduction in expected ASCVD events. Although calculated risk is well suited to predict benefits, individual characteristics can have modifying effects, e.g. giving a statin to a person with a low LDL-cholesterol vs a high LDL-cholesterol. The Authors introduced the threshold of 2.3% absolute risk reduction as a threshold for initiating statin treatment. This approach would add 9.5 million US citizens to be eligible for statins and could prevent an additional 266 508 cardiovascular events over 10 years’ time. Comparing both strategies for the thresholds of 7,5% risk and 2.3% absolute Risk Reductions would end up with a NNT’s of 21.2% (95%CI 20.4-22.0) and 24.2 (95%CI 23.1-25.5) respectively. What is a different outcome of the two approaches are NNT10 max, maximum number of patients treated with each strategy. This NNT10Max = 54 and 43.5 for the risk- vs the benefit based strategy. This is explained by the possibility that individuals with elevated baseline risk but a low expected benefit end up receiving statins. Treatment in these individuals is inefficient and hence the NNT10 benefit approach is considered a more rational approach by the authors. They conclude: “Before we can reap these benefits, however, we will need more consensus and updated guidelines that sanction this approach, as well as
clinician-friendly tools to calculate expected benefit like what is now available for calculating baseline risk”.
Pletcher MJ, Pignone M, Jarmul JA et al. Population Impact & Efficiency of Benefit-Targeted Versus Risk-Targeted Statin Prescribing for Primary Prevention of Cardiovascular Disease. J Am Heart Assoc 2017; 6. http://www.ncbi.nlm.nih.gov/pubmed/?term=28188251
 
Are statins beneficial in the physically active in primary prevention
Very little data exists on statin use in physically active relatively “healthy” individuals. This analysis was based on a retrospective propensity score-matched cohort of healthy active US military personal (2002 – 2011). Baseline data was collected from 2002-2004, outcome data from 2006-2011. Study outcomes included major acute cardiovascular events (MACE), diabetes mellitus and its complications, kidney diseases, musculoskeletal diseases, obesity, and malignancy. The study included 837 statins users and 2488 propensity matched controls.
Patients were followed-up for 19,443 person-years. Statin-users used statins for a mean period of 234 days (SD ± 97 days) and a median of 270 days; 75% of the prescriptions were for simvastatin, 19% for atorvastatin, 4% for pravastatin and lovastatin, and 2% for rosuvastatin. At some point during the study period, 19% used low-intensity statins, 82% used moderate- intensity statins, and 8% used high-intensity statins. Overall event rate for MACE was low: 2.63/1000 patient years for non-users and 2.58/1000 patient years for statin users
MACE were recorded in 1.6% of the statin users and 1.5% of the controls. OR: 1.05 (95% CI 0.55-1.99). Diabetes was diagnosed in 12.5% of the statins users and 5.8% of the controls. OR 2.34 (95%CI 1.79-3.04). Diabetes + complications were found in 1.7% of the statin users and 0.7% of the non-users. OR: 2.47 (95%CI 1.21-5.04). The authors concluded that Among healthy physically active individuals, statin use was associated with doubled risk of diabetes and diabetic complications without countervailing cardiovascular benefits. Limitation of observational studies need to be taken into consideration, and despite propensity matching confounding cannot be excluded. Results should be reproduced in a sufficiently powered randomized placebo controlled trial.
Mansi IA, English JL, Morris MJ et al. Statins for primary prevention in physically active individuals: Do the risks outweigh the benefits? Journal of science and medicine in sport 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28185810
 
Predicting PCSK9ab efficacy of LDL-cholesterol lowering
The LDL-Cholesterol lowering effects of PCSK9ab depends on several variables, by incorporating these variable in a mechanistic systems pharmacology model, more precise predictions are possible. The calculated forecasts were compared and validates wit available clinical data. Important parameters evaluated were baseline LDL-C; baseline PCSK9 concentrations; genetic mutations for familial hypercholesterolemia and background statin therapy. As expected PCSK9ab were more effective ins statin treated patients. Statins up-regulate PCSK9 synthesis and produce higher plasma levels of PCSK9. However higher PCSK9 was also related to an increased clearance of anti-PCSK9 and LDL-C rebound. These results were in-line with earlier, but limited, publications on mono therapy with anti-PCSK9. In FH patients functional recptor activity of 10-25% was not associated with a reduced response of antiPCSK9, however if LDL-receptor activity was < 10 % (Homozygous FH patients) the efficacy of antiPCSK9is significantly reduced. Finally there was a weak but significant reduced response to antiPCSK9 related to baseline LDL-C and PCSK9 concentrations. The model that the authors developed could be of value for new PCSK9 targeting compounds to help predict dose response. In a clinical setting, it is of limited to no value.
Gadkar K, Budha N, Baruch A et al. A Mechanistic Systems Pharmacology Model for Prediction of LDL Cholesterol Lowering by PCSK9 Antagonism in Human Dyslipidemic Populations. CPT Pharmacometrics Syst Pharmacol 2014; 3:1-9. http://www.ncbi.nlm.nih.gov/pubmed/?term=28188981
 
Immune mediated myopathy is distinctly different from toxic myopathy
Myopathy related to statin use is a frequently encountered side effect of statins. Autoimmune mediated statin induced myopathy is a distinctly different problem. Anti-HMGCR positive statin-associated immune-mediated necrotizing myopathy (IMNM) is characterized by a different etiology, disease development and management. In this comprehensive review, the authors provide a clear approach on how to recognize, diagnose and manage this serious type of statin related myopathy. The auto immune variant, in contrast with the better known toxic myopathy, manifests after prolonged statin use of sometimes several years. The etiology is a combination of genetic factors and use of statins that trigger a cascade of events that eventually results in HMGCR auto anti-bodies. Statin-induced IMNM is rare, commonly associated with proximal muscle weakness, higher creatine kinase values, HLA-DRB1 11: 01 positivity and persistence after statin discontinuation. Median duration of statin therapy before onset of muscle symptoms was 38 months. Statin dosage of statin intensity seem not to be associated with the risk of developing IMNM. The incidence is extremely rare 1-2/1000 000 year. Diagnosis is made by clinical criteria: muscle weakness and preference for the proximal muscles as well as abnormal laboratory-, functional and pathology tests:  HMGCR auto anti-bodies, abnormal- EMG, MRI (muscle Edema) and biopsy findings (necrosis and mild-no inflammations). Treatment is ased on immediate termination of statins + aggressive immunosuppression or immunomodulation. Prednisone is the first line therapy followed by methotrexate, azathioprine, intravenous immunoglobulin (IVIG), mycophenolate and rituximab in varying combinations. Alternative agents include plasmapheresis, cyclophosphamide and cyclosporine. Treatments can last from months to years and relapses can occur. Statin re-challenge is contra-indicated,  prompt and aggressive therapy is of considerable benefit and able to restore muscle strength and physical function
Christopher-Stine L, Basharat P. Statin-associated immune-mediated myopathy: biology and clinical implications. Curr Opin Lipidol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28207435

Issue 8

Chinese PTCA patients better off with high loading dose Rosuvastatin (20 mg)

This meta-analysis, that included studies with Chinese patients only, examined the benefit of Rosuvastatin 20 mg vs 10 mg as a loading dose pre-PTCA. Included were 11 studies and 802 patients. Of these patients 398 were in the high dose group and 404 in the 10 mg Rosuvastatin group. Patients were evaluated for changes in: hsCRP; cTnT; total cholesterol; LDL-cholesterol; HDL-cholesterol and triglycerides. After 24 hrs., significant improvements were observed for hsCRP and cTnT. At 48 hrs., this was found for: hsCRP, HDL-c and total cholesterol. After 30 days, significant improvements included: hsCRP, cTnT, LDL-C, total cholesterol and triglycerides. No information on tolerability or improved clinical endpoints were provided. Although the quality of the include trials could not be evaluated, this one of the first (simple) meta-analysis in exclusively Chinese patients evaluating a relatively high dose of a high intensity statin. The presented results seem to be on par with publications were non-Asian patients were included
Ye Z, Lu H, Su Q et al. Effect of high-dose rosuvastatin loading before percutaneous coronary intervention in Chinese patients with acute coronary syndrome: A systematic review and meta-analysis. PLoS One 2017; 12:e0171682. http://www.ncbi.nlm.nih.gov/pubmed/?term=28231287
 
Is Genetic profiling of primary prevention patients before starting statins necessary?
Using a genetic profile, based on 57 different SNP’s, patients in 3 different primary prevention studies. The WOSCOP study, examining the benefits of 40 mg pravastatin; and two observational studies: BIO-IMAGE, evaluating carotid plaque burden and CARDIA examining coronary artery calcifications were used to evaluate the impact of the highest quintile vs the lowest quintile of the poly genetic risk score(PRS). Not only was there an increase of atherosclerosis, reflected by the imaging studies, in WOSCOPS not only an increased risk for CVD events: HR 1.62 (95% CI 1.27-2.05, P< 0.001) but also a significantly improved response to statins was observed, in the patients with the highest PRS core vs the rest. The absoluter risk reduction in respectively the highest PRS vs the rest were 7.9% and 2.7; translating in NNT’s of 13 and 38.  Based on a study level meta-analysis across WOSCOPS, ASCOT and JUPITER, statin use was associated with 44% relative risk reduction in the high PRS vs. 26% in all others. (P=0.05). The absolute risk reduction was 3.6% (95% CI, 2.0%-5.1%) vs 1.3 % (95% CI, 0.6%-1.91%). Similar patterns emerged for coronary artery calcification and carotid plaque burden. Each standard deviation increase in the polygenic risk score was associated with 1.32-fold (95% CI, 1.04-1.68) greater likelihood of having coronary artery calcification and 9.7% higher (95% CI, 2.2-17.8%) burden of carotid plaque. The authors concluded that “Those at high genetic risk have a greater burden of subclinical atherosclerosis and derive greater relative and absolute benefit from statin therapy to prevent a first CHD event”
Natarajan P, Young R, Stitziel NO et al. Polygenic Risk Score Identifies Subgroup with Higher Burden of Atherosclerosis and Greater Relative Benefit from Statin Therapy in the Primary Prevention Setting. Circulation 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28223407
 
Severe rhabdomyolysis and accompanied by severe hypercalcemia post hemodialysis
An Asian patient treated with 80 mg of simvastatin (!) developed rhabdomyolysis and renal failure, one week post AMI, that was complicated by post procedural contrast induced nephropathy. One month after presenting with rhabdomyolysis the patient developed severe hypercalcemia with intact PTH and 1,25 (OH)D levels. Whole body bone scintigraphy showed generalized calcium phosphate deposits in his soft tissues and muscles of the chest wall, shoulders, proximal upper and lower extremities, pelvis and hips. One week after hemodialysis his calcium levels normalized. The most likely explanation of the hypercalcemia is mobilization and dissolution of calcium phosphate deposits in the injured muscle sites along with immobilization due to the complications. Although an uncommon manifestation of a rare complication, rhabdomyolysis, for seasoned lipidologists a diagnosis to remember!
Mirza ZB, Hu S, Amorosa LF. Bone scintigraphy of severe hypercalcemia following simvastatin induced rhabdomyolysis. Clinical cases in mineral and bone metabolism : the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases 2016; 13:257-261. http://www.ncbi.nlm.nih.gov/pubmed/?term=28228795
 
Renal disease and lipids not a simple story to tell! 
In 11 pages, the authors review the current evidence and guidelines regarding lipid management and use of statins in patients with chronic renal disease (CKD). They discuss the different dyslipidemias observed in different types and phases of CKD as well as studies and guidelines addressing dyslipidemia’s in CKD patients. No simple message on how to optimally manage these patients, due to a lack of high quality trials. They acknowledge that in advanced renal disease/hemodialysis patients there is not much we can expect in terms of risk reduction when statins are administered. Acting promptly in earlier stages of renal disease, statins do seem to provide some protection. They are right when stating that more trials are needed to properly address the benefits of lipid management/statins in the broad spectrum of the different types of CKD patients, but if this will be carried out by pharma companies or health authorities is questionable due to the costs of this large endpoint studies.  
Mikolasevic I, Zutelija M, Mavrinac V, Orlic L. Dyslipidemia in patients with chronic kidney disease: etiology and management. International journal of nephrology and renovascular disease 2017; 10:35-45. http://www.ncbi.nlm.nih.gov/pubmed/?term=28223836
 
Better understand statin myotoxicity?
Everything you need to know about statin myotoxicity explained in this paper. An important lesson: it takes a combination of factors in a single patient to develop statin induced myotoxicity (SIM) and in many cases (50%) a preventable drug–drug interaction was to blame! Genetic and epigenetic polymorphisms of multiple proteins involved in drug transport and metabolism as well as normal myocyte function, co-morbidities, age and gender play an important role. The rise in [Ca2+]s, lactate, and ROS, and reduced ATP and gCl lead to cramps, pains and fatigue. CK rises when the sarcolemma membranes of the muscle cell are damaged, triggered by muscle remodeling due to apoptosis and proteolysis. Blood concentrations of statins, and distinctly simvastatin, can be raised in carriers of variants of influx transporters such as SLCO1B1, and efflux transporters such as ABCB1 and ABCG2. However, SIM can be found in patients with normal transporter function and many patient that possess these variants do not present with SIMS. Specific myocyte and extra-myocyte conditions must coexist in the same individual to initiate SIM. The authors suggested that SIMS is less likely to develop with Pravastatin, Rosuvastatin or Pitavastatin, however myositis and rhabdomyolysis have been reported in patient using these statins as well. They advise to start with low dosages of pravastatin and slowly up titrate in patients at risk for developing SIM. The also advice to measure 25(OH)D3. Inhibition of HMG-CoA reduces the synthesis of 7-dehydrocholesterol, the precursor of vitamin D. Patients with vitamin D deficiency present with similar complaints as SIM; proximal myalgia and fatigue. Low plasma concentrations of vitamin D (< 15 mg/dl) was associated with an increased risk of developing SIM and complaints improved in patients with low vitamin D (< 30 mg/dl) that were given a high dose (50,000–100,000 IU/- week) of vitamin D. Alcohol consumption, and correcting hypothyroidism are two additional simple approaches to address the problem SIM in patients at risk for CVD and where statins are potentially lifesaving.
du Souich P, Roederer G, Dufour R. Myotoxicity of statins: Mechanism of action. Pharmacology & therapeutics 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28223230

Relevant publications
Issue 7
  1. Lin Wu FL, Wang J, Ho W et al. Effectiveness of a combination of ezetimibe and statins in patients with acute coronary syndrome and multiple comorbidities: A 6-year population-based cohort study. Int J Cardiol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28190615
  2. Yokomichi H, Nagai A, Hirata M et al. Statin use and all-cause and cancer mortality: BioBank Japan cohort. Journal of epidemiology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28196737
  3. Raymakers AJ, Sadatsafavi M, Sin DD et al. The impact of statin use on all-cause mortality in patients with COPD: a population based cohort study. Chest 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28202342
  4. Leiter LA, Zamorano JL, Bujas-Bobanovic M et al. Lipid-Lowering Efficacy and Safety of Alirocumab in Patients with or without Diabetes: A Sub-Analysis of ODYSSEY COMBO II. Diabetes Obes Metab 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28206704
  5. Hammersley D, Signy M. Ezetimibe: an update on its clinical usefulness in specific patient groups. Therapeutic advances in chronic disease 2017; 8:4-11. http://www.ncbi.nlm.nih.gov/pubmed/?term=28203346
  6. Giugliano RP, Mach F, Zavitz K et al. Design and rationale of the EBBINGHAUS trial: A phase 3, double-blind, placebo-controlled, multicenter study to assess the effect of evolocumab on cognitive function in patients with clinically evident cardiovascular disease and receiving statin background lipid-lowering therapy-A cognitive study of patients enrolled in the FOURIER trial. Clin Cardiol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28207168
  7. Clark D, Cho LS. Statin therapy in the frail elderly: A nuanced decision. Cleveland Clinic journal of medicine 2017; 84:143-145. http://www.ncbi.nlm.nih.gov/pubmed/?term=28198684
  8. Chang TI, Streja E, Soohoo M et al. Association of Serum Triglyceride to HDL Cholesterol Ratio with All-Cause and Cardiovascular Mortality in Incident Hemodialysis Patients. Clin J Am Soc Nephrol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28193609
  9. Zhao Y, Peng R, Zhao W et al. Zhibitai and low-dose atorvastatin reduce blood lipids and inflammation in patients with coronary artery disease. Medicine (Baltimore) 2017; 96:e6104. http://www.ncbi.nlm.nih.gov/pubmed/?term=28207527
  10. Wallert J, Lissaker C, Madison G et al. Young adulthood cognitive ability predicts statin adherence in middle-aged men after first myocardial infarction: A Swedish National Registry study. Eur J Prev Cardiol 2017:2047487317693951. http://www.ncbi.nlm.nih.gov/pubmed/?term=28195516
  11. Stone NJ, Robinson JG. Potential for Net Benefit Should Guide Preventive Therapy. Circulation 2017; 135:630-632. http://www.ncbi.nlm.nih.gov/pubmed/?term=28193796
  12. Southern WM, Nichenko AS, Shill DD et al. Skeletal muscle metabolic adaptations to endurance exercise training are attainable in mice with simvastatin treatment. PLoS One 2017; 12:e0172551. http://www.ncbi.nlm.nih.gov/pubmed/?term=28207880
  13. Sepehri Z, Masoumi M, Ebrahimi N et al. Correction: Atorvastatin, Losartan and Captopril Lead to Upregulation of TGF-beta, and Downregulation of IL-6 in Coronary Artery Disease and Hypertension. PLoS One 2017; 12:e0172404. http://www.ncbi.nlm.nih.gov/pubmed/?term=28192516
  14. Richard PO, Ahmad AE, Bashir S et al. Effect of statins as a secondary chemopreventive agent among individuals with non-muscle-invasive bladder cancer: A population-based analysis. Urologic oncology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28190747
  15. Reichert K, Pereira do Carmo HR, Galluce Torina A et al. Correction: Atorvastatin Improves Ventricular Remodeling after Myocardial Infarction by Interfering with Collagen Metabolism. PLoS One 2017; 12:e0172453. http://www.ncbi.nlm.nih.gov/pubmed/?term=28196119
  16. Parra A, Kreiter KT, Williams S et al. Effect of Prior Statin Use on Functional Outcome and Delayed Vasospasm after Acute Aneurysmal Subarachnoid Hemorrhage: A Matched Controlled Cohort Study. Neurosurgery 2005; 56:476-484. http://www.ncbi.nlm.nih.gov/pubmed/?term=28184638
  17. Nord JW, Jr., Berry A, Stults B et al. Evaluation of the Effectiveness of a Patient-Centered Educational Mailer Designed to Improve Statin Adherence: A Pragmatic Trial. EGEMS (Washington, DC) 2016; 4:1256. http://www.ncbi.nlm.nih.gov/pubmed/?term=28203610
  18. Munkhaugen J, Sverre E, Otterstad JE et al. Medical and psychosocial factors and unfavourable low-density lipoprotein cholesterol control in coronary patients. Eur J Prev Cardiol 2017:2047487317693134. http://www.ncbi.nlm.nih.gov/pubmed/?term=28196429
  19. Lynch JR, McGirt M, Laskowitz DT et al. 871 Simvastatin Reduces Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Results of a Pilot Randomized Clinical Trial. Neurosurgery 2005; 57:420. http://www.ncbi.nlm.nih.gov/pubmed/?term=28184829
  20. Kwok S, Pang J, Adam S et al. An online questionnaire survey of UK general practitioners' knowledge and management of familial hypercholesterolaemia. BMJ Open 2016; 6:e012691. http://www.ncbi.nlm.nih.gov/pubmed/?term=28186938
  21. Krumme AA, Sanfelix-Gimeno G, Franklin JM et al. Can purchasing information be used to predict adherence to cardiovascular medications? An analysis of linked retail pharmacy and insurance claims data. BMJ Open 2016; 6:e011015. http://www.ncbi.nlm.nih.gov/pubmed/?term=28186924
  22. Kramer AH, Bleck TP, Nathan BA et al. Statin Use Was not Associated with Less Vasospasm or Improved Outcome after Subarachnoid Hemorrhage. Neurosurgery 2008; 63:E1209. http://www.ncbi.nlm.nih.gov/pubmed/?term=28184873
  23. Keating P, Young J, George P et al. Anti-HMGCR autoantibodies in self-limiting statin-induced myopathy. International journal of rheumatic diseases 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28185416
  24. Guertin JR, Rahme E, LeLorier J. Use of Continuous Exposure Variables when Examining Dose-Dependent Pharmacological Effects - Application to the Association between Exposure to Higher Statin Doses and the Incidence of Diabetes. Journal of population therapeutics and clinical pharmacology = Journal de la therapeutique des populations et de la pharamcologie clinique 2017; 24:5-15. http://www.ncbi.nlm.nih.gov/pubmed/?term=28186711
  25. Durrington PN, Soran H. Cholesterol Levels Should Play a More Important Role in Identifying Statin Recipients. Circulation 2017; 135:627-629. http://www.ncbi.nlm.nih.gov/pubmed/?term=28193795
  26. Dong B, Singh AB, Shende VR, Liu J. Hepatic HNF1 transcription factors control the induction of PCSK9 mediated by rosuvastatin in normolipidemic hamsters. International journal of molecular medicine 2017; 39:749-756. http://www.ncbi.nlm.nih.gov/pubmed/?term=28204827
  27. Brinjikji W, Lehman VT, Kallmes DF et al. The effects of statin therapy on carotid plaque composition and volume: A systematic review and meta-analysis. Journal of neuroradiology. Journal de neuroradiologie 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28187866
  28. Balan A, Szaingurten-Solodkin I, Swissa SS et al. The effects of pravastatin on the normal human placenta: Lessons from ex-vivo models. PLoS One 2017; 12:e0172174. http://www.ncbi.nlm.nih.gov/pubmed/?term=28199380
Issue 8
  1. Steen DL, Khan I, Ansell D et al. Retrospective examination of lipid-lowering treatment patterns in a real-world high-risk cohort in the UK in 2014: comparison with the National Institute for Health and Care Excellence (NICE) 2014 lipid modification guidelines. BMJ Open 2017; 7:e013255. http://www.ncbi.nlm.nih.gov/pubmed/?term=28213597
  2. Stam-Slob MC, van der Graaf Y, Greving JP et al. Cost-Effectiveness of Intensifying Lipid-Lowering Therapy With Statins Based on Individual Absolute Benefit in Coronary Artery Disease Patients. J Am Heart Assoc 2017; 6. http://www.ncbi.nlm.nih.gov/pubmed/?term=28214794
  3. Koslik HJ, Meskimen AH, Golomb BA. Physicians' Experiences as Patients with Statin Side Effects: A Case Series. Drug safety - case reports 2017; 4:3. http://www.ncbi.nlm.nih.gov/pubmed/?term=28217821
  4. Kaminska E, Hennig M, Brandt A et al. [Treatment with statins in children with familial hypercholesterolemia]. Developmental period medicine 2016; 20:328-334. http://www.ncbi.nlm.nih.gov/pubmed/?term=28216488
  5. Grover A, Rehan HS, Gupta LK, Yadav M. Correlation of compliance to statin therapy with lipid profile and serum HMGCoA reductase levels in dyslipidemic patients. Indian Heart J 2017; 69:6-10. http://www.ncbi.nlm.nih.gov/pubmed/?term=28228309
  6. Amin K, Farley JF, Maciejewski ML, Domino ME. Effect of Medicaid Policy Changes on Medication Adherence: Differences by Baseline Adherence. Journal of managed care & specialty pharmacy 2017; 23:337-345. http://www.ncbi.nlm.nih.gov/pubmed/?term=28230447
  7. Mayor S. Statin side effects are strongest predictor of inadequate cholesterol control, study shows. Bmj 2017; 356:j869. http://www.ncbi.nlm.nih.gov/pubmed/?term=28219883
  8. Kuehn BM. Preventive Statin Use Recommended by US Task Force. Circulation 2017; 135:806-807. http://www.ncbi.nlm.nih.gov/pubmed/?term=28223326
  9. Geifman N, Brinton RD, Kennedy RE et al. Evidence for benefit of statins to modify cognitive decline and risk in Alzheimer's disease. Alzheimer's research & therapy 2017; 9:10. http://www.ncbi.nlm.nih.gov/pubmed/?term=28212683
  10. Mozetic V, Freitas CG, Riera R. Statins and Fibrates for Diabetic Retinopathy: Protocol for a Systematic Review. JMIR research protocols 2017; 6:e30. http://www.ncbi.nlm.nih.gov/pubmed/?term=28228373

Miscellaneous publications
Issue 7
  1. Yoo RJ, Kim MH, Woo SK et al. Monitoring of macrophage accumulation in statin-treated atherosclerotic mouse model using sodium iodide symporter imaging system. Nuclear medicine and biology 2017; 48:45-51. http://www.ncbi.nlm.nih.gov/pubmed/?term=28208058
  2. Wu X, Song M, Qiu P et al. Synergistic chemopreventive effects of nobiletin and atorvastatin on colon carcinogenesis. Carcinogenesis 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28207072
  3. N P, Abhilash A, Saquib S et al. Clinical Efficacy of Subgingivally Delivered 1.2 mg Simvastatin in the Treatment of Patients with Aggressive Periodontitis: A Randomized Controlled Clinical Trial. The International journal of periodontics & restorative dentistry 2017; 37:e135-e141. http://www.ncbi.nlm.nih.gov/pubmed/?term=28196160
  4. Morel J, Hargreaves I, Brealey D et al. Simvastatin pre-treatment improves survival and mitochondrial function in a three-day fluid-resuscitated rat model of sepsis. Clinical science (London, England : 1979) 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28202686
  5. Luu W, Gelissen IC, Brown AJ. Manipulating Cholesterol Status Within Cells. Methods in molecular biology (Clifton, N.J.) 2017; 1583:41-52. http://www.ncbi.nlm.nih.gov/pubmed/?term=28205165
  6. Komatsu R, Yilmaz HO, You J et al. Lack of Association between Preoperative Statin Use and Respiratory and Neurologic Complications after Cardiac Surgery. Anesthesiology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28207437
  7. Kapoor S. Rosuvastatin and Its Evolving Role as a Vascular Remodeling and Antiproliferative Agent in Different Systemic Malignancies. J Pharmacol Exp Ther 2017; 360:434. http://www.ncbi.nlm.nih.gov/pubmed/?term=28188271
  8. Kanshana JS, Khanna V, Singh V et al. Progression and characterization of the accelerated atherosclerosis in iliac artery of New Zealand White rabbits: effect of Simvastatin. Journal of cardiovascular pharmacology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28207427
  9. Ji T, Wentian L, Yukun Z et al. Simvastatin Inhibits IL-1beta-Induced Apoptosis and Extracellular Matrix Degradation by Suppressing the NF-kB and MAPK Pathways in Nucleus Pulposus Cells. Inflammation 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28188410
  10. Akhigbe T, Zolnourian A, Bulters D. Cholesterol-reducing agents for treatment of aneurysmal subarachnoid haemorrhage: systematic review and meta-analyses of randomized controlled trials. World neurosurgery 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28192263

Issue 8
  1. axWang ST, Ho HJ, Lin JT et al. Simvastatin-induced cell cycle arrest through inhibition of STAT3/SKP2 axis and activation of AMPK to promote p27 and p21 accumulation in hepatocellular carcinoma cells. Cell death & disease 2017; 8:e2626. http://www.ncbi.nlm.nih.gov/pubmed/?term=28230855
  2. Sigala F, Efentakis P, Karageorgiadi D et al. Reciprocal regulation of eNOS, H2S and CO-synthesizing enzymes in human atheroma: Correlation with plaque stability and effects of simvastatin. Redox biology 2017; 12:70-81. http://www.ncbi.nlm.nih.gov/pubmed/?term=28214453
  3. Santos L, Davel AP, Almeida TI et al. Soy milk versus simvastatin for preventing atherosclerosis and left ventricle remodeling in LDL receptor knockout mice. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas / Sociedade Brasileira de Biofisica ... [et al.] 2017; 50:e5854. http://www.ncbi.nlm.nih.gov/pubmed/?term=28225891
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