up-to-date with a click!
Update - Issue 11-12, 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 11

Lower stroke risk, in patients with improved statin adherence
Meta-analysis of 15 observational studies and 710,504 subjects, associates statins adherence with decreased risk of stroke. A cut-off value of proportion of days covered (PDC) by medication of ≥80% was used to define good adherence. This was in primary prevention as well as secondary prevention setting. Studies were heterogeneous in terms of quality, ethnic backgrounds, populations studied and outcome. Of the 15 studies 14 were positive and showed improved outcomes in patient adherent to statins, of which 12 proved statistically significant. One study showed no improved outcome but this was non-statistically significant. The overall relative risk reduction of statin adherence vs non-adherence was 28%; RR 0.72 (95%CI 0.65-0.79). For ischemic stroke: RR 0.83 (95% CI 0.74-0.92) for hemorrhagic stroke: RR 0.75 (95% CI 0.51-1.09). Improved statin adherence of 20% translated into an 8% lower risk of total stroke; RR:0.92 (95% CI 0.89-0.94). In the ischemic stroke subgroup, this translated to a 7% lower risk RR: 0.93 (95% CI 0.65-079).  The authors concluded that better adherence is associated with reduced risk of stroke but comment that better quality prospective studies are needed to confirm this.
Xu T, Yu X, Ou S et al. Statin Adherence and the Risk of Stroke: A Dose-Response Meta-Analysis. CNS drugs 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28290082
Statin intolerance translates into increased risk of CHD events
Post MI patients unable to tolerate statins had a markedly increased risk of recurrent MI and CHD. Data was collected from an US Medicare registry of 105 329 patients that started with moderate or high intensity statin after AMI discharge (2007 -2013). intolerance was defined as 1. down titrating statins, 2. initiating ezetimibe, 3. switching from statins to ezetimibe monotherapy, 4. diagnosed rhabdomyolysis or antihyperlipidemic event, followed by statin down titration or 5. discontinuation or switching between ≥3 types of statins after initiation. High statin adherence was defined as proportion of days covered ≥ 80%. Statin intolerance was observed in 1 741 (1.65%) patients; high statin adherence in 55 567 (52.8%) individuals. Number of recorded events during the median 1.9-2.3-year follow were: 4 450 MI’s  6 250 CHD events and 14 311 deaths: 14 311. Non-compliant patients statin intolerant patients had a 50% higher chance of a recurrent cardiac event. For MI HR: 1.50 (95%CI 1.30-1.73); for CHD events HR 1.51 (95% CI 1.34-1.70). no significant difference was observed for all-cause mortality HR: 0.96 (95%CI 0.87-1.06). Although this retrospective study has the standard vulnerabilities of observational data such as residual confounding. Also, statin intolerance could only be inferred and was not based on documented specific data. Despite this shortcoming collected data re-affirms the importance of using high intensity high dose statin daily. This guideline dictated regimen provides significant protection for CHD recurrences within a relative short period of approximately 2 years.  
Serban MC, Colantonio LD, Manthripragada AD et al. Statin Intolerance and Risk of Coronary Heart Events and All-Cause Mortality Following Myocardial Infarction. J Am Coll Cardiol 2017; 69:1386-1395. http://www.ncbi.nlm.nih.gov/pubmed/?term=28302290
Nissen SE. Statin Intolerance: An Elusive But Morbid Disorder. J Am Coll Cardiol 2017; 69:1396-1398. http://www.ncbi.nlm.nih.gov/pubmed/?term=28302291
When is LDL-C too low?
The introduction of PCSK9ab allows for reaching plasma LDL-C levels that are unattainable with statins or statin/ezetimibe combination therapy. LDL-C levels as low as < 25 mg/dl were not an uncommon finding in patients that participated the PCSK9ab trials. The question the authors of this review aim to address is: can LDL-C be too low? And at what level do we cross the threshold of benefit to harm. The presented data was discussed during an expert symposium: Risk and benefits of Extremely Low LDL Cholesterol in the summer of 2016. The authors discuss several topics: cellular cholesterol balance; the experience from abeta- and; hypobetalipoproteinemia’s; experience from PCSK9 mutations and ANGPLT3 mutations; lipid-lowering trials; LDL-C levels and effects on risk of type 2 diabetes, infections, immune system, bone metabolism and brain function. The authors concluded that based on current knowledge, cholesterol critical functions such as steroid hormone production, enterohepatic circulation of bile acids and neural cell function remain intact when LDL-C is extremely low. The impact of prolonged very low LDL-C concentrations on atherosclerotic complications as well possible side effects still needs to be determined.
Olsson AG, Angelin B, Assmann G et al. Can LDL cholesterol be too low? Possible risks of extremely low levels. Journal of internal medicine 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28295777
Calcium scoring in asymptomatic patients – Consensus paper
The role of Calcium score in determining risk for atherothrombotic events is gaining prominence. The expert consensus statement from the Society of Cardiovascular Computed Tomography presents a structured overview of the scientific evidence supporting the prognostic value of calcium scoring in primary prevention. The consensus statement promotes this imaging tool to reclassify patients after the global risk scores have been implemented. Improved adherence to preventive strategies such as healthy lifestyle and risk factor modifying medical treatments is observed in studies addressing this issue. Recommendations on techniques, different procedures and stressing the re-use imaging data that was generated for other diagnostic purposes e.g. Lung cancer and breast cancer screening are included as well. For those that are interested in using calcium scoring in their clinical practice this paper provides guidance and up to date background information on published studies.
Hecht H, Blaha MJ, Berman DS et al. Clinical indications for coronary artery calcium scoring in asymptomatic patients: Expert consensus statement from the Society of Cardiovascular Computed Tomography. Journal of cardiovascular computed tomography 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28283309
Better outcomes and no harms observed in patients with LDL-C < 30 mg/dl  

In the IMPROVE-IT study analyzing the benefits and harms of reaching an LDL-C < 30 mg/dl was a pre-specified endpoint. Patients who reached this target after one month (6.4%), were compared to patients that achieved LDL-C concentrations of 30-49 mg/dl (31%), 50-69 mg/dl (36%) and > 70 mg/dl. (26%). Patients reaching LDL-C <30 mg/dl (median 25 mg/dl; interquartile range 21-27 mg/dl) were older, male, nonwhite, diabetic, statin naïve, presenting with first MI, had lower baseline values and 85% received the combination of Ezetimibe/Simvastatin. No difference in the 9 prespecified safety endpoints was observed. The risk for the primary endpoint – a composite of cardiovascular death, major coronary events, or stroke - was significantly lower in the patients that were able to reach a very low LDL-C, compared to the ones with an LDL-C >70 mg/dl; HR: 0.79 (95%CI 0.69-0.91; P=0.001). the authors concluded that reaching LDL-C targets far beyond current guideline recommendations was not associated with adverse events. Numerical cardiovascular events were significantly less. This observational analysis supports the uses of intensive lipid lowering strategies in very high risk patients.
Giugliano RP, Wiviott SD, Blazing MA et al. Long-term Safety and Efficacy of Achieving Very Low Levels of Low-Density Lipoprotein Cholesterol : A Prespecified Analysis of the IMPROVE-IT Trial. JAMA cardiology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28291866

Issue 12

Do statin users forget healthy lifestyle?

In this retrospective analysis of the Australian Diabetes, Obesity and Lifestyle Study (2011–2012). 4614 participants (>37 yers of age) were queried for smoking status, physical activity, saturated fat intake and alcohol consumption. The Participants that were using a statin (N= 1108 – 24%) were no different in terms of smoking, exercise and alcohol consumption. There was however a significant difference in the saturated fatty acids consumption. Statin users were 29% less likely to be within the highest quartile vs the lowest quartile of daily saturated fatty acid intake. Despite the often-stated fear that taking a statin automatically translates into less adherence to a healthy lifestyle, this was not observed in this Australian cohort. There was even evidence of improved diet in statin users most likely related to heightened awareness of the impact of lifestyle, but most prominently diet, on plasma cholesterol levels. If this is a typical characteristic of Australians could not be distilled from this analysis and needs to be confirmed by prospective studies of a similar design in other geographical and ethnic populations. 
Johal S, Jamsen KM, Bell JS et al. Do statin users adhere to a healthy diet and lifestyle? The Australian Diabetes, Obesity and Lifestyle Study. Eur J Prev Cardiol 2017; 24:621-627. http://www.ncbi.nlm.nih.gov/pubmed/?term=28326830
Review of lipid management in ACS patients
ACS patients are considered to have a higher risk for atherothrombotic complications as patients with no clinical manifestations and stable CHD patients. One of the more prominent characteristics of these patients is inflammation and pro-thrombogenic features such as increased platelet reactivity. Lipid lowering has earned a prominent position in reducing this risk, partly by lowering LDL-C and partly because of the anti-inflammatory effect of statins persé. In this review, the data from the older statin trials e.g. PPROVE-IT and MIRACL as well as the more recent IMPROVE-IT (with Ezetimibe) and ODYSSEY Outcomes, GLAGOV, ODYSSEY J-IVUS and FOURIER (PCSK9ab) are reviewed. Based on the collected trial data, early and intensive statin treatment proved to reduce the risk of recurrent CVD events. Evidence is accumulating for non-statin lipid lowering as well, Ezetimibe and PCSK9ab trials have proven their contribution when added to statin treatment, reaching targets beyond what is possible with statins, translated in additional CVD risk reduction. Next generation agents e.g. CETP-inhibitors mRNA inhibition for PCSK9 or Apo CIII and PPAR-agonist are still in an early phase of their development but have potential to be promising as well.
Fujisue K, Tsujita K. Current status of lipid management in acute coronary syndrome. J Cardiol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28325524
CT-angio improves risk stratification based on the 2013 Pooled Cohort Equation
A meta-analysis based on two trials to determine the potential of CT angio to reclassify patients for statin therapy after risk assessment with the 2013 Pooled Cohort Risk Equation. The 2 studies included 2 295 patients; 66% male; non-obstructive CAD in 47% of the patients; a median follow-up of 49 months and 67 ASCVD events. Presence of non-obstructive CAD translated in a HR of 3.2 (95% CI 1.5-6.7). Adding this information into the Pooled Cohort Risk Equation resulted in a reclassification of 14% of the subjects. The presence of non-obstructive CAD automatically translates to increased risk and would shift an individual with a low 10-year risk being eligible for statin therapy. This effect was more prominent in men compared to women and African Americans compared to Caucasians. The modified risk scores were calculated in 169 patients with acute chest pain without acute coronary syndrome. The mean original 10-year ASCVD risk in this population was 7.2 ± 7.7%; 101 (60%) were without CAD, and 68 (40%) had non-obstructive CAD. statin eligibility was revised in 14% of the population (n=24 of 169). Specifically, 12 of 101 patients (12%) who had an original ASCVD score of >7.5% and who had no CAD were reclassified as non–statin eligible, whereas 12 of 68 patients (18%) who had non-obstructive CAD but an original ASCVD score <7.5% were reclassified as statin eligible. The authors caution there were important limitations of their analysis due to the small number of studies, participants and recorded events.
Emami H, Takx RA, Mayrhofer T et al. Nonobstructive Coronary Artery Disease by Coronary CT Angiography Improves Risk Stratification and Allocation of Statin Therapy. JACC. Cardiovascular imaging 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28330658
Timing and dose of statins important for reducing 30 day mortality after CABG surgery
Data collected in a retrospective cohort study, of 3,025 consecutive CABG patients
between July 2005 and May 2011 at the Texas Heart Institute, Catholic Health Initiatives St. Luke’s Health-Baylor St. Luke’s Medical Center. Statins were administered before the procedure < 24 hr. (N=1 788); 24-72 hrs. (N=452) and >72 hrs. or no statin (N=781). Patients were also grouped by statins dose: No statin (N=739); ≤20 mg Atorvastatin or equivalent (n= 920) and >20 mg atorvastatin or equivalent (N=1 284). The authors concluded that a statin of 20 mg atorvastatin or equivalent administered < 24 hr. before the procedure were both independently associated with reduced 20-day all-cause mortality. For early timing an OR: 0.52 (95%CI 0.28-0.98; P=0.04). Atorvastatin >20 mg (or equivalent statin) compared to no statins translated into an OR: 0.32 (95%CI 0.13-0.82; P=0.02). A dose of 20 mg or less provided not protection. Considering the limitations of this retrospective observational analysis, this study provides insights that are indications that statin started just before CABG and in a dosage of > 20mg of Atorvastatin could have impressive protective effects for these high-risk patients. The results are comparable to benefits observed in randomized trials that analyzed the effects of a single tablet of 80 mg + 40 mg Atorvastatin 24hrs and 1hr. before a scheduled PTCA procedure.  
Curtis M, Deng Y, Lee VV et al. Effect of Dose and Timing of Preoperative Statins on Mortality After Coronary Artery Bypass Surgery. The Annals of thoracic surgery 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28318515
Statins protect patients suffering from severe hepatitis B and C
Increase in transaminases are frequently reported with statin use and not seldom a reason to stop statins. In this analysis statin use provides hepatic protection, not harm, in patients with severe hepatitis B/C. Based on a retrospective analysis of the large Taiwanese National Health Insurance registry. Patients with cirrhotic liver disease (N=1350) were selected and statins users were propensity matched with non-users. The benefit provided by statin use was mainly in decreasing the risk of ascites-related complications and hepatic encephalopathy. Reduced risk in variceal bleeding could be observed in HBV- and alcohol-related cirrhotic patients. Statin use was associated with significantly lower mortality (by approximately 60%) in mainly patients with HBV-cirrhosis. Statin also reduced the HCC risk in cirrhotic patients, but lack of significance in subgroup analysis. Overall patients using statins had a reduced risk for decompensations due to chronic HBV and HCV.; HR 0.39 (95% CI 0.25-0.62) and HR 0.51 (95% CI 0.29-0.93) respectively. A dose dependend reduced risk for decompensation, mortality and hepato cellular carcinoma was observed as well (p for trend: < .0001, < .0001, and 0.009). The authors conclude that based on this study,and additional accumulating evidence, statins may now be considered as an adjuvant therapy to prevent decompensation among cirrhotic patients.
Chang FM, Wang YP, Lang HC et al. Statins decrease the risk of decompensation in HBV- and HCV-related cirrhosis: A population-based study. Hepatology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28318053

Relevant publications
Issue 11
  1. Fang JX, Wang EQ, Wang W et al. The efficacy and safety of high-dose statins in acute phase of ischemic stroke and transient ischemic attack: a systematic review. Internal and emergency medicine 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28303440
  2. Thongtang N, Sitthananun C, Sriussadaporn S, Nitiyanant W. Efficacy of low- and moderate-intensity statins for achieving low- density lipoprotein cholesterol targets in Thai type 2 diabetic patients. Journal of diabetes and metabolic disorders 2017; 16:6. http://www.ncbi.nlm.nih.gov/pubmed/?term=28289653
  3. Sabatine MS, Giugliano RP, Keech AC et al. Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease. N Engl J Med 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28304224
  4. Ridker PM, Tardif JC, Amarenco P et al. Lipid-Reduction Variability and Antidrug-Antibody Formation with Bococizumab. N Engl J Med 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28304227
  5. Ran D, Nie HJ, Gao YL et al. A randomized, controlled comparison of different intensive lipid-lowering therapies in Chinese patients with non-ST-elevation acute coronary syndrome (NSTE-ACS): Ezetimibe and rosuvastatin versus high-dose rosuvastatin. Int J Cardiol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28291622
  6. Lin CM, Liao KF, Lin CL, Lai SW. Use of Simvastatin and Risk of Acute Pancreatitis: A Nationwide Case-Control Study in Taiwan. Journal of clinical pharmacology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28301063
  7. Koren MJ, Sabatine MS, Giugliano RP et al. Long-term Low-Density Lipoprotein Cholesterol-Lowering Efficacy, Persistence, and Safety of Evolocumab in Treatment of Hypercholesterolemia: Results Up to 4 Years From the Open-Label OSLER-1 Extension Study. JAMA cardiology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28291870
  8. Kitagawa K, Hosomi N, Nagai Y et al. Reduction in High-Sensitivity C-Reactive Protein Levels in Patients with Ischemic Stroke by Statin Treatment: Hs-CRP Sub-Study in J-STARS. J Atheroscler Thromb 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28302952
  9. Holzhauser L, Hovnanians N, Eshtehardi P et al. Statin therapy improves survival in patients with severe pulmonary hypertension: a propensity score matching study. Heart Vessels 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28303379
  10. Choi KS, Kim JM, Yi HJ et al. Dose-related effect of statins in patients with endovascular coiling or microsurgical clipping for aneurysmal subarachnoid hemorrhage: updated study-level meta-analysis. Eur J Clin Pharmacol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28293714
  11. Carroll C, Tappenden P, Rafia R et al. Evolocumab for Treating Primary Hypercholesterolaemia and Mixed Dyslipidaemia: An Evidence Review Group Perspective of a NICE Single Technology Appraisal. PharmacoEconomics 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28285379
  12. Agarwal S, Chaubey KK, Chaubey A et al. Clinical efficacy of subgingivally delivered simvastatin gel in chronic periodontitis patients. Journal of Indian Society of Periodontology 2016; 20:409-416. http://www.ncbi.nlm.nih.gov/pubmed/?term=28298823
  13. Xie R, Yang Y, Cui W et al. Atorvastatin Can Ameliorate Left Atrial Stunning Induced by Radiofrequency Ablation for Atrial Fibrillation. Canadian journal of physiology and pharmacology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28301729
  14. Wang Q, Zheng M, Leil T. Investigating Transporter-Mediated Drug-Drug Interactions Using a Physiologically Based Pharmacokinetic Model of Rosuvastatin. CPT Pharmacometrics Syst Pharmacol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28296193
  15. Thompson PD. Adverse Effects of Statins-Reply. Jama 2017; 317:1080. http://www.ncbi.nlm.nih.gov/pubmed/?term=28291889
  16. Stone NJ, Blum CB. Use of Statins in Adults Older Than 75 Years. Jama 2017; 317:1081. http://www.ncbi.nlm.nih.gov/pubmed/?term=28291887
  17. Samorukova EI, Adasheva TV, Zadionchenko VS, Rosliakova GA. [Pleiotropic Effects of Rosuvastatin in Patients With High Cardiovascular Risk]. Kardiologiia 2015; 55:32-37. http://www.ncbi.nlm.nih.gov/pubmed/?term=28294912
  18. Salastekar N, Desai T, Hauser T et al. Salsalate Improves Glycemia in Overweight Persons With Diabetes Risk Factors of Stable Statin-Treated Cardiovascular Disease: a 30-month Randomized Placebo-Controlled Trial. Diabetes Obes Metab 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28295931
  19. Ponomareva AI, Kompaniets OG, Linchak RM, Agafonova GA. [Pharmacoepidemiology of Statins in Patients With Hypertension and Dyslipidemia]. Kardiologiia 2015; 55:25-31. http://www.ncbi.nlm.nih.gov/pubmed/?term=28294791
  20. Panov AV, Gordeev ML, Mitrofanova LB et al. [Rosuvastatin in Coronary Bypass Surgery: Whether Only Secondary Prevention?]. Kardiologiia 2016; 56:18-23. http://www.ncbi.nlm.nih.gov/pubmed/?term=28294868
  21. Mikhin VP, Zhilyaeva YA, Gromnaky NI. [Pleotropic Effects of Atorvastatin in Patients With Chronic Ischemic Heart Disease]. Kardiologiia 2016; 56:42-46. http://www.ncbi.nlm.nih.gov/pubmed/?term=28294872
  22. Malachowski SJ, Quattlebaum AM, Miladinovic B. Adverse Effects of Statins. Jama 2017; 317:1079-1080. http://www.ncbi.nlm.nih.gov/pubmed/?term=28291886
  23. Li J, Liu J, Liang Z et al. Simvastatin and Atorvastatin inhibit DNA replication licensing factor MCM7 and effectively suppress RB-deficient tumors growth. Cell death & disease 2017; 8:e2673. http://www.ncbi.nlm.nih.gov/pubmed/?term=28300827
  24. Koshelskaya OA, Vinnitskaya IV, Konko TY et al. [Comparative Randomized Study of the Effects of Long-Term Therapy With Rosuvastatin and With Combination of Atorvastatin and Ezetimibe on Carbohydrate Metabolism and Adipokynes Levels in Patients With Coronary Artery Disease and Diabetes Mellitus]. Kardiologiia 2015; 55:67-74. http://www.ncbi.nlm.nih.gov/pubmed/?term=28294846
  25. Kohler-Forsberg O, Gasse C, Berk M, Ostergaard SD. Do Statins Have Antidepressant Effects? CNS drugs 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28303466
  26. Kobalava ZD, Stavtseva YV. [The Efficacy and Safety of Rosuvastatin in Patients With oronary Heart Disease]. Kardiologiia 2015; 55:80-87. http://www.ncbi.nlm.nih.gov/pubmed/?term=28294722
  27. Gurwitz JH, Go AS, Fortmann SP. Use of Statins in Adults Older Than 75 Years-Reply. Jama 2017; 317:1081. http://www.ncbi.nlm.nih.gov/pubmed/?term=28291890
  28. Goldstein LB. Adverse Effects of Statins. Jama 2017; 317:1079. http://www.ncbi.nlm.nih.gov/pubmed/?term=28291885
  29. Fania L, Didona D, Tonanzi T et al. Simvastatin-associated dermatomyositis. Dermatologic therapy 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28296009
  30. Dunphy L, Morhij R, Tucker S. Rhabdomyolysis-induced compartment syndrome secondary to atorvastatin and strenuous exercise. BMJ case reports 2017; 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28302660
  31. Chen W, Huang Z, Bi M et al. Effects of simvastatin on serum adiponectin: a meta-analysis of randomized controlled trials. Lipids Health Dis 2017; 16:53. http://www.ncbi.nlm.nih.gov/pubmed/?term=28288631
  32. Chaudhary R, Garg J, Shah N, Sumner A. PCSK9 inhibitors: A new era of lipid lowering therapy. World J Cardiol 2017; 9:76-91. http://www.ncbi.nlm.nih.gov/pubmed/?term=28289523
  33. Bertolotti M, Franchi C, Rocchi MB et al. Prevalence and Determinants of the Use of Lipid-Lowering Agents in a Population of Older Hospitalized Patients: the Findings from the REPOSI (REgistro POliterapie Societa Italiana di Medicina Interna) Study. Drugs Aging 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28299634
  34. Bayat N, Ebrahimi-Barough S, Norouzi-Javidan A et al. Anti-inflammatory Effects of Atorvastatin by Suppressing TRAF3IP2 and IL-17RA in Human Glioblastoma Spheroids Cultured in a Three-dimensional Model: Possible Relevance to Glioblastoma Treatment. Mol Neurobiol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28283885
  35. Bart BY, Luchinkina EE, Gordeev IG et al. [Comparative Analysis of the Efficacy and Safety of Rosuvastatin and Original Rosuvastatin]. Kardiologiia 2016; 56:46-49. http://www.ncbi.nlm.nih.gov/pubmed/?term=28290847
  36. Baranova EI, Berezina AV, Melioranskaya EI, Polyakova EA. [Safety and Efficacy of Amlodipine, Lisinopril and Rosuvastatin Therapy in Patients With Metabolic Syndrome and Nonalcoholic Fatty Liver Disease]. Kardiologiia 2015; 55:68-75. http://www.ncbi.nlm.nih.gov/pubmed/?term=28294798
  37. Andrade C. Relative to SSRI users, SSRI-statin users have fewer psychiatric hospital contacts and no increase in suicidal behaviour or all-cause mortality. Evidence-based mental health 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28283544

Issue 12
  1. Yu S, Chu Y, Li G et al. Statin Use and the Risk of Cataracts: A Systematic Review and Meta-Analysis. J Am Heart Assoc 2017; 6. http://www.ncbi.nlm.nih.gov/pubmed/?term=28320745
  2. Toyama K, Sugiyama S, Oka H et al. A Pilot Study: The Beneficial Effects of Combined Statin-exercise Therapy on Cognitive Function in Patients with Coronary Artery Disease and Mild Cognitive Decline. Intern Med 2017; 56:641-649. http://www.ncbi.nlm.nih.gov/pubmed/?term=28321063
  3. Stellaard F, Lutjohann D. The Interpretation of Cholesterol Balance Derived Synthesis Data and Surrogate Noncholesterol Plasma Markers for Cholesterol Synthesis under Lipid Lowering Therapies. Cholesterol 2017; 2017:5046294. http://www.ncbi.nlm.nih.gov/pubmed/?term=28321334
  4. Rodriguez-Broadbent H, Law PJ, Sud A et al. Mendelian randomisation implicates hyperlipidaemia as a risk factor for colorectal cancer. International journal of cancer. Journal international du cancer 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28340513
  5. Qian LJ, Gao Y, Zhang YM et al. Therapeutic efficacy and safety of PCSK9-monoclonal antibodies on familial hypercholesterolemia and statin-intolerant patients: A meta-analysis of 15 randomized controlled trials. Scientific reports 2017; 7:238. http://www.ncbi.nlm.nih.gov/pubmed/?term=28331223
  6. Hamzei E, Alavi A, Khorami Saber M, Azad M. The effect of statins on National Institutes of Health Stroke Scale (NiHSS) in Ischemic stroke. Journal of medicine and life 2015; 8:52-55. http://www.ncbi.nlm.nih.gov/pubmed/?term=28316706
  7. Bouchonville MF, Matani S, DuBroff JJ, DuBroff RJ. Are diabetes guidelines truly evidence based? Diabetes Res Clin Pract 2017; 127:70-79. http://www.ncbi.nlm.nih.gov/pubmed/?term=28319804
  8. Arian A, Moghadam SG, Kazemi T, Hajihosseini M. The Effects of Statins on Pulmonary Artery Pressure in Patients with Chronic Obstructive Pulmonary Disease: A Randomized Controlled Trial. Journal of research in pharmacy practice 2017; 6:27-30. http://www.ncbi.nlm.nih.gov/pubmed/?term=28331863
  9. Tomcsanyi J. [Adherence to statins in patients with myocardial infarction in Hungary]. Orvosi hetilap 2017; 158:443-446. http://www.ncbi.nlm.nih.gov/pubmed/?term=28328244
  10. Stiles ZE, Sparks DA. Acute Extremity Compartment Syndrome Secondary to Statin-Induced Myopathy. The American surgeon 2017; 83:74-75. http://www.ncbi.nlm.nih.gov/pubmed/?term=28316293
  11. Shah RV, Spahillari A, Mwasongwe S et al. Subclinical Atherosclerosis, Statin Eligibility, and Outcomes in African American Individuals: The Jackson Heart Study. JAMA cardiology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28315622
  12. Salado-Font SM, Lopez-Munoz F, Povedano-Montero FJ, Labella Quesada F. Bibliometric analysis of the scientific production as regards statin use for ophthalmological symptoms of myasthenia gravis. Archivos de la Sociedad Espanola de Oftalmologia 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28318833
  13. Patti AM, Toth PP, Giglio RV et al. Nutraceuticals as an Important Part of Combination Therapy in Dyslipidaemia. Current pharmaceutical design 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28317482
  14. Palumbo I, Matrone F, Montesi G et al. Statins Protect Against Acute RT-related Rectal Toxicity in Patients with Prostate Cancer: An Observational Prospective Study. Anticancer research 2017; 37:1453-1457. http://www.ncbi.nlm.nih.gov/pubmed/?term=28314317
  15. Okerson T, Patel J, DiMario S et al. Effect of 2013 ACC/AHA Blood Cholesterol Guidelines on Statin Treatment Patterns and Low-Density Lipoprotein Cholesterol in Atherosclerotic Cardiovascular Disease Patients. J Am Heart Assoc 2017; 6. http://www.ncbi.nlm.nih.gov/pubmed/?term=28314797
  16. Millar JS, Lassman ME, Thomas T et al. Effects of CETP Inhibition with Anacetrapib on Metabolism of VLDL TG and Plasma Apolipoproteins C-II, C-III, and E. Journal of lipid research 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28314859
  17. Lash TL, Riis AH, Ostenfeld EB et al. Associations of Statin Use With Colorectal Cancer Recurrence and Mortality in a Danish Cohort. American journal of epidemiology 2017:1-9. http://www.ncbi.nlm.nih.gov/pubmed/?term=28338891
  18. Kashihara Y, Ieiri I, Yoshikado T et al. Small-dosing Clinical Study: Pharmacokinetic, Pharmacogenomic (SLCO2B1 and ABCG2), and Interaction (Atorvastatin and Grapefruit Juice) Profiles of Five Probes for OATP2B1 and BCRP. Journal of pharmaceutical sciences 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28322941
  19. Dogra K, Goyal A, Khadgawat R et al. Low-density lipoprotein apheresis in a pediatric patient of familial hypercholesterolemia: Primi experientia from a tertiary care center in North India. Asian journal of transfusion science 2017; 11:58-61. http://www.ncbi.nlm.nih.gov/pubmed/?term=28316443
  20. Colantonio LD, Richman JS, Carson AP et al. Performance of the Atherosclerotic Cardiovascular Disease Pooled Cohort Risk Equations by Social Deprivation Status. J Am Heart Assoc 2017; 6. http://www.ncbi.nlm.nih.gov/pubmed/?term=28314800
  21. Capoulade R, Chan KL, Mathieu P et al. Autoantibodies and immune complexes to oxidation-specific epitopes and progression of aortic stenosis: Results from the ASTRONOMER trial. Atherosclerosis 2017; 260:1-7. http://www.ncbi.nlm.nih.gov/pubmed/?term=28319871
  22. Bernelot Moens SJ, Neele AE, Kroon J et al. PCSK9 monoclonal antibodies reverse the pro-inflammatory profile of monocytes in familial hypercholesterolaemia. Eur Heart J 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28329114
  23. Baruch A, Luca D, Kahn RS et al. A phase 1 study to evaluate the safety and LDL cholesterol-lowering effects of RG7652, a fully human monoclonal antibody against proprotein convertase subtilisin/kexin type 9. Clin Cardiol 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28326559
  24. Correction to: "Intracellular Unbound Atorvastatin Concentrations in the Presence of Metabolism and Transport.". J Pharmacol Exp Ther 2017; 361:198. http://www.ncbi.nlm.nih.gov/pubmed/?term=28314732

Miscellaneous publications
Issue 11
  1. Zhang Z, Tang L, Yu W et al. Improvement in erectile function in a rat model of high cholesterol diet-induced atherosclerosis by atorvastatin in a manner that is independent of its lipid-lowering property. Andrologia 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28295458
  2. Yu WL, Sun TW, Qi C et al. Enhanced osteogenesis and angiogenesis by mesoporous hydroxyapatite microspheres-derived simvastatin sustained release system for superior bone regeneration. Scientific reports 2017; 7:44129. http://www.ncbi.nlm.nih.gov/pubmed/?term=28287178
  3. Mohamed MT, Abuelezz SA, Atalla SS et al. The anti-osteoporotic and anti-atherogenic effects of alendronate and simvastatin in ovariectomized rats fed high fat diet: A comparative study of combination therapy versus monotherapy. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2017; 89:1115-1124. http://www.ncbi.nlm.nih.gov/pubmed/?term=28298072
  4. Mendes Junior D, Domingues JA, Hausen MA et al. Study of mesenchymal stem cells cultured on a poly(lactic-co-glycolic acid) scaffold containing simvastatin for bone healing. Journal of applied biomaterials & functional materials 2017:0. http://www.ncbi.nlm.nih.gov/pubmed/?term=28291900
  5. Kida K, Tanabe K, Sasaki H et al. Release properties of atelocollagen-gelatin complexes as carriers for local administration of fluvastatin. Dent Mater J 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28302944
  6. Goto N, Okazaki K, Akasaki Y et al. A single intra-articular injection of fluvastatin-PLGA microspheres reduces cartilage degradation in rabbits with experimental osteoarthritis. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28303595
  7. Brower V. Pravastatin has no advantage in small-cell lung cancer. The Lancet. Oncology 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28285843
  8. Salem HF, Kharshoum RM, Halawa AK, Naguib DM. Preparation and optimization of tablets containing a self-nano-emulsifying drug delivery system loaded with rosuvastatin. Journal of liposome research 2017:1-12. http://www.ncbi.nlm.nih.gov/pubmed/?term=28287014
  9. Chavan BB, Kalariya PD, Nimbalkar RD et al. Identification and characterization of fluvastatin metabolites in rats by UHPLC/Q-TOF/MS/MS and in silico toxicological screening of the metabolites. Journal of mass spectrometry : JMS 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28295913

Issue 12
  1. Yamada-Nomoto K, Yoshino O, Akiyama I et al. PAI-1 in granulosa cells is suppressed directly by statin and indirectly by suppressing TGF-beta and TNF-alpha in mononuclear cells by insulin-sensitizing drugs. American journal of reproductive immunology (New York, N.Y. : 1989) 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28337819
  2. Chen Y, Yu S, Zhang N et al. Atorvastatin prevents Angiotensin II induced myocardial hypertrophy in vitro via CCAAT/enhancer-binding protein beta. Biochem Biophys Res Commun 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28315329
  3. Luo D, Kim JH, Park C et al. Design of fixed dose combination and physicochemical characterization of enteric-coated bilayer tablet with circadian rhythmic variations containing telmisartan and pravastatin sodium. Int J Pharm 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28330645
  4. Affandi MM, Tripathy M, Majeed A. Arginine Complexes with Simvastatin: Apparent Solubility, In Vitro Dissolution and Solid State Characterization. Current drug delivery 2017. http://www.ncbi.nlm.nih.gov/pubmed/?term=28322162

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