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PubMed2005

Statins and the response to myocardial injury.

The benefits of long-term statin (HMG-CoA reductase inhibitor) treatment for preventing coronary events have been well documented in several large-scale prospective clinical trials. By influencing the determinants of myocardial injury, statins may produce direct cardioprotective effects in the ischemic myocardium and prevent further damaging recurrent events. Although not proven fully in a clinical setting, cholesterol-independent or 'pleiotropic' effects of statins are thought to protect against myocardial injury and may occur via a number of mechanisms. Endothelial dysfunction occurs early in the development of atherosclerosis and is associated with a reduction in endothelial nitric oxide (NO) production. Statins have been shown to increase the expression of endothelial NO synthase, with subsequent augmentation of NO in the vasculature. Statins have also been reported to have anti-inflammatory effects, reducing the release of cytokines and chemokines, decreasing the expression of pro-inflammatory cell adhesion molecules, and reducing the accumulation of neutrophils in myocardial tissue following ischemia and reperfusion. Indeed, the role of statins in reducing infarct size is supported by data from a number of preclinical studies. Statin treatment, administered at the onset of reperfusion, has been shown to reduce infarct size by approximately 50% following ischemia in various animal models, and this may be an NO-dependent effect. Randomized clinical trials have indicated that early initiation of statin treatment is associated with a reduction in both the rate of recurrence of cardiovascular events and death in patients with acute coronary syndrome. In addition, decreased rates of myocardial infarction and mortality were demonstrated in several retrospective studies where statin treatment was administered before an interventional procedure. There is a need for further clinical trials to fully elucidate the importance of pre-procedural statin therapy and to determine the extent and mechanisms by which statins exert their cardioprotective effects.

Animals↗
PubMed2004

Non-lipid effects of statins: emerging new indications.

Statins are beneficial both in the primary and secondary prevention of atherosclerotic vascular disease and acute events in a broad spectrum of patient subgroups. However, the observed clinical benefit with statin therapy is much greater than expected through the reduction of cholesterol levels alone. Clinical and experimental studies suggested that several antiatherosclerotic effects other than lipid lowering also contribute to the observed benefit of statin therapy. These 'pleiotropic effects' include improvement of endothelial function, antitrombotic actions, plaque stabilization, reduction of the vascular inflammatory process and anti-oxidation. Statins may also exhibit a wide variety of actions other than antiatherosclerotic effects. Recent observational data documented a potential association between statin use and improvement of fracture risk in osteoporosis. Despite the lack of randomized trials, epidemiological and limited clinical data suggested that statins might retard the pathogenesis of Alzheimer's disease. Observational data indicated that the progression of aortic stenosis and valvular calcification might be delayed in statin users. In addition, the deterioration of congestive heart failure may be delayed with statins via anti-inflammatory, vascular endothelial and antiatherosclerotic actions. Furthermore, preliminary clinical studies suggested that, by their immunosuppressive actions statins might reduce the incidence of rejection following organ transplantation. Currently, there is not enough evidence to prescribe therapy for such patients. However, ongoing studies are exploring the role of statin therapy for these new indications. This review will discuss several non-lipid effects of statin therapy currently under investigation.

Animals↗
PubMedDate not supplied

Statin use is associated with reduced all-cause mortality after endovascular abdominal aortic aneurysm repair.

It has been shown that preoperative statin therapy reduces all-cause and cardiovascular mortality in patients undergoing major noncardiac vascular surgery. In this report, we investigated the influence of statin use on early and late outcome following endovascular abdominal aortic aneurysm repair (EVAR). The study population, consisting of patients collated in the EUROSTAR registry, was stratified in two groups according to statin use. Baseline characteristics between the two groups were compared by chi-square and Wilcoxon rank sum tests for discrete and continuous variables. The effects of statin use on outcomes after EVAR were analyzed by multivariate regression models. Of the 5,892 patients enrolled in the EUROSTAR registry, 731 (12.4%) patients used statins for hyperlipidemia. Statin users were younger, were more obese, and had a higher prevalence of diabetes, cardiovascular disease, and hypertension. After 5 years of follow-up, the cumulative survival rate was 77% for nonusers of statin versus 81% for statin users (p = .005). After adjustment for age and other risk factors, statin use was still an independent predictor of improved survival (p = .03). Our results revealed that statin prescription was more frequent in younger patients. However, when adjusted for age and medical risk factors, the use of statin in patients who underwent EVAR was still independently associated with reduced overall mortality.

Age Factors↗
PubMed2006

Protective role of chronic statin therapy in reducing myocardial damage during percutaneous coronary intervention.

OBJECTIVE: Percutaneous coronary intervention (PCI) is frequently associated with troponin I (TnI) elevation. Experimental studies suggest that statins may reduce ischaemia-reperfusion myocardial injury. The study objective was to verify whether chronic treatment with statins might reduce the occurrence and the extent of periprocedural myocardial damage in patients undergoing PCI. METHODS: Five hundred and fifty-two consecutive patients undergoing PCI were included: 279 were not on statins before PCI, 273 were on statins. TnI levels >or= 0.3 ng/ml were considered indicative of myocardial injury. RESULTS: Statin-treated patients had a higher prevalence of hyperlipidaemia, previous myocardial infarction, and revascularization procedures. Coronary angiography also documented a higher prevalence of multivessel disease. No difference between the two groups was observed regarding the PCI-treated vessel, type of lesions, use of stents and of anti-IIb/IIIa inhibitors. Patients on statins showed the lowest incidence of TnI >or= 0.3 ng/ml (29 vs. 48%, P = 0.00001) and of creatine kinase-MB elevation (7 vs. 12%, P = 0.04). The mean peak TnI levels were significantly lower in patients on statins (1.07 +/- 3.8 vs. 2.73 +/- 12.3, P = 0.00006). Multivariate analysis identified preprocedural statin therapy as the only independent negative predictor of postprocedural abnormal TnI levels (odds ratio = 0.52; 95% confidence intervals 0.34-0.79; P = 0.003). CONCLUSIONS: This study shows that chronic therapy with statins reduces the incidence of periprocedural myocardial damage after PCI. The beneficial effect of statins was independent of either the most important clinical and angiographic characteristics or the use of other cardiovascular drugs including beta-blockers. These data support the specific cardioprotective role of statins.

Angina Pectoris↗
PubMedDate not supplied

[Adverse effects of statins].

The safety of the hydroxymethyl glutaryl-coenzyme A reductase inhibitors (statins) has been called into question following the recent withdrawal from the market of one of the class, cerivastatin. The withdrawal of cerivastatin highlighted concerns regarding the safety of the entire class. According to data from several large clinical trials, the statins (except cerivastatin) are well tolerated. The most important and clinically relevant adverse effect reported with statins is myopathy. Myopathy is a clinical diagnosis of elevated creatine phosphokinase and/or myalgia along with fatigue. However, the severe from (i.e. statin-associated rhabdomyolysis) is an uncommon syndrome and occurs at a rate of approximately 1/100,000 patients/years. Statin-associated myopathy is related to statin doses, and often to drug/drug interactions. Other clinically relevant adverse effects associated with statin therapy include liver transminases elevation, which is relatively mild and often self-limiting There is no evidence from clinical trials of a significant alteration of ophthalmological function with statins. The issue of statin-induced cancer remains inconclusive. Overall, the statins seem to exhibit a favourable risk/benefit ratio, and this undoubtedly justifies life-long clinical use of statins for cardiovascular prevention.

Anticholesteremic Agents↗
PubMed2003

Statins differ in their ability to block NF-kappaB activation in human blood monocytes.

OBJECTIVE: The benefits of statin therapy in cardiovascular medicine are ascribed to its lipid-lowering effect as well as its anti-inflammatory properties. Whereas all statins have been shown to reduce cholesterol plasma levels, their effect on inflammatory markers has been inconsistent. Here, we show that statins differ markedly in their effectiveness in preventing activation of NF-kappaB, a transcription factor involved in the activation of immediately early genes during inflammation. METHODS: Six statins (atorvastatin (Atv), cerivastatin (Cer), fluvastatin (Flu), lovastatin (Lov), pravastatin (Pra), simvastatin (Sim)) were tested for their ability to influence the induction of NF-kappaB in human monocytes (Mo) during inflammation. Mo isolated from healthy blood donors were incubated with LPS (10 microg/ml) in the presence and absence of statin (0.001-5 microM). NF-kappaB binding activity (EMSA), degradation and phosphorylation of the inhibitor protein IkappaB-alpha (Western blotting), tissue factor (TF) mRNA (rtPCR), and TF activity (clotting assay) were analyzed. RESULTS: All statins inhibited LPS-induced NF-kappaB binding activity in Mo in a dose-dependent manner. The inhibitory effect was due to reduced phosphorylation and degradation of the NF-kappaB inhibitor protein IkappaB, and was primarily dependent on the absence of mevalonate. Whilst this effect appeared with all statins, there were marked differences in the degree of inhibition between the statins. Cer (45 +/- 9% inhibition, p < 0.05) was 9-fold more effective in reducing NF-kappaB activation than Flu (5 +/- 10% inhibition). The differences in the potency of statins (Cer > Atv > Sim > Pra > Lov > Flu) were also reflected at the transcriptional level and the protein level of NF-kappaB controlled tissue factor expression. CONCLUSIONS: The finding that statins differ in their potency in interfering with the activation of NF-kappaB signaling in human monocytes further supports the hypothesis that some statins inhibit the inflammatory response more than others.

Cells, Cultured↗
PubMed2003

Statin use, clinical fracture, and bone density in postmenopausal women: results from the Women's Health Initiative Observational Study.

BACKGROUND: 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been shown to stimulate bone formation in laboratory studies, both in vitro and in vivo. While early epidemiologic studies showed lower risk for hip fracture among statin users than nonusers, subsequent studies have produced mixed results. OBJECTIVE: To examine the association of statin use with incidence of hip, lower arm or wrist, and other clinical fractures and with baseline levels of bone density. DESIGN: Prospective study. SETTING: Women's Health Initiative Observational Study conducted in 40 clinical centers in the United States. PARTICIPANTS: 93 716 postmenopausal women ages 50 to 79 years. MEASUREMENTS: Rates of hip, lower arm or wrist, and other clinical fractures were compared among 7846 statin users and 85 870 nonusers over a median follow-up of 3.9 years. In 6442 women enrolled at three clinical centers, baseline levels of total hip, posterior-anterior spine, and total-body bone density measured by using dual-energy x-ray absorptiometry were compared according to statin use. RESULTS: Age-adjusted rates of hip, lower arm or wrist, and other clinical fractures were similar between statin users and nonusers regardless of duration of statin use. The multivariate-adjusted hazard ratios for current statin use were 1.22 (95% CI, 0.83 to 1.81) for hip fracture, 1.04 (CI, 0.85 to 1.27) for lower arm or wrist fracture, and 1.11 (CI, 1.00 to 1.22) for other clinical fracture. Bone density levels did not statistically differ between statin users and nonusers at any skeletal site after adjustment for age, ethnicity, body mass index, and other factors. CONCLUSION: Statin use did not improve fracture risk or bone density in the Women's Health Initiative Observational Study. The cumulative evidence does not warrant use of statins to prevent or treat osteoporosis.

Aged↗
PubMed2001

The use over time of statins in coronary patients in an Italian tertiary referral center.

BACKGROUND: In the last decade, large-scale clinical trials have consistently shown that therapy with statins is of great benefit to patients with and at risk of developing coronary artery disease. We assessed, in a sample of patients with coronary artery disease in whom coronary angiography was indicated and hospitalized in the last 10 years, the use of statins at admission. METHODS: One hundred patients with stable coronary artery disease were randomly selected per year from 1991 to 2000. The final study population consisted of 1000 patients. The prescription of statins for > or = 6 months before hospital admission was determined from a hospital-wide clinical database. RESULTS: From 1995, the prevalence of patients treated with statins at hospital admission progressively increased. In 1991, only 2% of patients were treated with statins before hospital admission while in the year 2000, 38% of patients were receiving this treatment. The mean prevalence of patients treated with statins before and after 1995 was 3 vs 22% (p < 0.0001) respectively. The distribution of the demographic and clinical parameters and the prevalence of conventional cardiovascular risk factors were similar in patients treated or not treated with statins. CONCLUSIONS: After 1994, in coincidence with the publication of the results of clinical trials showing the benefit of statins in patients with coronary artery disease, the use of these drugs increased significantly. This finding suggests that the widespread diffusion of the results of the major clinical trials and of guidelines drawn up by medical associations have had a significant impact on statin prescription in patients with coronary artery disease. Nevertheless our data also indicate that, despite overwhelming evidence on the benefits of statin therapy, in current clinical practice cardiologists are not optimally utilizing lipid management and that statins are frequently prescribed without an appropriate analysis of risk factors.

Aged↗
PubMed2003

Statin therapy in the heart and estrogen/progestin replacement study.

AIM: Limited data exists to guide secondary prevention in postmenopausal women with coronary heart disease (CHD). Treatment with HMG-CoA reductase inhibitors (statins) is likely to be beneficial for these patients. Yet, clinical trial results are conflicting. Moreover, significant interactions may exist between statins and hormone replacement therapy (HRT) that may complicate this approach. METHODS: In a post hoc analysis of the HERS trial, patients who were taking a statin were compared to those who were not. Subjects were randomized to HRT or placebo. Statin therapy was not controlled by the trial investigators, but may have been prescribed by the patients' primary physicians. Use of statins was monitored throughout the trial. The primary outcome was the composite of myocardial infarction and death resulting from CHD, with all-cause mortality and venous thromboembolism (VTE) as secondary outcome measures. RESULTS: At baseline, 1004 subjects were taking a statin, with 1234 subjects randomized to receive HRT, and 1237 to receive placebo. Baseline statin use was associated with lower rates of the primary outcome (MI or fatal CHD, RH=0.78, 95% CI 0.61 to 0.99, p=0.044), and all-cause mortality (RH=0.74, 95% CI 0.56 to 0.99, p=0.04). Statin therapy was associated with a reduced incidence of VTE in both the HRT group and the placebo arm. The negative effect of HRT on the primary outcome seen in the 1st year of treatment was much reduced among baseline statin users and was no longer statistically significant (RH=1.34, 95% CI 0.63 to 2.86, p=0.45). CONCLUSION: Data from HERS supports the use of statins for secondary prevention in postmenopausal women with a history of cardiovascular disease. Statins may attenuate the increased cardiovascular risk of hormone replacement therapy.

Aged↗
PubMed2003

[Efficacy and safety of combined statin-fenofibrates therapy compared with monotherapy in patients with mixed hyperlipidemia and high risk of coronary heart disease].

UNLABELLED: In most patients with mixed hyperlipidemia and coronary heart disease (CHD) the treatment targeted both at triglyceride and LDL cholesterol levels is very difficult, when one lipid-lowering drug is used. We performed a prospective study evaluating the efficacy and safety of statins (simvastatin 20 mg, fluvastatin 40 mg, lovastatin 20 mg, atorvastatin 10 mg) and fibrates (fenofibrate 200 mg, ciprofibrate 100 mg) used alone, and then compared with statin-fibrate combinations in 180 patients. Each of three periods of therapy lasted 8-12 weeks. All regimens of statins and fibrates normalised the lipid profile more effectively than monotherapy. Monotherapy with statins lowered total cholesterol by 23.8% in relation to the baseline; compared with 13% for fibrates monotherapy and 34.3% for statins plus fibrates combinations. Triglyceride concentration decreased by 25.5% with statins alone, 34.0% with fibrates alone and 44.5% with combined therapy. LDL cholesterol was reduced by 28.1%, 12.7%, 40.3%, respectively. Statins increased HDL cholesterol by 4%, fibrates by 18% and combined therapy by 15.2%. The target levels for LDL cholesterol were achieved in 3.7% patients on statins therapy, in 1.1% on fibrates and 21.7% on the combined therapy. For total cholesterol the changes were 8.3%, 2.2% and 41.7%, respectively and for triglycerides the were 27.7%, 45% and 66.7%, respectively. The safety of the treatment was assessed by recording adverse events and measuring clinical laboratory parameters. No significant increase in CPK or ALT levels was observed. Only 7 patients had a history of moderate ALT increase (< 3 times) and 27 of CPK increase (< 3 times) when receiving combined statins plus fibrates. CONCLUSIONS: We conclude that combined therapy with statins and fibrates can improve lipid abnormalities in mixed hyperlipidaemia more effective then statins or fibrates monotherapy. The combined therapy was well tolerated and safe.

Adult↗
PubMed2005

[Statins and stroke].

The occurrence of stroke increases with age, particularly affecting the older elderly, a population also at higher risk for coronary heart disease (CHD). Epidemiological and observational studies have not shown a clear association between cholesterol levels and all causes of stroke. Nevertheless, large, long-term statin trials in patients with established CHD or et high risk for CHD (diabetes, hypertension) have shown that statins decrease stroke incidence in these populations even with a normal baseline cholesterol concentration. In patients with previous stroke statins reduce the incidence of coronary events, but whether they actually reduce the incidence of recurrent strokes in secondary prevention is unproved. In this review we discuss the potential reason for the effects of statins on stroke and the mechanisms of action. Statins probably reduce stroke by a variety of mechanisms. Several studies indicate that statins have multiple effects beyond lowering the cholesterol level. There is evidence that statins have neuroprotective properties for the acute ischaemic brain. Statins interfere with platelet aggregation and have anti-inflammatory and antioxidative properties. Also statins promote stabilisation of atherosclerotic plaques and improve blood flow to the ischaemic brain. The protective effects of statins might be due to their direct effect on endothelial cells leading to improved nitric oxide (NO) bioavailability. However further studies are needed to understand the full role of statins in the prevention of stroke in patients without established cardiovascular disease, representative of the typical stroke population.

Aged↗
PubMed2006

The effects of prescription drug copayments on statin adherence.

BACKGROUND: High copayments may present a barrier to medication adherence among patients with chronic conditions such as hyperlipidemia. OBJECTIVE: To assess the effects of statin copayments on statin adherence among individuals with employer-based insurance. STUDY DESIGN: We used a cross-sectional time-series design, with patient as the cross section and month as the time unit. METHODS: Medical and pharmacy claims among continuously enrolled statin users were selected from the 2000-2003 Medstat MarketScan database. Generalized estimating equation models were used to estimate the effects of copayment changes on statin adherence. Adherence was derived from the medication possession ratio, which represents the percentage of days on therapy each month. Separate estimates were obtained for new statin users (n = 142 341) and for continuing statin users (n = 92 344). RESULTS: Higher copayments were associated with lower statin adherence rates. A 100% index copayment increase had a larger effect on monthly adherence (2.6 and 1.1 percentage point decreases in adherence among new users and continuing users, respectively [both P < .01]) than a 100% copayment increase over time (a 1.1 percentage point decrease among new users [P < .01] and a nonsignificant decrease among continuing users). In all models, new statin users were more price sensitive than continuing users. CONCLUSIONS: High copayments are a financial barrier to statin adherence. The index copayment amount can affect compliance with statin use. Given the relationship between statin use and decreased frequency of cardiovascular events and procedures, the implications of high copayments should be considered by policy makers.

Aged↗
PubMed2004

Use of statins and fracture: results of 4 prospective studies and cumulative meta-analysis of observational studies and controlled trials.

BACKGROUND: The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are widely used for the treatment of hyperlipidemia, and recent in vitro and animal data suggest that statins promote bone formation and increase bone strength. METHODS: To determine whether statin use is associated with a reduced risk for fracture, we analyzed statin use and fracture rates in 4 large prospective studies (the Study of Osteoporotic Fractures, the Fracture Intervention Trial, the Heart and Estrogen/Progestin Replacement Study, and the Rotterdam Study). We searched MEDLINE through January 2002 and abstracts from major scientific meetings and performed a cumulative meta-analysis of published and unpublished observational studies and clinical trials. The meta-analysis included 8 observational studies and 2 clinical trials that reported statin use and documented fracture outcomes. RESULTS: After adjustment for multiple factors, including age, body mass index, and estrogen use, we found a trend toward fewer hip fractures (relative hazards [RHs], 0.19-0.62) and, to a lesser extent, nonspine fractures (RHs, 0.49-0.95) among statin users in each of the 4 prospective studies. The meta-analysis of observational studies was consistent with these findings. The summary odds ratio (OR) for statin use and hip fracture was 0.43 (95% confidence interval [CI], 0.25-0.75), whereas that for nonspine fracture was 0.69 (95% CI, 0.55-0.88). The meta-analysis of clinical trial results did not support a protective effect with statin use for hip fracture (summary OR, 0.87; 95% CI, 0.48-1.58) or nonspine fracture (OR, 1.02; 95% CI, 0.83-1.26). CONCLUSIONS: Observational studies suggest that the risk for hip and nonspine fractures is lower among older women taking statin medications for hyperlipidemia, but post hoc analyses of cardiovascular trials do not. Controlled trials specifically designed to test the effect of statins on skeletal metabolism and fracture are needed.

Aged↗
PubMed2005

Do statins reduce risk of incident dementia and Alzheimer disease? The Cache County Study.

BACKGROUND: Prior reports suggest reduced occurrence of dementia and Alzheimer disease (AD) in statin users, but, to our knowledge, no prospective studies relate statin use and dementia incidence. OBJECTIVE: To examine the association of statin use with both prevalence and incidence of dementia and AD. DESIGN: Cross-sectional studies of prevalence and incidence and a prospective study of incidence of dementia and AD among 5092 elderly residents (aged 65 years or older) of a single county. Participants were assessed at home in 1995-1997 and again in 1998-2000. A detailed visual inventory of medicines, including statins and other lipid-lowering agents, was collected at both assessments. MAIN OUTCOME MEASURES: Diagnosis of dementia and of AD. RESULTS: From 4895 participants with data sufficient to determine cognitive status, we identified 355 cases of prevalent dementia (200 with AD) at initial assessment. Statin use was inversely associated with prevalence of dementia (adjusted odds ratio, 0.44; 95% confidence interval, 0.17-0.94). Three years later, we identified 185 cases of incident dementia (104 with AD) among 3308 survivors at risk. Statin use at baseline did not predict incidence of dementia or AD (adjusted hazard ratio for dementia, 1.19; 95% confidence interval, 0.53-2.34; adjusted hazard ratio for AD, 1.19; 95% confidence interval, 0.35-2.96), nor did statin use at follow-up (adjusted odds ratio for dementia, 1.04; 95% confidence interval, 0.56-1.81; adjusted odds ratio for AD, 0.85; 95% confidence interval, 0.32-1.88). CONCLUSIONS: Although statin use might be less frequent in those with prevalent dementia, we found no association between statin use and subsequent onset of dementia or AD. Further research is warranted before costly dementia prevention trials with statins are undertaken.

Aged↗
PubMed1991

Statin immunolocalization in human brain tumors. Detection of noncycling cells using a novel marker of cell quiescence.

Surgical specimens of 35 human brain tumors were examined with a novel monoclonal antibody, S-44, immunoreactive to statin, a nuclear protein specifically expressed in quiescent (noncycling) G0-phase cells. Benign tumors typically were statin positive with labeling indices (LI) between 22% and 96%: acoustic schwannomas (n = 3, mean = 29.9 +/- 19.4%); meningiomas (n = 4, mean = 59.0 +/- 15.1%); pituitary adenomas (n = 3, mean = 79.9 +/- 28.2%), and an epidermoid cyst (41.0%). By contrast, the statin LI of 18 of 24 (75%) malignant brain tumors was less than or equal to 2%: medulloblastomas (n = 7, mean = 0.3 +/- 0.2%); anaplastic astrocytomas (n = 3, mean = 1.6 +/- 2.7%); glioblastomas (n = 10, mean = 10.3 +/- 14.4%); metastatic carcinomas (n = 3, mean = 3.0 +/- 4.6); and a germinoma (0.2%). The vascular endothelium among diverse tumors typically was statin positive. All 21 tumors with a statin LI less than 10% were malignant, and all nine tumors with a statin LI greater than 40% were benign. The statin LI of benign tumors (n = 11, mean = 55.1 +/- 26.7%) was significantly higher than that of the malignant tumors (n = 24, mean = 5.2 +/- 10.5%, P less than 0.001). The absence of statin expression is a new way to determine the malignancy of human brain tumors. The statin LI may be useful to guide the prognosis and treatment of individual patients. The mechanisms that control statin expression are important in therapy seeking to shift the proliferating, cycling cells to the quiescent, G0 compartment.

Adolescent↗
PubMed2006

The comparative safety of rosuvastatin: a retrospective matched cohort study in over 48,000 initiators of statin therapy.

PURPOSE: The purpose of this study was to compare incidence rates of hospitalization associated with rhabdomyolysis, myopathy, renal, or hepatic dysfunction, and of in-hospital death, between initiators of rosuvastatin and other statins. METHODS: This was a matched cohort study of statin initiators from the administrative database of a large health insurer in the US, during the first 6 months of rosuvastatin availability with up to 18 months of follow-up. All outcome events were verified by medical record review. Incidence rates, risk ratios, and associated 95% confidence intervals were estimated. RESULTS: From an initial pool of 12,217, 11,249 eligible rosuvastatin initiators were matched to 37,282 initiators of other statins. The incidence rate (IR) per 1000 person-years for rhabdomyolysis was 0.10 [0.00, 0.55] for rosuvastatin initiators (n = 1) and 0.06 [0.01, 0.22] for other statin initiators (n = 2), for a hazard ratio (HR) of 1.98 [0.18, 21.90]. The IR for myopathy was 0.20 [0.02, 0.71] for rosuvastatin initiators (n = 2) and 0.00 [0.00, 0.09] for other statin initiators (n = 0). The IR for renal dysfunction was 1.18 [0.61, 2.06] for rosuvastatin initiators (n = 12) and 1.26 [0.91, 1.71] for other statin initiators (n = 42), for a HR of 0.90 [0.47, 1.73]. The IR for hepatic dysfunction was 0.20 (0.02, 0.71) for rosuvastatin initiators (n = 2) and 0.24 (0.10, 0.47) for other statin initiators (n = 8), for a HR of 0.87 (0.18, 4.14). CONCLUSIONS: This study found no difference between rosuvastatin and the other statins in the incidence of hospitalizations associated with renal or hepatic events, or death. The absolute incidence rates of rhabdomyolysis and myopathy were reassuringly low among all statin initiators but remain too small for firm conclusions to be drawn on any difference between the statins.

Adolescent↗
PubMed2007

The impact of over-the-counter simvastatin on the number of statin prescriptions in the United Kingdom: a view from the General Practice Research Database.

PURPOSE: The United Kingdom (UK) government changed the prescription policy of statins, making low-dose simvastatin (10 mg) available as an over-the-counter (OTC) drug in August 2004. We assessed the impact of this policy change on statin prescribing. METHODS: We examined all statin prescriptions in the General Practice Research Database (GPRD), a well-validated database of approximately 3.5 million patients, from the first quarter of 2001 to the second quarter of 2005. RESULTS: From 2001, the number of statin prescriptions written for GPRD patients was increasing by approximately 437 prescriptions per 100,000 people per quarter until the time of the policy change. Over the four quarters post-policy implementation, however, this trend changed abruptly (p < 0.0001) with a decrease of 281 prescriptions per 100,000 people per quarter. This decrease was not restricted to prescriptions of 10 mg statins but was also observed for statin prescriptions of >or=20 mg. Several other cardiovascular medications displayed a similar trend as that observed in the number of statin prescriptions. This trend was not observed among non-cardiovascular control medications. CONCLUSIONS: Our study suggests that the policy allowing the OTC sale of 10 mg simvastatin has had a significant impact on statin prescriptions by general practitioners. However, this new policy may also be leading to less aggressive statin therapy. An alternative explanation for the observed decrease in statin prescriptions may be related to the unknown factors responsible for the overall decrease observed with other cardiovascular prescription drugs.

Databases, Factual↗
PubMed2005

Statin lipid-lowering drugs and bone mineral density.

BACKGROUND: HMG Co-A reductase inhibitors (statin lipid-lowering drugs) have been associated with a reduced rate of fractures in some studies, but not in others. We examined the relationship between statin use and bone density among postmenopausal women. METHODS: We conducted a cross-sectional survey at one academic medical center. Postmenopausal women who underwent bone densitometry and agreed to a telephone interview were surveyed about osteoporosis risk factors, use of hormone replacement therapy and osteoporosis medications and statin exposure. We then developed linear regression models adjusting for known counfounders to assess the relationship between statin use and bone mineral density (BMD). RESULTS: Of 339 women studied, 162 were current or past users of statins, and 177 were not. Statin users and non-users were similar with respect to age, race, prior fracture history, the presence of medical conditions associated with osteoporosis, use of medications for osteoporosis, use of tobacco and use of oral glucocorticoids. Statin users had significantly higher body mass index (BMI) and rates of thiazide use, and were more likely to abstain from alcohol. After adjusting for important confounders, we found that statin use was associated with a significantly higher t-score at the total hip (-0.53 +/- 0.17) compared with non-users (-0.83 +/- 0.18; p = 0.02). At the lumbar spine, there was a trend toward higher t-scores in statin users (-0.91 +/- 0.24) compared with non-users (-1.21 +/- 0.23; p = 0.08). CONCLUSIONS: These results support the hypothesis that statin use is associated with higher BMD. While it is unclear whether their relationship is causal, further controlled studies examining bone formation and resorption would help determine the clinical implications of these findings.

Bone Density↗