Journal articles: 'Statin-associated muscle symptoms'

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Palapinyo, Sirinoot. "Statin-Associated Muscle Symptoms: SAM." Bangkok Medical Journal 14, no. 01 (2018): 69–75. http://dx.doi.org/10.31524/bkkmedj.2018.02.013.

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Sarzani, Riccardo, Federico Giulietti, Massimiliano Allevi, et al. "Statin-Associated Muscle Symptoms: Clinical Index in a hypertensive population candidated to lipid-lowering therapy but not taking statins." European Atherosclerosis Journal 2, no. 1 (2023): 19. http://dx.doi.org/10.56095/eaj.v2i1.30.

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Aim: Statin-associated muscle symptoms (SAMS) are claimed to be frequent in clinical practice. The SAMS-clinical index (SAMS-CI) assesses the likelihood that muscle symptoms are related to statin use. We evaluated the prevalence and characteristics of muscle symptoms in hypertensive patients eligible for statin therapy according to their individual cardiovascular risk. Methods: Observational study on 390 consecutive outpatients referred to our Centre. All patients were asked the following question: “Have you ever taken a drug/nutraceutical that you think gave you muscle symptoms?”. Patients who answered “yes” were evaluated with SAMS-CI. Results: Mean age: 60.5±13.5 years. Male prevalence: 53.8%. Patients who have ever taken a statin (“statin+” group): 250. Patients who have never taken a statin but have taken at least one other drug (“statin-” group): 140. Prevalence of muscle symptoms did not differ between the groups (p=0.217). Age and number of drugs taken were significantly associated with muscle symptoms at multivariate analysis. A not clinically significant higher SAMS-CI score emerged in the “statin+” group (p=0.004). Localization and pattern of muscle symptoms did not differ between the groups (p=0.170). Timing of muscle symptoms onset after starting the drug (p=0.036) and timing of symptom improvement after withdrawal (p=0.002) were associated with statin therapy. Conclusions: Prevalence of patient-reported muscle symptoms was not associated with statin therapy in our real life clinical study, confirming the growing evidence that subjective muscle-related symptoms are often misattributed to statins, while they may more likely be related to the nocebo/drucebo effect or other common undiagnosed conditions.

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Bouitbir, Jamal, Gerda M. Sanvee, Miljenko V. Panajatovic, François Singh, and Stephan Krähenbühl. "Mechanisms of statin-associated skeletal muscle-associated symptoms." Pharmacological Research 154 (April 2020): 104201. http://dx.doi.org/10.1016/j.phrs.2019.03.010.

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Baggett, Mary Caitlin, and Diane Nykamp. "Statin-Associated Bilateral Foot Myopathy." Journal of Pharmacy Practice 33, no. 6 (2019): 899–902. http://dx.doi.org/10.1177/0897190019857851.

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Objective: To report a case of statin-induced bilateral foot myopathy that resulted from 2 different statins. Case Summary: A 44-year-old Caucasian male with a history of ventricular fibrillation cardiac arrest, hyperlipidemia, and coronary artery disease experienced bilateral foot pain, weakness, and soreness while taking atorvastatin 20 mg daily. The pain subsided within weeks of discontinuing atorvastatin but returned years later after the initiation of rosuvastatin. The Naranjo probability scale indicates that this is a definite association between bilateral foot myopathy and statin use. Discussion: There is an association with statin use and lowering cardiovascular risk in patients with dyslipidemia and cardiovascular disease. However, statin metabolites can accumulate in the myocytes of muscle groups to cause a common side effect of myopathy. Statin myopathy typically occurs in large, bilateral, or proximal muscle groups, such as the thighs, back, calves, or buttocks. This patient was unusual in that his muscle symptoms only occurred in his feet and was severe enough to affect his ambulation. Conclusion: Stain-associated muscle symptoms have been reported to lessen medication adherence. There is also a risk with muscle symptoms that the patient could develop rhabdomyolysis, a rare but serious condition. Recognizing statin-associated muscle symptoms even in uncommon locations is important, so that alternative lipid-lowering strategies can be implemented to lower cardiovascular risk.

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Turashvili, N. "Statin-associated muscle symptoms and vitamin D." Atherosclerosis 315 (December 2020): e279-e280. http://dx.doi.org/10.1016/j.atherosclerosis.2020.10.882.

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Stock, Jane K. "Update on SAMS: Statin-associated muscle symptoms." Atherosclerosis 269 (February 2018): 260–61. http://dx.doi.org/10.1016/j.atherosclerosis.2017.12.032.

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Pennisi, Manuela, Giuseppe Di Bartolo, Giulia Malaguarnera, Rita Bella, Giuseppe Lanza, and Michele Malaguarnera. "Vitamin D Serum Levels in Patients with Statin-Induced Musculoskeletal Pain." Disease Markers 2019 (March 25, 2019): 1–6. http://dx.doi.org/10.1155/2019/3549402.

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Introduction. Statin-associated muscle symptoms are common side effects of statin therapy. These symptoms include myopathy, myalgia, and rhabdomyolysis. Vitamin D has been associated with musculoskeletal health; thus, its deficiency may produce detrimental effects in this tissue. Indeed, one symptom of vitamin D deficiency is myalgia, and the normalization of low vitamin D levels can relieve it. Patients and Methods. This cross-sectional study examined 1210 statin-treated patients to assess vitamin D status. These patients were divided into two groups: 287 with statin-associated muscle symptoms (SAMS) and 923 control patients without SAMS. Results. We have found a significant association between deficient and insufficient vitamin D status and statin-associated muscle symptoms (SAMS). Vitamin D deficiency (<30 nmol/L) presents 77% (95% C.I. 71.6% to 81.7%) sensitivity and 63.4% (95% C.I. 60.2% to 66.5%) specificity in diagnosing SAMS. Odds ratio analysis showed that this association is moderate-strong both for deficient and for insufficient status. Conclusion. We found a correlation between vitamin D deficiency and SAMS. Therefore, vitamin D levels may be useful for the diagnosis and management of SAMS.

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Dyadyk, A. I., T. E. Kugler, S. R. Zborowskyy, and Yu V. Suliman. "Statin-associated muscle symptoms: epidemiology, risk factors, mechanisms and treatment." Kardiologiia 59, no. 5S (2019): 4–12. http://dx.doi.org/10.18087/cardio.2522.

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Statins are widely prescribed and the risk of adverse drug reactions of lipid-lowering therapy is actively discussed, including muscle symptoms. This review synthesizes the knowledge about the clinical aspects of statin-associated muscle symptoms, which is important for the practitioner. Potential mechanisms of their development, risk factors, clinical manifestations, treatment and prevention are described. Timely detection the side effects of statins makes it possible to diagnose and eliminate, which is crucial for conducting lipid-lowering therapy for patients with atherosclerotic cardiovascular diseases. Management of statin-associated muscle symptoms requires altering (reduced dosages, use of another statin or alternative lipid-lowering drugs) or discontinuing the statin treatment.

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Lugovaya, Liya A., Alexey A. Nekrasov, Leonid G. Strongin, and Tatyana A. Nekrasova. "Clinical case of statin-induced myopathy in female patient with compensated hypothyroidism and unfavorable polymorphic variant of SLCO1B1*5 (c.521T>C)." Clinical review for general practice 2, no. 5 (2021): 21–24. http://dx.doi.org/10.47407/kr2021.2.5.00066.

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Statin-associated muscle symptoms are one of the statin-induced side effects. The incidence of the condition is increased by the presence of associated risk factors, one of which is hypothyroidism. The paper reports clinical case of statin-associated muscle symptoms in patient with compensated hypothyroidism carrying a SLCO1B1 mutation. Optimal assessment and treatment algorithms are discussed.

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Thompson, Paul D. "MY APPROACH to Managing Statin-Associated Muscle Symptoms." Trends in Cardiovascular Medicine 27, no. 2 (2017): 160–61. http://dx.doi.org/10.1016/j.tcm.2016.09.007.

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Backes, James M., Janelle F. Ruisinger, Cheryl A. Gibson, and Patrick M. Moriarty. "Statin-associated muscle symptoms—Managing the highly intolerant." Journal of Clinical Lipidology 11, no. 1 (2017): 24–33. http://dx.doi.org/10.1016/j.jacl.2017.01.006.

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Ochs‐Balcom, Heather M., Ly Minh Nguyen, Changxing Ma, et al. "Clinical features related to statin‐associated muscle symptoms." Muscle & Nerve 59, no. 5 (2019): 537–43. http://dx.doi.org/10.1002/mus.26397.

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Herrett, Emily, Elizabeth Williamson, Danielle Beaumont, et al. "Study protocol for statin web-based investigation of side effects (StatinWISE): a series of randomised controlled N-of-1 trials comparing atorvastatin and placebo in UK primary care." BMJ Open 7, no. 12 (2017): e016604. http://dx.doi.org/10.1136/bmjopen-2017-016604.

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IntroductionStatins are effective at preventing cardiovascular disease, widely prescribed and their use is growing. Uncertainty persists about whether they cause symptomatic muscle adverse effects, such as pain and weakness, in the absence of statin myopathy. Discrepancies between data from observational studies, which suggest statins are associated with excess muscle symptoms, and from randomised trials, which suggest no such excess, have caused confusion. N-of-1 trials offer the opportunity to establish whether muscle symptoms during statin use are caused by statins in particular individuals.Methods and analysisThis series of 200 randomised, double-blinded N-of-1 trials in primary care will determine (1) the effect of statins on all muscle symptoms and (2) the effect of statins on muscle pain that is perceived to be statin related. Patients who are considering discontinuing statin use due to muscle symptoms and those who have discontinued in the last 3 years due to such symptoms will be recruited. Participants will be randomised to a sequence of six 2-month treatment periods during which they will receive atorvastatin 20 mg per day or matched placebo. On each of the last 7 days of each treatment period, participants will rate their muscle symptoms on a Visual Analogue Scale (VAS).At the end of their trial, participants will be shown numerical and graphical summaries of their own symptom data during statin and placebo periods. The primary analysis on the aggregate data from all participants will be a linear mixed model for VAS muscle symptom score, comparing scores during treatment with statin and placebo.Ethics and disseminationThis trial received a favourable opinion from South Central-Hampshire A Research Ethics Committee. Results will be published in a peer-reviewed medical journal. Dissemination of results to patients will take place via the media, website (statinwise.lshtm.ac.uk) and patient organisations.Trial registration numberISRCTN30952488.

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Herrett, Emily, Elizabeth Williamson, Danielle Beaumont, et al. "Study protocol for statin web-based investigation of side effects (StatinWISE): a series of randomised controlled N-of-1 trials comparing atorvastatin and placebo in UK primary care." BMJ Open 7, no. 12 (2017): e016604. https://doi.org/10.1136/bmjopen-2017-016604.

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IntroductionStatins are effective at preventing cardiovascular disease, widely prescribed and their use is growing. Uncertainty persists about whether they cause symptomatic muscle adverse effects, such as pain and weakness, in the absence of statin myopathy. Discrepancies between data from observational studies, which suggest statins are associated with excess muscle symptoms, and from randomised trials, which suggest no such excess, have caused confusion. N-of-1 trials offer the opportunity to establish whether muscle symptoms during statin use are caused by statins in particular individuals.Methods and analysisThis series of 200 randomised, double-blinded N-of-1 trials in primary care will determine (1) the effect of statins on all muscle symptoms and (2) the effect of statins on muscle pain that is perceived to be statin related. Patients who are considering discontinuing statin use due to muscle symptoms and those who have discontinued in the last 3 years due to such symptoms will be recruited. Participants will be randomised to a sequence of six 2-month treatment periods during which they will receive atorvastatin 20 mg per day or matched placebo. On each of the last 7 days of each treatment period, participants will rate their muscle symptoms on a Visual Analogue Scale (VAS).At the end of their trial, participants will be shown numerical and graphical summaries of their own symptom data during statin and placebo periods. The primary analysis on the aggregate data from all participants will be a linear mixed model for VAS muscle symptom score, comparing scores during treatment with statin and placebo.Ethics and disseminationThis trial received a favourable opinion from South Central-Hampshire A Research Ethics Committee. Results will be published in a peer-reviewed medical journal. Dissemination of results to patients will take place via the media, website (statinwise.lshtm.ac.uk) and patient organisations.Trial registration numberISRCTN30952488.

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Cibičková, Ľubica, and David Karásek. "Statin associated muscle symptoms - literature review and our experience." Interní medicína pro praxi 18, no. 2 (2016): 74–76. http://dx.doi.org/10.36290/int.2016.018.

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Mangone, Laura A., Beth A. Taylor, Robert Schmelzer, et al. "Skeletal muscle mitochondrial capacity in patients with statin-associated muscle symptoms (SAMS)." Open Heart 11, no. 1 (2024): e002551. http://dx.doi.org/10.1136/openhrt-2023-002551.

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ObjectiveThe objective of this article is to evaluate near-infrared spectroscopy (NIRS), a non-invasive technique to assess tissue oxygenation and mitochondrial function, as a diagnostic tool for statin-associated muscle symptoms (SAMS).MethodsWe verified SAMS in 39 statin-treated patients (23 women) using a double-blind, placebo-controlled, cross-over protocol. Subjects with suspected SAMS were randomised to simvastatin 20 mg/day or placebo for 8 weeks, followed by a 4-week no treatment period and then assigned to the alternative treatment, either simvastatin or placebo. Tissue oxygenation was measured before and after each statin or placebo treatment using NIRS during handgrip exercise at increasing intensities of maximal voluntary contraction (MVC).Results44% (n=17) of patients were confirmed as having SAMS (11 women) because they reported discomfort only during simvastatin treatment. There were no significant differences in percent change in tissue oxygenation in placebo versus statin at all % MVCs in all subjects. The percent change in tissue oxygenation also did not differ significantly between confirmed and unconfirmed SAMS subjects on statin (−2.4% vs −2.4%, respectively) or placebo treatment (−1.1% vs −9%, respectively). The percent change in tissue oxygenation was reduced after placebo therapy in unconfirmed SAMS subjects (−10.2%) (p≤0.01) suggesting potential measurement variability.ConclusionsNIRS in the forearm cannot differentiate between confirmed and unconfirmed SAMS, but further research is needed to assess the usability of NIRS as a diagnostic tool for SAMS.Trial registration numberNCT03653663.

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Taylor, Beth A., Gregory Panza, and Paul D. Thompson. "Increased creatine kinase with statin treatment may identify statin-associated muscle symptoms." International Journal of Cardiology 209 (April 2016): 12–13. http://dx.doi.org/10.1016/j.ijcard.2016.02.028.

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Austin, Publishing Group. "Are Chronic Pain Syndromes the Reason for Statin-Associated Muscle Symptoms?" Journal of Family Medicine 9, no. 2 (2022): 1300. https://doi.org/10.26420/jfammed.2022.1300.

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Background: Statin induced myalgia is defined as muscle pain without elevation of serum creatine phosphokinase levels, and is a well-known complaint among statin users. Chronic pain syndromes affect a high percentage of the population; and it may be possible that these pain syndromes confound the reports of statin induced myalgia. We sought to compare the occurrence of chronic pain among patients on statin therapy who developed myalgia with those who did not. Methods: This study included 112 statin-treated patients, followed up at the clinic of the Lipid Center in Sheba Medical Center. Fifty-six of the subjects had a diagnosis of statin associated muscle symptoms (SAMS) and 56 did not. Verified questionnaires were used to assess the diagnoses of fibromyalgia, pain intensity, functional impairment, anxiety and depression in the study population. Results: Patients with statin myalgia were more likely to fulfil the diagnostic criteria for fibromyalgia than patients without statin myalgia (11 (19.6%) vs. zero, respectively). Patients in the SAMS group also exhibited higher levels of anxiety and depression in comparison with the control group. Female sex, higher scores on the Brief Pain Inventory pain intensity scale, and a Hamilton rating scale level indicative of an anxiety disorder were found to be significant predictors for fibromyalgia in patients suffering from statin myalgia. Conclusion: A significant percentage of patients, diagnosed with statin myalgia actually fulfilled the diagnostic criteria for fibromyalgia, depression or anxiety disorder. Detection of these patients and treatment of their primary pain disorder or psychiatric illness has the potential to prevent unnecessary cessation of effective statin therapy. Keywords: Statin; Myalgia; Pain; Adherence; Fibromyalgia; Anxiety; Depression

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Barry, Arden R., Jessica E. Beach, and Glen J. Pearson. "Prevention and management of statin adverse effects: A practical approach for pharmacists." Canadian Pharmacists Journal / Revue des Pharmaciens du Canada 151, no. 3 (2018): 179–88. http://dx.doi.org/10.1177/1715163518768534.

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Statin-associated adverse effects, primarily muscle-related symptoms, occur in up to approximately one-third of patients in clinical practice. Recently, a Canadian Consensus Working Group outlined 6 key principles to assess and manage patients with goal-inhibiting statin intolerance, defined as a syndrome characterized by symptoms or biomarker abnormalities that prevent the long-term use of and adherence to indicated statin therapy, which includes a trial of at least 2 statins and precludes reversible causes of statin adverse effects. These principles ensure patients are appropriately receiving a statin and aware of both the benefits and risks of therapy. As well, they address factors that may increase the risk of statin-associated myopathy. A thorough assessment of patients’ clinical and laboratory history should be performed in any patient presenting with muscle symptoms on statin therapy, followed by a systematic dechallenge/rechallenge approach. In practice, most patients with statin intolerance due to muscle symptoms will be able to tolerate another statin. This is of particular importance because of the relative paucity of compelling evidence demonstrating a cardiovascular benefit with nonstatin therapies. Pharmacists are ideally situated to provide patient education, recommend changes to therapy and monitor patients with goal-inhibiting statin intolerance.

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Pedro-Botet, Juan, and Juan Rubiés-Prat. "Statin-associated muscle symptoms: beware of the nocebo effect." Lancet 389, no. 10088 (2017): 2445–46. http://dx.doi.org/10.1016/s0140-6736(17)31163-7.

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Stoekenbroek, Robert M., and John J. P. Kastelein. "Statin-associated muscle symptoms — really all in the mind?" Nature Reviews Cardiology 14, no. 8 (2017): 445–46. http://dx.doi.org/10.1038/nrcardio.2017.92.

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González, Coral Perez, Chandni Bardolia, Katie Pizzolato, and Nishita Shah Amin. "Utilizing Pharmacogenomics Results to Improve Statin-Associated Muscle Symptoms." Senior Care Pharmacist 39, no. 4 (2024): 151–58. http://dx.doi.org/10.4140/tcp.n.2024.151.

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The objective of this aims to demonstrate the advantage of a pharmacogenomics (PGx)-informed medication review in mitigating adverse drug events (ADEs) and optimizing therapeutic outcomes. PGx testing and PGx-informed medication reviews assist in mitigating ADEs. PGx testing was performed on a 68-year-old male presenting with uncontrolled chronic pain. The PGx results highlighted a drug-gene interaction, aiding in identification of the increased risk of statin-associated muscle symptoms (SAMS) attributing to uncontrolled chronic pain. This patient case report illustrates how incorporating PGx results can help improve chronic pain and mitigate ADEs, such as SAMS.

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Brennan, Emily T., and Tisha R. Joy. "Management Strategies for Statin-Associated Muscle Symptoms: How Useful Is Same-Statin Rechallenge?" Canadian Journal of Cardiology 33, no. 5 (2017): 666–73. http://dx.doi.org/10.1016/j.cjca.2017.02.013.

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Webster, Patrick, Nicholas Wiemer, Abdalhamid Al Harash, Cody Marshall, Nazia Khatoon, and Michael Lucke. "Challenges in Treating Statin-Associated Necrotizing Myopathy." Case Reports in Rheumatology 2021 (February 24, 2021): 1–5. http://dx.doi.org/10.1155/2021/8810754.

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Myalgia and mild elevation in muscle enzymes are common side effects of statin therapy. While these symptoms are generally self-limited, in rare cases, statin use is associated with an immune-mediated necrotizing myopathy caused by development of autoantibodies against HMG-CoA reductase. The primary presenting symptom of this condition is progressive symmetric proximal weakness that does not abate or worsens even after cessation of statin therapy and is associated with markedly elevated creatine kinase (CK) levels. To date, no randomized controlled trials have been conducted to identify the most effective treatment for statin-associated autoimmune myopathy. Treatment recommendations involve a combination of steroids and immunosuppressive drugs. This single-center case series highlights the clinicopathologic features diagnostic for statin-associated autoimmune myopathy as well as treatment challenges for the patient population. The series highlights a range of potential presentations, from mildly symptomatic despite highly elevated CK, to severe muscle weakness including dysphagia. Multiple patients required several immunosuppressant medications as well as intravenous immunoglobulin (IVIG) to achieve disease control. In this case series, marked improvement was noted in several diabetic patients with IVIG.

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Schetz, Daria, Jacek Sein Anand, Karolina Kuźbicka, Marcin Wirtwein, and Ivan Kocić. "COVID-19 Vaccination Protects Skeletal Muscle Against Statin-Related Side Effects." Vaccines 13, no. 4 (2025): 357. https://doi.org/10.3390/vaccines13040357.

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Introduction: COVID-19, caused by SARS-CoV-2, has disrupted global health systems, with vaccines being essential to mitigating its impact. Statins, widely prescribed for dyslipidemia, are associated with muscle-related side effects, which may worsen during COVID-19. This study explores the association between statin use, COVID-19 vaccination, and skeletal muscle-related symptoms. Aims: To evaluate the association between statin use and muscle symptoms (pain and creatine kinase (CK) levels) in COVID-19 patients and investigate whether vaccination is associated with changes in these symptoms. Methods: This observational study included 147 symptomatic COVID-19 patients: 74 chronic statin users (SG) and 73 non-users (CG). Vaccination status (unvaccinated, one-dose, or two-dose Pfizer–BioNTech) was recorded. Muscle pain was assessed using the Numerical Rating Scale (NRS), and CK levels were measured. Additional factors, including age, sex, BMI, and smoking status, were analyzed. Statistical tests examined the potential associations between statin use, vaccination, and muscle-related outcomes. Results: Higher CK levels were more frequently reported in SG, with severe rhabdomyolysis occurring slightly more often in the SG (4% vs. 3%). Men had higher CK values, while women appeared to be at greater risk of severe rhabdomyolysis. Older adults (≥65 years) in the SG had significantly higher CK levels. Fully vaccinated individuals had lower CK values and reported less muscle pain, while unvaccinated participants had the highest incidence of CK abnormalities and severe muscle pain. No significant differences in CK levels were observed between SARS-CoV-2 variants. Conclusions: Statin use was associated with elevated CK levels and increased muscle pain severity. Older adults and women appeared more susceptible to severe muscle complications. Full vaccination was linked to lower CK values and reduced muscle symptoms. Further research is needed to confirm these findings.

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Leonova, M. V. "Effects of nocebo and drusebo in determining statin-induced muscle symptoms." Meditsinskiy sovet = Medical Council, no. 17 (October 16, 2022): 136–42. http://dx.doi.org/10.21518/2079-701x-2022-16-17-136-142.

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Statins represent an important class of cardiovascular drugs for the prevention of atherogenic complications. However, despite the effectiveness of statins, non-adherence and discontinuation of therapy with these drugs is a problem worldwide. Reasons for not using statins in patients at high CV risk include statin-associated muscle symptoms (SAMS), which are not usually associated with significant elevations of serum creatine kinase. SAMS are the most common side effects of statins: 3–5% in RCTs, 15–20% in observational studies, and 60% in patient surveys. This range is possibly due to misinterpretation of symptoms, as well as patients’ expectation of harm from statin treatment (“statin fear”). The article highlights the problem of studying the role of nocebo and drusebo effects for SAMS, presents differences in definitions and methods of detection. The concept of the drucebo effect was proposed by the International Lipid Expert Group (ILEP, 2018) as a harm to the patient, unrelated to the pharmacological action of the drug (negative effect of the drucebo). The results of studies and meta-analyses evaluating the effects of nocebo and drusebo for SAMS are presented, in which no difference was found in the frequency and severity of muscle symptoms between statin and placebo; the nocebo rate was 90% of the statin effect, and the contribution of the drusebo effect to SAMS and statin discontinuation ranged from 38 to 78%. Also presented are current international guidelines and principles of patient management aimed at preventing discontinuation of statin use in connection with SAMS.

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Lowe, Kimberly, Khadija Tul Kubra, Ze Yang He, and Katherine Carey. "Vitamin D Supplementation to Treat Statin-Associated Muscle Symptoms: A Review." Senior Care Pharmacist 34, no. 4 (2019): 253–57. http://dx.doi.org/10.4140/tcp.n.2019.253.

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For the past 15 years, cardiovascular disease (CVD) has been the leading cause of death for both men and women in the United States and worldwide. With an aging population, there has been increasing use of statin therapy to reduce the risk of CVD. However, statin-associated muscle symptoms (SAMS) remain an obstacle to this treatment, leading to discontinuation and nonadherence to statin therapy. Signs and symptoms of SAMS include muscle pain, tenderness, and increased serum creatine kinase. Despite the idiopathic pathophysiology of SAMS, some studies have shown an association between vitamin D deficiency and SAMS; the use of vitamin D supplements can lead to relief of these symptoms. The purpose of this review was to critique evidence for the association between low serum vitamin D and SAMS and the use of vitamin D supplementation for treatment.

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Muntean, Danina M., Paul D. Thompson, Alberico L. Catapano, et al. "Statin-associated myopathy and the quest for biomarkers: can we effectively predict statin-associated muscle symptoms?" Drug Discovery Today 22, no. 1 (2017): 85–96. http://dx.doi.org/10.1016/j.drudis.2016.09.001.

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Thompson, Paul D., and Beth Taylor. "A Novel Mechanism to Explain Statin-Associated Skeletal Muscle Symptoms." JACC: Basic to Translational Science 4, no. 4 (2019): 524–26. http://dx.doi.org/10.1016/j.jacbts.2019.07.001.

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Di Giorgio, Leo, and Michael Fleischmann. "Commentary: Does my patient have statin associated muscle symptoms (SAMS)?" International Journal of Osteopathic Medicine 29 (September 2018): 32–35. http://dx.doi.org/10.1016/j.ijosm.2018.05.001.

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Brinton, Eliot A., Kevin C. Maki, Terry A. Jacobson, Craig A. Sponseller, and Jerome D. Cohen. "Metabolic syndrome is associated with muscle symptoms among statin users." Journal of Clinical Lipidology 10, no. 4 (2016): 1022–29. http://dx.doi.org/10.1016/j.jacl.2016.05.003.

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Peyrel, Paul, Pascale Mauriege, Jérôme Frenette, et al. "IMPACT OF VITAMIN D SUPPLEMENTATION ON STATIN-ASSOCIATED MUSCLE SYMPTOMS." Journal of the American College of Cardiology 81, no. 8 (2023): 1761. http://dx.doi.org/10.1016/s0735-1097(23)02205-2.

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Ballard, Kevin D., Lindsay Lorson, C. Michael White, Paul D. Thompson, and Beth A. Taylor. "Effect of Simvastatin on Arterial Stiffness in Patients with Statin Myalgia." Advances in Preventive Medicine 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/351059.

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Statins reduce arterial stiffness but are also associated with mild muscle complaints. It is unclear whether individuals with muscle symptoms experience the same vascular benefit or whether statins affect striated and smooth muscle cells differently. We examined the effect of simvastatin treatment on arterial stiffness in patients who did versus those who did not exhibit muscle symptoms. Patients with a history of statin-related muscle complaints (n=115) completed an 8 wk randomized, double-blind, cross-over trial of daily simvastatin 20 mg and placebo. Serum lipids and pulse wave velocity (PWV) were assessed before and after each treatment. Muscle symptoms with daily simvastatin treatment were reported by 38 patients (33%). Compared to baseline, central PWV decreased (P=0.01) following simvastatin treatment but not placebo (drug ∗ time interaction:P=0.047). Changes in central PWV with simvastatin treatment were not influenced by myalgia status or time on simvastatin (P≥0.15). Change in central PWV after simvastatin treatment was inversely correlated with age (r=-0.207,P=0.030), suggesting that advancing age is associated with enhanced statin-mediated arterial destiffening. In patients with a history of statin-related muscle complaints, the development of myalgia with short-term simvastatin treatment did not attenuate the improvement in arterial stiffness.

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Stanek, Jakub, Patrycja Sornek, Wiktoria Izdebska, et al. "impact of the nocebo effect on discontinuation of statin therapy due to myopathy in patients with cardiovascular disease – a review." Quality in Sport 31 (November 18, 2024): 55769. http://dx.doi.org/10.12775/qs.2024.31.55769.

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Introduction and purpose of review: Statins are widely used drugs in the prevention of cardiovascular diseases, yet many patients experience side effects of statin use, mainly muscle symptoms, such as myopathy, which often lead to discontinuation of treatment. The aim of this literature review is to assess the role of the nocebo effect in reported muscle symptoms and its impact on statin discontinuation in patients with cardiovascular diseases. Methods: The review analysed the results of several studies, including key publications such as the N-of-1 trial by Wood et al.[1] and the work of Collins et al.[2] on the safety and efficacy of statin therapy. The review covered articles published between 2000 and 2023 that examined the impact of the nocebo effect on statin discontinuation[3-10]. Results: The collected data indicate that the nocebo effect plays a significant role in the reported muscle symptoms during statin use. The study by Wood et al.[1] showed no significant differences in reported symptoms between the groups taking statins, placebo, or receiving no treatment, suggesting that a substantial portion of the symptoms results from the nocebo effect. Similar findings were obtained in the study conducted by the StatinWISE group[4], where patients taking statins and placebo reported a comparable frequency of muscle symptoms. An analysis conducted by Collins et al.[2] indicates that the actual incidence of myopathy associated with statin therapy is much lower than commonly reported. Conclusions: The nocebo effect significantly influences the perceived adverse effects of statins, which may lead to the unjustified discontinuation of these drugs by patients with cardiovascular diseases. Further research is needed to better understand the psychological mechanisms affecting statin tolerance and to develop educational and clinical strategies aimed at minimizing the nocebo effect and improving long-term adherence to therapy.

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Lowe, Kimberly, Khadija Tul Kubra, Ze Yang He, and Katherine Carey. "Vitamin D Supplementation to Treat Statin-Associated Muscle Symptoms: A Review." Senior Care Pharmacist 34, no. 4 (2019): 253–57. http://dx.doi.org/10.4140/tcp.n.2019.253.

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Isackson, Paul J., Jianxin Wang, Mohammad Zia, et al. "RYR1 and CACNA1S genetic variants identified with statin-associated muscle symptoms." Pharmacogenomics 19, no. 16 (2018): 1235–49. http://dx.doi.org/10.2217/pgs-2018-0106.

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Laufs, Ulrich, Krysztof J. Filipiak, Ioanna Gouni-Berthold, Alberico L. Catapano, Giuseppe Mandraffino, and Pascale Benlian. "Practical aspects in the management of statin-associated muscle symptoms (SAMS)." Atherosclerosis Supplements 26 (April 2017): 45–55. http://dx.doi.org/10.1016/s1567-5688(17)30024-7.

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Khan, Abdullah, Kevin C. Maki, Matthew K. Ito, et al. "Statin Associated Muscle Symptoms: Characteristics of Patients and Recommendations by Providers*." Journal of Clinical Lipidology 9, no. 3 (2015): 460. http://dx.doi.org/10.1016/j.jacl.2015.03.080.

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Gazzotti, M., M. Casula, E. Olmastroni, F. Bonaiti, L. Grigore, and A. L. Catapano. "Prevalence Of Statin-Associated Muscle Symptoms In Italy: The Prosisa Study." Atherosclerosis 287 (August 2019): e88. http://dx.doi.org/10.1016/j.atherosclerosis.2019.06.257.

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Glueck, Charles J., Kevin Lee, Marloe Prince, Alexander Milgrom, Frini Makadia, and Ping Wang. "Low serum vitamin D, statin associated muscle symptoms, vitamin D supplementation." Atherosclerosis 256 (January 2017): 125–27. http://dx.doi.org/10.1016/j.atherosclerosis.2016.11.027.

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Laboy, Shannon M., and Michael T. PULLEY. "Statin‐associated muscle symptoms: Does the benefit outweigh the risk factor?" Muscle & Nerve 59, no. 5 (2019): 525–27. http://dx.doi.org/10.1002/mus.26470.

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Sahebkar, Amirhossein, Nikou Saboni, Matteo Pirro, and Maciej Banach. "Curcumin: An effective adjunct in patients with statin-associated muscle symptoms?" Journal of Cachexia, Sarcopenia and Muscle 8, no. 1 (2016): 19–24. http://dx.doi.org/10.1002/jcsm.12140.

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Garrett, Timothy J., Michelle A. Puchowicz, Edwards A. Park, et al. "Effect of statin treatment on metabolites, lipids and prostanoids in patients with Statin Associated Muscle Symptoms (SAMS)." PLOS ONE 18, no. 12 (2023): e0294498. http://dx.doi.org/10.1371/journal.pone.0294498.

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Background Between 5–10% of patients discontinue statin therapy due to statin-associated adverse reactions, primarily statin associated muscle symptoms (SAMS). The absence of a clear clinical phenotype or of biomarkers poses a challenge for diagnosis and management of SAMS. Similarly, our incomplete understanding of the pathogenesis of SAMS hinders the identification of treatments for SAMS. Metabolomics, the profiling of metabolites in biofluids, cells and tissues is an important tool for biomarker discovery and provides important insight into the origins of symptomatology. In order to better understand the pathophysiology of this common disorder and to identify biomarkers, we undertook comprehensive metabolomic and lipidomic profiling of plasma samples from patients with SAMS who were undergoing statin rechallenge as part of their clinical care. Methods and findings We report our findings in 67 patients, 28 with SAMS (cases) and 39 statin-tolerant controls. SAMS patients were studied during statin rechallenge and statin tolerant controls were studied while on statin. Plasma samples were analyzed using untargeted LC-MS metabolomics and lipidomics to detect differences between cases and controls. Differences in lipid species in plasma were observed between cases and controls. These included higher levels of linoleic acid containing phospholipids and lower ether lipids and sphingolipids. Reduced levels of acylcarnitines and altered amino acid profile (tryptophan, tyrosine, proline, arginine, and taurine) were observed in cases relative to controls. Pathway analysis identified significant increase of urea cycle metabolites and arginine and proline metabolites among cases along with downregulation of pathways mediating oxidation of branched chain fatty acids, carnitine synthesis, and transfer of acetyl groups into mitochondria. Conclusions The plasma metabolome of patients with SAMS exhibited reduced content of long chain fatty acids and increased levels of linoleic acid (18:2) in phospholipids, altered energy production pathways (β-oxidation, citric acid cycle and urea cycles) as well as reduced levels of carnitine, an essential mediator of mitochondrial energy production. Our findings support the hypothesis that alterations in pro-inflammatory lipids (arachidonic acid pathway) and impaired mitochondrial energy metabolism underlie the muscle symptoms of patients with statin associated muscle symptoms (SAMS).

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Fedacko, Jan, Daniel Pella, Petra Fedackova, et al. "Coenzyme Q10and selenium in statin-associated myopathy treatment." Canadian Journal of Physiology and Pharmacology 91, no. 2 (2013): 165–70. http://dx.doi.org/10.1139/cjpp-2012-0118.

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The objective of this study was to evaluate the possible benefits of coenzyme Q10and selenium supplementation administered to patients with statin-associated myopathy (SAM). Sixty eligible patients entered the pilot study. Laboratory examination (CoQ10, selenium, creatin kinase) and intensity of SAM (visual scale) were performed at baseline, after 1 month, and at the end of study at month 3. Plasma levels of CoQ10 increased from 0.81 ± 0.39 to 3.31 ± 1.72 μmol/L in the active group of patients treated by CoQ10, compared with the placebo (p = 0.001). Also, the symptoms of SAM significantly improved in the active group (p < 0.001): the intensity of muscle pain decreased from 6.7 ± 1.72 to 3.2 ± 2.1 (p < 0.01, –53.4 ± 28.2%); muscle weakness decreased from 7.0 ± 1.63 to 2.8 ± 2.34 (p < 0.01, –60 ± 24.0%); muscle cramps decreased from 5.33 ± 2.06 to 1.86 ± 2.42, p < 0.01, –65 ± 28%); tiredness decreased from the initial 6.7 ± 1.34 to 1.2 ± 1.32 (p < 0.01, –82 ± 22%). We did not observe any significant changes in the placebo group. In conclusion, supplementation of statin-treated patients with CoQ10 resulted in a decrease in the symptoms of SAM, both in absolute numbers and intensity. Additional selenium supplementation was not associated with any statistically significant decrease of SAM. However, it is not possible to draw any definite conclusions, even though this study was carried out in double-blind fashion, because it involved a small number of patients.

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Saeed, M. K., J. Shah, R. Damani, F. Rahman, P. Patel, and P. Gupta. "Risk Factors Associated with Statin-Associated Muscle Symptoms in Patients Attending a Specialized Regional Lipid Clinic." Journal of Lipids 2021 (March 19, 2021): 1–5. http://dx.doi.org/10.1155/2021/8882706.

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Background. Statin-associated muscle symptoms (SAMS) are the major side effects reported for statins. Data from previous studies suggest that 7–29% of patients on statin had associated muscle symptoms. In the UK, there is a lack of corresponding data on SAMS and factors associated with the development of SAMS. Objective. This analysis is aimed at establishing the prevalence of SAMS and identifying major contributory risk factors in patients attending a lipid clinic. Methods. Clinical records of 535 consecutive patients, who visited the lipid clinic in the University Hospitals of Leicester, were studied retrospectively between 2009 and 2012. SAMS were defined by the presence of muscle symptoms with two or more different statins. Patients who reported muscle symptoms to statin with one or no rechallenge were excluded. The association of SAMS with clinical characteristics such as age and BMI, sex, smoking, excess alcohol, comorbidities, and medications was tested for statistical significance. A binomial logistic regression model was applied to adjust for risk factors significantly associated with SAMS. Results. The prevalence of SAMS was found to be 11%. On unadjusted analysis, the mean age of patients who had SAMS was significantly higher than those without SAMS ( 59.4 ± 10.5 years vs. 50.3 ± 13.4 years, respectively, P < 0.001 ). Nonsmokers were more likely to develop SAMS in comparison to active smokers ( P = 0.037 ). Patients taking antihypertensive medications were more likely to develop SAMS ( P = 0.010 ). In binomial logistic regression analysis, only age was positively and significantly associated with SAMS after adjusting for other risk factors ( β = 0.054 , P = 0.001 ). Conclusion. To the best of our knowledge, this study is the largest cohort of patients with SAMS in the United Kingdom. Our data suggest that the prevalence of SAMS is 11% and increased age is a risk factor associated with the development of SAMS in our cohort of patients.

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Taylor, Beth A., Robert J. Sanchez, Terry A. Jacobson, et al. "Application of the Statin-Associated Muscle Symptoms-Clinical Index to a Randomized Trial on Statin Myopathy." Journal of the American College of Cardiology 70, no. 13 (2017): 1680–81. http://dx.doi.org/10.1016/j.jacc.2017.07.767.

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Ruscica, Massimiliano, Alessandra Bertoletti, Cecilia Gobbi, Cesare R. Sirtori, Stefano Carugo, and Alberto Corsini. "Lipid-lowering approaches to manage statin-intolerant patients." European Heart Journal Supplements 26, Supplement_1 (2024): i56—i59. http://dx.doi.org/10.1093/eurheartjsupp/suae007.

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Abstract Statins have improved the potential to prevent cardiovascular disease events and to prolong the lives of patients. Statins, among the most widely used drugs worldwide, reduce the levels of low-density lipoprotein cholesterol (LDL-C) by an average of 30–50%. However, non-adherence to statin therapy, due to statin intolerance, might be as high as 60% after 24 months of treatment and is associated with a 70% increase in the risk of cardiovascular disease events. Statin intolerance can be classified as a complete inability to tolerate any dose of a statin or a partial intolerance with the inability to tolerate the dose necessary to achieve the patient-specific therapeutic objective. Reasons for discontinuation are many, with statin-associated muscle symptoms being cited as the most frequent reason for stopping therapy and the incidence of muscle symptoms increasing with treatment intensity. Considering the causal effect of LDL-C in the atherosclerotic process, clinicians should consider that regardless of the lipid-lowering drugs patients are willing to take, any reduction in LDL-C they achieve will afford them some benefit in reducing cardiovascular risk. Besides statins, the current therapeutic armamentarium offers different strategies to reach LDL-C targets in statin-intolerant patients (i.e. a fixed combination between a lower dose of statin plus ezetimibe, bempedoic acid, or proprotein convertase subtilisin/kexin type 9 inhibition).

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Bosco, Giosiana, Francesco Di Giacomo Barbagallo, Salvatore Spampinato, et al. "Management of Statin Intolerant Patients in the Era of Novel Lipid Lowering Therapies: A Critical Approach in Clinical Practice." Journal of Clinical Medicine 12, no. 6 (2023): 2444. http://dx.doi.org/10.3390/jcm12062444.

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Statins are the cornerstone of lipid-lowering therapies effective for cardiovascular risk reduction. Although they are generally well tolerated, statin intolerance (SI) is frequent in clinical practice, and it is usually related to the onset of muscle symptoms, which are defined under the acronym SAMS (Statin-Associated Muscle Side Effects). These side effects are responsible for statin treatment discontinuation that results in increased cardiovascular risk. The National Lipid Association (NLA) has recently provided an updated definition of statin intolerance, and a distinction between complete and partial statin intolerance has been reported. The evaluation of symptom severity and the presence of muscle damage biomarker alterations make it essential to adopt a patient-centered approach aimed at obtaining a personalized therapeutic strategy. Firstly, it could be useful to administer a different statin, reduce the dosage or adopt an alternate dosage regimen. However, some patients are unable to tolerate any statin at every dosage, or despite taking statins at the maximum tolerated dose, they fail to achieve the recommended LDL-C target, and thus it is necessary to introduce a non-statin hypolipidemic treatment. Ezetimibe, proprotein-convertase subtilisin/kexin type 9 (PCSK9) inhibitors such as monoclonal antibodies (alirocumab and evolocumab) or RNA messenger silencing (inclisiran), bempedoic acid or nutraceuticals are non-statin lipid-lowering therapies that could be used as an alternative or in addition to statins to achieve an early and sustained LDL-C reduction in clinical practice. In this review, we evaluated SI management focusing on non-statin lipid lowering therapies and their implications in lipid lowering approaches in clinical practice.

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Vinci, Pierandrea, Emiliano Panizon, Letizia Maria Tosoni, et al. "Statin-Associated Myopathy: Emphasis on Mechanisms and Targeted Therapy." International Journal of Molecular Sciences 22, no. 21 (2021): 11687. http://dx.doi.org/10.3390/ijms222111687.

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Hyperlipidemia is a major risk factor for cardiovascular morbidity and mortality. Statins are the first-choice therapy for dyslipidemias and are considered the cornerstone of atherosclerotic cardiovascular disease (ASCVD) in both primary and secondary prevention. Despite the statin-therapy-mediated positive effects on cardiovascular events, patient compliance is often poor. Statin-associated muscle symptoms (SAMS) are the most common side effect associated with treatment discontinuation. SAMS, which range from mild-to-moderate muscle pain, weakness, or fatigue to potentially life-threatening rhabdomyolysis, are reported by 10% to 25% of patients receiving statin therapy. There are many risk factors associated with patient features and hypolipidemic agents that seem to increase the risk of developing SAMS. Due to the lack of a “gold standard”, the diagnostic test for SAMS is based on a clinical criteria score, which is independent of creatine kinase (CK) elevation. Mechanisms that underlie the pathogenesis of SAMS remain almost unclear, though a high number of risk factors may increase the probability of myotoxicity induced by statin therapy. Some of these, related to pharmacokinetic properties of statins and to concomitant therapies or patient characteristics, may affect statin bioavailability and increase vulnerability to high-dose statins.

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Munkhaugen, John, Nils Tore Vethe, Morten Wang Fagerland, et al. "Statin-associated muscle symptoms in coronary patients: design of a randomized study." Scandinavian Cardiovascular Journal 53, no. 3 (2019): 162–68. http://dx.doi.org/10.1080/14017431.2019.1612085.

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Journal articles on the topic 'Statin-associated muscle symptoms'

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