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PubMedDate not supplied

Statins in the prevention and treatment of Alzheimer disease.

Vascular risk factors such as hypertension and hypercholesterolemia during midlife increase the risk for Alzheimer's disease (AD). Treatment of hypercholesterolemia and other vascular risk factors may have great implications in the prevention of AD. Recent findings illustrate that the sterol metabolism in the brain is an active process, well controlled and regulated by 24-hydroxylase, an enzyme that is uniquely expressed in the brain. The use of statins in ischemic heart disease (IHD) has proven to be a phenomenal advance in pharmacological disease prevention and treatment. A growing body of evidence, suggest that statins exhibit additional benefits that are independent of their cholesterol-lowering actions. Statin treatment has also considerable effect in prevention of ischemic stroke. In animal models of ischemic stroke, statins have proven to reduce infarct size through up-regulation of endothelial nitric oxide synthases. Data from recent observational studies have revealed a potential role for statins in prevention of AD. The following review comments the processes leading to dementia including the involvement of cholesterol regulation, cerebral circulation and inflammation in development of dementia. The mechanisms by which statins may be beneficial in controlling these processes is discussed.

Aged↗
PubMed2001

Statin therapy decreases the risk of osteonecrosis in patients receiving steroids.

Osteonecrosis is a devastating complication of systemic steroid use. Prolonged steroid use produces a hyperlipidemic state in most patients and puts them at risk for osteoporosis and osteonecrosis. The fat content within the femoral head increases, resulting in increased intracortical pressure that may lead to sinusoidal collapse and osteonecrosis. Statins are lipid-clearing agents that dramatically reduce lipid levels in blood and tissues. Statins are widely used to prevent cardiovascular disease and have been shown to reduce the adverse effects of steroids on lipid metabolism. The purpose of this study was to determine whether the use of statin drugs affects later development of osteonecrosis in patients receiving steroids. The records of 284 patients who were taking statin drugs at the time they were started on high dose steroids were examined to determine whether osteonecrosis had developed. The patients remained on statin drugs during the entire time of steroid exposure. Magnetic resonance imaging scans were used to verify the osteonecrosis unless it was visible by radiograph. After an average of 7.5 years (minimum followup, 5 years), only three patients (1%) from the group had osteonecrosis develop. This 1% incidence is much less than the 3% to 20% incidence usually reported for patients receiving high-dose steroids. Statins may offer some protection against having osteonecrosis develop when steroid treatment is necessary.

Adrenal Cortex Hormones↗
PubMed2006

Autoimmune hepatitis triggered by statins.

Although the cause of autoimmune hepatitis (AIH) is unknown, drugs are believed to be potential triggers in some patients. In isolated case reports, statins have been considered such triggers. Here we describe 3 patients in whom it is probable that statins initiated the development of AIH. Two men (aged 47 and 51) and one woman (aged 57) developed AIH after the initiation of statin therapy. They developed positive titers of antinuclear antibodies, antismooth muscle antibodies (1/40 to 1/160), and hypergammaglobulinemia. Features of all 3 patients met the criteria for AIH according to the International Autoimmune Hepatitis Panel. Liver biopsies in all 3 showed varying stages of fibrosis and plasma cell infiltration, compatible with AIH. The woman developed hepatitis due to statins on 2 separate occasions: the first in 1999, due to simvastatin, and the second in 2001 to 2002, due to atorvastatin, which was severe and persisted even after discontinuing medication. Similarly, in the 2 other cases, exposure to statins preceded development of AIH, which persisted despite discontinuing medications. All 3 patients responded well to prednisone and azathioprine or mycophenolate therapy. 3 similar previously reported cases are reviewed. We conclude that the 3 cases reported here and 3 similar previously reported cases, indicate that severe, ongoing AIH on rare occasions can be triggered by statins.

Atorvastatin↗
PubMed2001

Statin induced myopathy does not show up in MIBI scintigraphy.

Statin induced myopathy is the most commonly seen side effect in users of this family of drugs. Their different forms present with either creatine phosphokinase (CK) elevation or not, signs of in vivo oxidation injury or not or a combination of both. The pathogenetic background, however, still remains obscure. As MIBI, beside myocardial and tumour scintigraphy, is useful in detecting muscle metabolic abnormalities, an increased uptake of MIBI in the diseased muscular segments could be expected. We investigated seven patients (five males, two females; aged 36-56 years) with statin induced myopathy with either elevated CK, isoprostanes or muscle pains at varying combinations. MIBI whole-body imaging was done immediately, the patients still being on the respective statin. Sixteen patients (six males, 10 females) suffering from lung or breast cancer and being on statins served as controls. No uptake abnormalities in any muscular segment either in the patients or the control group were seen. Thus, MIBI scintigraphy is not useful, apparently, in diagnosing and eventually localizing statin induced myopathy. These findings indicate that MIBI scintigraphy is of no help for diagnosis and gaining further insight into statin induced myopathy.

Adult↗
PubMed2002

The effectiveness of hydroxy-methylglutaryl coenzyme A reductase inhibitors (statins) in the elderly is not influenced by apolipoprotein E genotype.

We aimed to assess whether the effectiveness of statins in the prevention of myocardial infarction, stroke and total mortality is influenced by apolipoprotein E (apoE) genotype in an elderly population. We used data from the Rotterdam Study, a prospective population-based cohort study in the Netherlands which started in 1990 and included 7983 subjects aged 55 years and older. Subjects who were treated with cholesterol lowering drugs at baseline or with a serum total cholesterol > or = 6.5 mmol/l at baseline were included. We compared the incidence of myocardial infarction, stroke and total mortality in subjects who received > or = 2 years of statin treatment with that in subjects who had been treated for less than 2 years, and in untreated subjects, using a Cox proportional hazard model with cumulative statin use defined as time-dependent covariates. The adjusted relative risk of all-cause mortality was 0.79 [95% confidence interval (CI) 0.51-1.22] and of myocardial infarction and stroke 0.50 (95% CI 0.28-0.91) for subjects treated with statins for > or = 2 years compared to untreated subjects. The adjusted relative risks for subjects with the epsilon4 allele were 0.91 (95% CI 0.45-1.84) for all-cause mortality and 0.63 (95% CI 0.23-1.78) for myocardial infarction and stroke. In subjects without the epsilon4 allele, adjusted relative risks were 0.71 (95% CI 0.41-1.24) for all-cause mortality and 0.46 (95% CI 0.22-0.95) for myocardial infarction and stroke. We found a protective effect of statins on the risk of myocardial infarction and stroke that was independent of apoE genotype. The protective effect of statins on total mortality was not statistically significant, but did not seem to differ between subjects with different apoE genotypes.

Aged↗
PubMed2004

Statin therapy in kidney disease populations: potential benefits beyond lipid lowering and the need for clinical trials.

PURPOSE OF REVIEW: This review outlines the limited information currently available on the effects of statins among patients with chronic kidney disease, and summarizes the ongoing randomized trials designed to address this question. RECENT FINDINGS: The effects of fluvastatin on major coronary events among renal transplant patients, and the effects of pravastatin and simvastatin in small subgroups of coronary patients with minor degrees of renal impairment, appear broadly compatible with those observed in trials conducted in non-renal populations. In addition, recent evidence from trials among patients with vascular disease or diabetes suggests that statin therapy may delay progressive loss of renal function. However, there remains substantial uncertainty regarding the effects of statin therapy among patients with established chronic kidney disease (pre-dialysis or dialysis patients). In particular, there does not appear to be a strongly positive relationship between blood cholesterol and cardiovascular events in such patients. This may be because uraemic cardiomyopathy and arteriosclerosis, which cause the majority of these events in chronic kidney disease patients, do not depend strongly on blood cholesterol. SUMMARY: Statins appear effective for the prevention of vascular events in people with established vascular disease and mild renal impairment, and may delay renal disease progression in such individuals. However, the effects of statins in patients with established chronic kidney disease are unknown, and we await the results of ongoing large-scale randomized trials of statin therapy among such patients.

Cardiovascular Diseases↗
PubMed2003

Dyslipidemia, statins, and venous thromboembolism: a potential risk factor and a potential treatment.

The optimal drug for the prevention of venous thromboembolism is one that is efficacious, associated with minimal bleeding risk, and easy to administer. Statins fulfill the latter two criteria, but their efficacy remains unproved. By examining the association between dyslipidemia and venous thromboembolism, as well as the evidence that statins might prevent venous thromboembolism, there may be a new rationale for the use of this class of drugs. There may be a common link between arterial and venous thrombosis. Dyslipidemia may be one of the many systemic factors associated not only with arterial thrombosis, but with venous thromboembolism as well. This may occur through the effects of circulating lipid molecules on the vascular endothelium, platelet function, and coagulation factors. By impeding these mechanisms, statins may be protective against venous thrombosis, but epidemiologic studies are few in number, and no randomized clinical trials have been conducted. Better epidemiologic evidence is required to establish whether dyslipidemia is a risk factor for venous thromboembolism. If future observational studies can demonstrate that statins are associated with a lower risk of venous thromboembolism, then consideration should be given to conducting a randomized clinical trial comparing statins with placebo for the prevention of venous thromboembolism. Until then, the efficacy of statins for the prevention or treatment of venous thromboembolism remains uncertain.

Clinical Trials as Topic↗
PubMed2003

The impact of reimbursement criteria on the appropriateness of 'statin' prescribing.

BACKGROUND: In Belgium, regulations restrict the reimbursement of statins to patients with total serum cholesterol above 250 mg/dl (6.41 mmol/l) after a three-month lipid-lowering diet. We investigated the possible impact of these regulations on characteristics of Belgian patients receiving a lipid-lowering drug. DESIGN: From 1998 to 2000, standard questionnaires on coronary risk factors and treatments with lipid-lowering drugs were completed by 301 GPs sampled at random in the 11 Belgian Provinces. Questionnaires had to be completed for 18 consecutive patients 35 years old or more attending GPs' practices, irrespective of the underlying motive for attendance. RESULTS: Of the 5511 patients included in the study, 1519 (28%) had established coronary disease or diabetes mellitus, or > or = 2 non-cholesterol coronary risk factors. Most (70%) of these patients were not treated with a lipid-lowering drug. Only 22% of patients with established coronary disease, 10% of patients with diabetes mellitus and 9% of patients with > or = 2 coronary risk factors were treated with a statin. Fifty-nine percent of fibrate users and 50% of statin users had a pre-treatment cholesterol level above 250 mg/dl, but had no or only one non-cholesterol coronary risk factor. CONCLUSIONS: In Belgium, the majority of patients at higher risk of coronary event do not benefit from lipid-lowering drugs, particularly the statins. In contrast, one of two statin users and three of five fibrate users should probably not receive the drug prescribed. Regulation based on blood cholesterol level encourages the overlooking of other risk factors relevant for selecting patients having the greatest chance to benefit from statin treatment.

Adult↗
PubMed2004

Statin therapy in the elderly.

PURPOSE OF REVIEW: The clinical efficacy and safety of statin therapy have been well established from a series of large-scale, randomized controlled trials. These trials, however, have predominantly recruited patients under the age of 70 years. As a consequence, the use of statins in older patients has remained controversial. RECENT FINDINGS: The results of the first trial to look exclusively at the elderly--the Prospective Study of Pravastatin in the Elderly at Risk--have added enormously to our understanding of the use of statins in the elderly. These findings, together with those from the large elderly cohort within the Heart Protection Study and the smaller elderly subgroups within the other major statin trials, have forced us to re-evaluate any systematic exclusion of elderly patients from statin therapy. SUMMARY: The collective evidence now strongly supports the use of statins in the at-risk elderly population.

Aged↗
PubMed2005

Statin pharmacogenomics: what have we learned, and what remains unanswered?

PURPOSE OF REVIEW: Statins are widely prescribed and are established as first-line therapy for the primary and secondary prevention of coronary heart disease. Response to treatment varies considerably from person to person; however, inherited traits (genetic variability) may play a central role in this inter-individual variation. The purpose of this review is to summarize recent progress in the research for exploring genetic determinants of clinical efficacy and safety of statin therapy. RECENT FINDINGS: In addition to 41 previous studies of 19 genes, the results of 17 pharmacogenomic studies investigating the relationship between common genetic variants and response to statin therapy in terms of lipid responses, clinical outcomes, and adverse events have been reported since January 2004 - 15 candidate genes related to pharmacodynamics and three to pharmacokinetics of statins. These reported data suggest that genetic variations influencing intestinal cholesterol absorption, cholesterol production, and lipoprotein catabolism may all play a role in modulating responsiveness, as well as genes involved in drug metabolism of statins. They also suggest that combined analysis of multiple variants in several genes, all of which have possible functional relations, is more likely to give significant results, especially when being performed with a larger number of participants. SUMMARY: Pharmacogenomic studies of statin therapy will provide a better picture as to who is most likely and least likely to benefit from treatment, which results in more individualized management of coronary artery disease.

Biotransformation↗
PubMed2007

Non-antiarrhythmic agents for prevention of postoperative atrial fibrillation: role of statins.

PURPOSE OF REVIEW: Atrial fibrillation is the most common arrhythmia following cardiac surgery, having both serious medical and socioeconomic consequences. Although there are established antiarrhythmic agents for preventing and treating postoperative atrial fibrillation, these therapies are neither 100% reliable, nor without risks and limitations. Thus, there remains a strong need for non-antiarrhythmic, adjunctive therapies for the prevention of postoperative atrial fibrillation. RECENT FINDINGS: Long-term statin administration in ambulatory patients is associated with a reduced risk of adverse cardiovascular events, including death, myocardial infarction, stroke, renal dysfunction and atrial fibrillation. Recent evidence suggests, however, that statins may also reduce the risk of acute adverse outcomes following invasive procedures, including postoperative atrial fibrillation. Although the exact mechanisms by which statins may reduce postoperative atrial fibrillation are unclear, accumulating evidence suggests that statins exert multiple effects independent of their effect on LDL cholesterol. For example, in patients with acute coronary syndromes, statin therapy has been shown to modulate remodeling of the cardiac extracellular matrix and to reduce markers of inflammation, including C-reactive protein, serum amyloid A, tumor necrosis factor-alpha, and IL-6. SUMMARY: Perioperative statin therapy may represent an important non-antiarrhythmic, adjunctive therapeutic strategy for the prevention of postoperative atrial fibrillation.

Anti-Arrhythmia Agents↗
PubMedDate not supplied

Statin drugs do not affect serum complement activation in vitro.

Statin drugs prevent coronary heart disease through anti-inflammatory mechanisms in addition to the well-known reduction of low-density lipoproteins. The complement system plays an essential role in the inflammatory response and has been postulated to be modified by statins. A direct role for statins in complement activation, however, has not been previously investigated. We therefore studied the effect of statins on in vitro complement activation. Pravastatin, atorvastatin and the active metabolite of the latter, ortho-hydroxy atorvastatin, were added to normal human serum and incubated for 1 h in the absence or presence of aggregated immunoglobulin (classical pathway activation) or cobra venom factor (alternative pathway activation). The degree of complement activation, as detected by specific complement-activation products for the classical pathway (C1rs-C1-inhibitor complexes), the combined classical and lectin pathway (C4bc), the alternative pathway (C3bBbP) and the final common pathway (C3bc and TCC), was not affected by pre-incubation of the serum with any of the statins. Statins do not affect complement activation directly, but indirect effects in vivo may well be operative.

Atorvastatin↗
PubMed2004

Statins: novel additions to the dermatologic arsenal?

The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins), atorvastatin, cerivastatin, fluvastatin, pravastatin, lovastatin and simvastatin, reduce atherogenesis and cardiovascular morbidity. Besides, there is growing evidence that statins have immunomodulatory activities. Statins downregulate the expression of adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), monocyte chemotactic protein-1 (MAC-1) and lymphocyte function-associated antigen-1 (LFA-1), on leucocytes and endothelial cells and, through binding to LFA-1, interfere with ICAM-1-LFA-1 interaction, which is crucial for activation of lymphocytes by antigen-presenting cells, ingress of leucocytes into the inflammation sites and immunologic cytotoxicity. Statins inhibit the inducible expression of major histocompatibility complex class II in several cell types including macrophages and downregulate the expression of T-helper-1 (Th1) chemokine receptors on T cells, leading further to inhibition of activation of lymphocytes and their infiltration into the inflammation sites. Statins block the induction of inducible nitric oxide synthase and the expression of several proinflammatory cytokines such as tumour necrosis factor-alpha and interferon-gamma in macrophages and possess antioxidant effects. These agents inhibit the proliferation of immunocytes and the activation of natural killer cells. Regarding the above facts and in view of their safety and inexpensiveness, statins may prove invaluable in the treatment of a multiplicity of dermatologic disorders, especially those characterized by ingress of activated leucocytes into the skin, such as alopecia areata, vitiligo, lichen planus, subacute cutaneous lupus erythematosus, erythema multiforme, psoriasis, bullous pemphigoid, systemic sclerosis, mycosis fungoides, toxic epidermal necrolysis and Behcet's disease.

Humans↗
PubMed2006

Statins and the risk of acute pancreatitis: a population-based case-control study.

BACKGROUND: Case reports have suggested that statins may cause acute pancreatitis. AIM: To examine if statins are associated with risk of acute pancreatitis. METHODS: We identified 2576 first-time admitted cases of acute pancreatitis from hospital discharge registers in three Danish counties, and 25 817 age- and gender-matched controls from the general population. Prescriptions for statins prior to admission with acute pancreatitis or index date among controls were retrieved from prescription databases. We used conditional logistic regression analysis to estimate odds ratios for acute pancreatitis among ever (ever before), current (0-90 days before), new (first prescription in 0-90 days before) and former (>90 days, but not 0-90 days before) users of statins. RESULTS: Adjusted odds ratios for acute pancreatitis among ever, current, new and former users of statins were 1.44 (95% confidence interval: 1.115-1.80), 1.26 (95% confidence interval: 0.96-1.64), 1.01 (95% confidence interval: 0.43-2.37) and 2.02 (95% confidence interval: 1.37-2.97), respectively. There was an indication of an inverse association between the number of filled prescriptions and risk of acute pancreatitis. CONCLUSIONS: Our findings speak against a strong causative effect of statins on the risk of acute pancreatitis, and may even indicate a mild protective effect.

Acute Disease↗
PubMed2005

Statin therapy: a potentially useful peri-operative intervention in patients with cardiovascular disease.

Statin cardiovascular protection is mediated by lipid lowering and pleiotropic effects. The efficacy of statins has been established in non-surgical patients with cardiovascular disease and also more recently in non-surgical patients who sustain an acute coronary event. Peri-operative statin administration has been shown to improve both short-term and long-term cardiac outcome following non-cardiac and coronary bypass graft surgery. This cardioprotection may be independent of peri-operative haemodynamics due to a positive effect on plaque stability. Recommendations for the peri-operative statin administration are suggested. These include indications for peri-operative statin therapy, timing of administration, therapeutic targets, duration of administration, the adverse implications of peri-operative statin withdrawal, safety and cost-effectiveness.

Cardiovascular Diseases↗
PubMed2004

Professional athletes suffering from familial hypercholesterolaemia rarely tolerate statin treatment because of muscular problems.

AIMS: Muscular problems are the major group of side-effects during statin treatment. They are known to occur much more frequently during and after exercise. METHODS AND RESULTS: For the last 8 years we have monitored 22 professional athletes in whom, because of familial hypercholesterolaemia, treatment with different statins was attempted. Only six out of the 22 finally tolerated at least one member of this family of drugs. In three of these six the first statin prescribed allowed training performance without any limitation. Changing the drug demonstrated that only two tolerated all the four or five statins examined (atorvastatin, fluvastatin, lovastatin, pravastatin, simvastatin). Cerivastatin was not among the statins prescribed. CONCLUSIONS: These findings indicate that in top sports performers only about 20% tolerate statin treatment without side-effects. Clinical decision making as to lipid lowering therapy thus becomes a critical issue in this small subgroup of patients.

Adolescent↗
PubMed2004

Association between adherence to statin therapy and lipid control in Hong Kong Chinese patients at high risk of coronary heart disease.

AIMS: To examine the pattern of adherence to statin therapy and to determine the association of adherence to statin therapy and the control of serum low-density lipoprotein (LDL)-cholesterol in a cohort of Hong Kong Chinese patients at high risk of coronary heart disease (CHD). METHODS: This was a prospective observational cohort study conducted at the outpatient clinics of a public teaching hospital in Hong Kong. Patients at high risk of CHD who had been initiated on statin monotherapy for < 12 months were recruited. The statin prescription was dispensed in a bottle with the Medication Event Monitoring System (MEMS). Adherence was assessed in two dimensions: dose-count was defined as the percentage of doses taken, and dose-time was defined as the percentage of doses taken within the suggested time interval. Lipid profiles were obtained at baseline and during two follow-up visits at month 3 and month 6. RESULTS: Eighty-three patients completed the study. The median adherence to dose-count and to dose-time were 95% (25-75th percentile = 87-99%) and 78% (25-75th percentile = 17-92%), respectively. Both dose-count and dose-time adherence declined slightly over the first 6 months of therapy. Living with family [relative risk (RR) = 0.79, 95% confidence interval (CI) 0.63, 0.91] and duration of therapy (RR = 0.99, 95% CI 0.98, 1.00) were negative predictors while number of family members (among those living with family) (RR = 1.05, 95% CI 1.00, 1.08) was a positive predictor for adherence to dose-count. Monthly household income (RR = 1.01, 95% CI 1.00, 1.02) and angina (RR = 1.29, 95% CI 1.05, 1.58) were positive predictors while living with family (RR = 0.74, 95% CI 0.55, 0.90) was a negative predictor for dose-time adherence. Percent reduction in serum LDL-cholesterol was correlated to dose-count (P < 0.001) and dose-time (P = 0.047) adherence. Statistically significant correlations were observed between adherence to dose-count and LDL reduction (R(2) = 0.130; P = 0.001), and between dose-time adherence and LDL reduction (R(2) = 0.048; P = 0.047). CONCLUSION: High adherence to statin therapy was found in a cohort of Chinese patients at high risk of CHD and the adherence declined slightly over time. A weak association between adherence to statin dose-count and LDL reduction and a marginal association between dose-time adherence and LDL reduction were observed.

Adult↗
PubMed2004

Statins: potent vascular anti-inflammatory agents.

Atherosclerosis is a multifactorial condition that can result in cardiovascular disease. Statin therapy is thought to mediate cardioprotective effects that influence endothelial function, inflammatory responses, plaque stability and thrombus formation, processes involved in atherosclerosis. Although reduction in low-density lipoprotein cholesterol (LDL-C) potentially plays a role in all of these effects, several lines of evidence also implicate nonlipidmediated 'pleiotropic' effects. For example, statin therapy confers a lower risk for coronary heart disease than placebo in patients with comparable serum cholesterol levels, and confers a greater magnitude of clinical benefit than expected based on LDL-C levels alone. Moreover, while nonstatin lipid-lowering therapy does not necessarily reduce stroke risk, statins have shown a significant reduction in stroke. Statins exert their pleiotropic effects, in part, by improving endothelial function via up-regulation of endothelial nitric oxide synthase enzyme activity. Markers of inflammation such as high sensitivity C-reactive protein have been also shown to add further prognostic information about patients at risk of cardiovascular disease who may benefit from statin therapy. Further studies are still needed to determine whether statins have direct effects on inflammatory pathways.

Anti-Inflammatory Agents↗