Statin-related adverse events: A meta-analysis

Silva, Matthew A.; Swanson, Anna C.; Gandhi, Pritesh J.; Tataronis, Gary

doi:10.1016/j.clinthera.2006.01.005

Cited by 228 publications

(142 citation statements)

References 24 publications

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“…In contrast, a meta-analysis 61 of 18 placebocontrolled trials involving 71,108 patients (trial duration 6-317 weeks) found that statins (mostly moderate-dose statins) have a 39% higher rate of any adverse effect [odds ratio (OR) 1.4; 95% CI 1.09 to 1.80; p = 0.008; number needed to harm 197) than placebo. However, serious adverse events (creatine phosphokinase greater than 10 times the upper normal limit) were infrequent and rhabdomyolysis was rare.…”

Section: Moderate-dose Statinsmentioning

confidence: 99%

Early high-dose lipid-lowering therapy to avoid cardiac events: a systematic review and economic evaluation

Ara

Pandor²,

Stevens³

et al. 2009

Health Technol Assess

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How to obtain copies of this and other HTA programme reports An electronic version of this publication, in Adobe Acrobat format, is available for downloading free of charge for personal use from the HTA website (www.hta.ac.uk). A fully searchable CD-ROM is also available (see below).Printed copies of HTA monographs cost £20 each (post and packing free in the UK) to both public and private sector purchasers from our Despatch Agents.Non-UK purchasers will have to pay a small fee for post and packing. For European countries the cost is £2 per monograph and for the rest of the world £3 per monograph.You can order HTA monographs from our Despatch Agents:-fax (with credit card or official purchase order) -post (with credit card or official purchase order or cheque) -phone during office hours (credit card only).Additionally the HTA website allows you either to pay securely by credit card or to print out your order and then post or fax it. Contact details are as follows: Payment methods Paying by chequeIf you pay by cheque, the cheque must be in pounds sterling, made payable to Direct Mail Works Ltd and drawn on a bank with a UK address. Paying by credit cardThe following cards are accepted by phone, fax, post or via the website ordering pages: Delta, Eurocard, Mastercard, Solo, Switch and Visa. We advise against sending credit card details in a plain email.Paying by official purchase order You can post or fax these, but they must be from public bodies (i.e. NHS or universities) within the UK. We cannot at present accept purchase orders from commercial companies or from outside the UK. How do I get a copy of HTA on CD?Please use the form on the HTA website (www.hta.ac.uk/htacd.htm). Or contact Direct Mail Works (see contact details above) by email, post, fax or phone. HTA on CD is currently free of charge worldwide.The website also provides information about the HTA programme and lists the membership of the various committees. HTA NIHR Health Technology Assessment programmeT he Health Technology Assessment (HTA) programme, part of the National Institute for Health Research (NIHR), was set up in 1993. It produces high-quality research information on the effectiveness, costs and broader impact of health technologies for those who use, manage and provide care in the NHS. 'Health technologies' are broadly defined as all interventions used to promote health, prevent and treat disease, and improve rehabilitation and long-term care. The research findings from the HTA programme directly influence decision-making bodies such as the National Institute for Health and Clinical Excellence (NICE) and the National Screening Committee (NSC). HTA findings also help to improve the quality of clinical practice in the NHS indirectly in that they form a key component of the 'National Knowledge Service'. The HTA programme is needs led in that it fills gaps in the evidence needed by the NHS. There are three routes to the start of projects. First is the commissioned route. Suggestions for research are actively sought from people working in t...

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Section: Moderate-dose Statinsmentioning

confidence: 99%

Early high-dose lipid-lowering therapy to avoid cardiac events: a systematic review and economic evaluation

Ara

Pandor²,

Stevens³

et al. 2009

Health Technol Assess

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“…Because cardioprotection by statins was also observed in patients with normal cholesterol levels, it has been proposed that statins may exert a broad spectrum of cholesterol-independent protective effects including plaque stabilization, preservation of endothelial function, and scavenging of free radicals, as well as antiproliferative, anti-ischemic, antiinflammatory, and antiapoptotic effects (Kaneider et al, 2001;Laufs et al, 1998;Lefer et al, 1999;Leung et al, 1993;Weber et al, 1997). On the other hand, it is well known that chronic treatment with statins may exhibit a number of extrahepatic adverse effects, such as myopathy and rhabdomyolysis (Thompson et al, 2003;Jamal et al, 2004;Silva et al, 2006); however, the mechanisms of these side effects are not entirely clear. Di Napoli et al (2001) showed that acute application of 25 M simvastatin protects the ischemic/reperfused heart against contractile dysfunction, release of creatine kinase, and postischemic hyperpermeability.…”

Section: Interaction Of Hyperlipidemia and Antihyperlipidemic Statinsmentioning

confidence: 99%

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

Ferdinándy¹,

Schulz²,

Baxter³

2007

Pharmacol Rev

648

615

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“…Di Napoli et al (4) showed that acute application of simvastatin protects the ischemic-reperfused heart, possibly via increased expression of endothelial nitric oxide synthase in rat hearts. On the other hand, it is well known that chronic treatment with statins may exhibit a number of extrahepatic adverse effects, such as myopathy and rhabdomyolysis (20); however, the mechanisms of these side effects are not entirely clear.…”

mentioning

confidence: 99%

Lovastatin interferes with the infarct size-limiting effect of ischemic preconditioning and postconditioning in rat hearts

Kocsis

Pipis

Fekete

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Kocsis GF, Pipis J, Fekete V, Kovács-Simon A, Odendaal L, Molnár É , Giricz Z, Janáky T, van Rooyen J, Csont T, Ferdinandy P. Lovastatin interferes with the infarct size-limiting effect of ischemic preconditioning and postconditioning in rat hearts. Am J Physiol Heart Circ Physiol 294: H2406-H2409, 2008. First published March 21, 2008 doi:10.1152/ajpheart.00862.2007.-Statins have been shown to be cardioprotective; however, their interaction with endogenous cardioprotection by ischemic preconditioning and postconditioning is not known. In the present study, we examined if acute and chronic administration of the 3-hydroxy-3-methylglutaryl CoA reductase inhibitor lovastatin affected the infarct size-limiting effect of ischemic preconditioning and postconditioning in rat hearts. Wistar rats were randomly assigned to the following three groups: 1) vehicle (1% methylcellulose per os for 12 days), 2) chronic lovastatin (15 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 per os for 12 days), and 3) acute lovastatin (1% methylcellulose per os for 12 days and 50 mol/l lovastatin in the perfusate). Hearts isolated from the three groups were either subjected to a nonconditioning (aerobic perfusion followed by 30-min coronary occlusion and 120-min reperfusion, i.e., test ischemia-reperfusion), preconditioning (three intermittent periods of 5-min ischemia-reperfusion cycles before test ischemia-reperfusion), or postconditioning (six cycles of 10-s ischemia-reperfusion after test ischemia) perfusion protocol. Preconditioning and postconditioning significantly decreased infarct size in vehicle-treated hearts. However, preconditioning failed to decrease infarct size in acute lovastatin-treated hearts, but the effect of postconditioning remained unchanged. Chronic lovastatin treatment abolished postconditioning but not preconditioning; however, it decreased infarct size in the nonconditioned group. Myocardial levels of coenzyme Q9 were decreased in both acute and chronic lovastatin-treated rats. Western blot analysis revealed that both acute and chronic lovastatin treatment attenuated the phoshorylation of Akt; however, acute but not chronic lovastatin treatment increased the phosphorylation of p42 MAPK/ERK. We conclude that, although lovastatin may lead to cardioprotection, it interferes with the mechanisms of cardiac adaptation to ischemic stress. coronary occlusion; coenzyme Q9; Akt; p42 mitogen-activated protein kinase/extracellular signal-regulated kinase; statin STATINS, 3-hydroxy-3-methylglutaryl (HMG) CoA reductase inhibitors, inhibit the synthesis of mevalonate, a rate-limiting step in cholesterol biosynthesis. A number of large clinical trials have shown that chronic administration of statins have potent cholesterol-lowering effects and reduce cardiovascular morbidity and mortality (16,17). Since cardioprotection by statins was also observed in patients with normal cholesterol levels, it was proposed that statins may exert a broad spectrum of cholesterol-independent protective effects (13, 14, 19). Di Napoli et al. (4) showed that acute applicati...

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Statin-related adverse events: A meta-analysis

Cited by 228 publications

References 24 publications

Early high-dose lipid-lowering therapy to avoid cardiac events: a systematic review and economic evaluation

Early high-dose lipid-lowering therapy to avoid cardiac events: a systematic review and economic evaluation

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

Lovastatin interferes with the infarct size-limiting effect of ischemic preconditioning and postconditioning in rat hearts

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