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At least 991 records · Page 55Linked to original sources
PubMed2001

Clinical relevance of statins: instituting treatment early in acute coronary syndrome patients.

The efficacy of statins in lowering the total and low-density lipoprotein cholesterol and reducing the risk of cardiac events is now well established. The secondary prevention studies started treatment several months after the acute event. However, the greatest risk of recurrence is shortly after the index event. Recent evidence from small-scale clinical trials shows that standard doses of statins can be both safe and effective when given early after an acute coronary event, including early after thrombolytic therapy for myocardial infarction. Angiographic studies have shown beneficial effects of pravastatin on coronary stenosis when initiated after a coronary event. While none of these studies have been powered to demonstrate an effect on outcome, each has shown a reduction in major cardiovascular events. Two large observational studies have shown a reduction in 6- and 12-month risk-adjusted mortality among post-MI patients treated early with statins. Large-scale trials of all statins are now in progress to evaluate further the efficacy of early initiation of statin therapy in acute coronary syndromes. The largest of these is the Australian Pravastatin Acute Coronary Treatment (PACT) study, which will compare early outcomes in patients treated with pravastatin versus placebo prescribed within the first 24 h of an acute coronary event.

Anticholesteremic Agents↗
PubMed1989

X-ray studies of aspartic proteinase-statine inhibitor complexes.

The conformation of a statine-containing renin inhibitor complexed with the aspartic proteinase from the fungus Endothia parasitica (EC 3.4.23.6) has been determined by X-ray diffraction at 2.2-A resolution (R = 0.17). We describe the structure of the complex at high resolution and compare this with a 3.0-A resolution analysis of a bound inhibitor, L-364,099, containing a cyclohexylalanine analogue of statine. The inhibitors bind in extended conformations in the long active-site cleft, and the hydroxyl of the transition-state analogue, statine, interacts strongly with the catalytic aspartates via hydrogen bonds to the essential carboxyl groups. This work provides a detailed structural analysis of the role of statine in peptide inhibitors. It shows conclusively that statine should be considered a dipeptide analogue (occupying P1 to P1') despite lacking the equivalent of a P1' side chain, although other inhibitor residues (especially P2) may compensate by interacting at the unoccupied S1' specificity subsite.

Amino Acids↗
PubMed2001

HMG-CoA reductase inhibitors (statins) characterized as direct inhibitors of P-glycoprotein.

PURPOSE: HMG-CoA reductase inhibitors (statins) are commonly prescribed for lipid lowering to treat hypercholesterolemia. Although they are well tolerated, their pharmacokinetic interactions with other drugs can lead to some adverse clinical consequences. The avenue of interaction has been asserted to be CYP3A4 because most (or all) known interactions are with CYP3A4 inhibitors, and statin oxidative metabolism is mediated by CYP3A4 as well as other CYP enzymes. However, these same drugs that exert a clinical pharmacokinetic effect on statin disposition are generally also P-gp substrates/inhibitors; hence, this transporter may be, or may contribute to, the mechanism of interaction. METHODS: This study shows directly, as well as quantifies, the inhibition of P-gp-mediated transport of a fluorescent marker substrate. RESULTS: Lovastatin and simvastatin are very potent and effective inhibitors of P-gp transport with IC50's of 26 and 9 microM, respectively, for the human enzyme. Atorvastatin is also an effective P-gp inhibitor, but at higher concentrations. Uniquely, pravastatin, whose functional groups render it an inferior inhibitor of P-gp in the whole cell, had no effect in this assay. This result is consistent with known clinical interactions. The effect of these statins on ATP consumption by P-gp was also assessed, and the Km results were congruent with the IC50 observations. CONCLUSIONS: Therefore, the clinical interactions of statins with other drugs may be due, in part or all, to inhibition of P-gp transport.

3T3 Cells↗
PubMed2003

Prevention of nitrate tolerance by long-term treatment with statins.

UNLABELLED: Recent studies have shown that statins seem to upregulate the endothelial NO synthase pathway (eNOS) and may, therefore, enhance NO availability, a direct scavenger of O2- and an inhibitor of oxidative enzymes. METHODS: To assess whether the oxidative stress produced by an in vivo exposure to nitroglycerin (NTG) is attenuated by statins, 4 groups of normocholesterolemic rats were treated; group 1 received pravastatin (20 mg/kg/d p.o) and group 2 atorvastatin (10 mg/kg/d) both for 5 weeks and the last 3 days, a cotreatment with the statin plus NTG (50 mg/kg/d, s.c. injections b.i.d.); group 3 (NTG) received only NTG (50 mg/kg/d, b.i.d. for 3 days) and group 4 served as control. Rings of thoracic aortas from these groups were studied in organ baths. Relaxations to NTG (0.1 nM to 0.1 mM) were determined on phenylephrine-preconstricted rings and O2- production (counts/10 s/mg) was assessed by lucigenin chemiluminescence technique. RESULTS: In vivo NTG exposure induced a rightward shift of the concentration-response curves to NTG: the pD2 (-log NTG concentration evoking a half maximal relaxation) was 5.8 +/- 0.3 (n=7) vs. 7.2 +/- 0.2 in the control group (not exposed to NTG, n=7) and O2- production was enhanced (1259 +/- 71 vs. 787 +/- 76, (n=5) P<.05). In contrast, groups 1 (n=7) and 2 (n=7) behaved as the control group (pD2 values were 7.4 +/- 0.1 (n=7) and 6.9 +/- 0.1 (n=7); O2- production was 721 +/- 109 and 647 +/- 121). The protective effect on nitrate tolerance disappeared when L-NAME (an eNOS inhibitor, 100 mg/kg/d) was co-administered with NTG in groups 1 and 2. Incubation of aortic rings with NAD(P)H (100 microM) also impaired the protective effect of both statins. Moreover, before NTG exposure, aortic cGMP content, reflecting EDNO availability, was significantly enhanced in group 1 (P<.05 vs. control). CONCLUSION: Long-term statin treatment protects against nitrate tolerance by counteracting NTG-induced increase in O2- production. Both eNOS pathway and NAD(P)H oxidases seem to be involved in this protective mechanism.

Administration, Oral↗
PubMed2000

Inhibition of monocyte chemotactic protein-1 synthesis by statins.

The beneficial effects of statins on the reduction of cardiovascular events has been partly attributed to their anti-inflammatory properties. In the complex of the different pathogenetic events leading to atherosclerosis, recent data suggest a central role of monocyte chemotactic protein-1 (MCP-1), because mice knock-out for MCP-1 or its receptor CC-chemokine receptor 2 were considerably resistant to plaque formation. In this study we investigated the effect of different statins on in vitro and in vivo production of MCP-1. Lovastatin and simvastatin caused a dose-dependent inhibition of MCP-1 production in peripheral blood mononuclear cells exposed to lipopolysaccharide or inactivated Streptococcus hemoliticus and in human endothelial cells exposed to interleukin-1beta. The addition of mevalonate overrode the inhibitory effect of statins indicating that mevalonate-derived products are important for chemokine production. The in vivo anti-inflammatory effect of statins was investigated using the mouse air-pouch model of local inflammation. Lovastatin and pravastatin were orally administered to mice according to a treatment schedule that significantly inhibited the hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activity without affecting total blood cholesterol. At the dose of 10 mg/kg, lovastatin and pravastatin reduced by approximately 50% the lipopolysaccharide-induced leukocytes recruitment and the exudate MCP-1 production. In conclusion, statins, by inhibiting mevalonate-derived products, reduced both in vitro and in vivo the production of chemokines involved in leukocyte migration, and this effect is unrelated to their cholesterol-lowering action.

Cells, Cultured↗
PubMed2005

Drug Insight: statins and stroke.

Stroke is the third leading cause of death in the US and a common cause of long-term disability worldwide. Ischemic strokes, which are often atherothrombotic, account for more than 80% of all strokes. Current stroke prevention focuses on optimizing the treatment of modifiable risk factors, such as hypertension, diabetes and dyslipidemia. The epidemiologic association between serum cholesterol levels and adjusted stroke rates is not as strong as the link between serum cholesterol levels and coronary heart disease. Clinical trials of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins), which are potent inhibitors of cholesterol synthesis, have demonstrated, however, a marked reduction in stroke risk in hypercholesterolemic and atherosclerotic individuals, with benefits extending to normocholesterolemic individuals. These findings suggest that statins might have additional effects in stroke protection beyond cholesterol reduction. Because statins inhibit the synthesis of isoprenoid intermediates in the cholesterol biosynthetic pathway, which are important lipid attachments for intracellular signaling molecules, they might have direct noncholesterol-dependent effects on inflammatory and endothelial cells. Here we discuss data from clinical trials assessing the effects of statins on stroke risk, as well as outline the mechanisms underlying the cholesterol-independent effects of statins and provide evidence-based recommendations for stroke prevention, based on achieved serum cholesterol levels in patients at risk of stroke.

Aged↗
PubMed2006

Drug insight: statins and gastrointestinal cancer.

Statins are popular lipid-lowering drugs that have had a great impact on the primary and secondary prevention of cardiovascular diseases. Basic and clinical research have also revealed that statins have biologic activities that go beyond lipid lowering, and suggest that they might have other therapeutic benefits. Perhaps the most exciting of these additional biologic effects is the finding that statins can exert an anticancer effect on cultured cancer cells, and in animal models. Clinical studies of statins for the treatment and prevention of cancer have, however, produced conflicting results. This review critically evaluates the current body of literature on the role of statins in the treatment and prevention of gastrointestinal cancers, with particular focus on clinical and observational studies.

Biliary Tract Neoplasms↗
PubMed2006

Statin therapy and autoimmune disease: from protein prenylation to immunomodulation.

Statins have been prescribed extensively for their cholesterol-lowering properties and efficacy in cardiovascular disease. However, compelling evidence now exists that statins also have extensive immunomodulatory properties that operate independently of lipid lowering. Consequently, much attention has been directed towards their potential as therapeutic agents for the treatment of autoimmune disease. Modulation of post-translational protein prenylation seems to be a key mechanism by which statins alter immune function. In this Review, the effect of statin therapy on immune function, and how this relates to the pathogenesis of autoimmune disease, is reviewed alongside current opinion of what the key biological targets of statins are.

Animals↗
PubMed2002

Statin use, hyperlipidaemia, and the risk of breast cancer.

Hydroxymethyl glutaryl coenzyme A inhibitors ("statins") are carcinogenic in rodents and an increased incidence of breast cancer was reported among pravastatin users in one randomised trial. We conducted a case-control study in the General Practice Research Database to evaluate the risk of breast cancer among 50- to 79-year old women treated with statins for hyperlipidaemia. Case and control women were matched by age, general practice, duration of prescription history in the General Practice Research Database, and index date. Adjusting for history of benign breast disease, body mass index, and use of hormone replacement therapy, women currently treated with statins had an estimated relative risk for breast cancer of 1.0 (95% confidence interval 0.6-1.6) compared to women without hyperlipidaemia. Untreated hyperlipidaemia was associated with an increased risk of breast cancer (estimated relative risk 1.6; 95% confidence interval 1.1-2.5). The estimated relative risk among women currently receiving only non-statin lipid-lowering drugs was similar to that of women with untreated hyperlipidaemia (1.8; 95% confidence interval 0.9-3.4). We found no evidence for an increasing trend in breast cancer risk with increasing duration of statin use (median duration 1.8 years, maximum 8.6 years).

Aged↗
PubMed2005

Effects of statins on vascular function of endothelin-1.

1. Although statins have been reported to inhibit the prepro-endothelin-1 (ET-1) gene transcription in endothelial cells, their effects on the vascular function of ET-1 have not been explored. We, therefore, examined the effects of statins on contraction and DNA synthesis mediated by ET-1 in vascular smooth muscle. The effects of statins on contraction induced by ET-1 were compared to those mediated by noradrenaline (NA) and KCl. 2. Simvastatin (SV) induced a concentration-dependent relaxation of tonic contraction mediated by ET-1 (10 nM) (IC50 value of 1.3 microM). The relaxation was also observed in rings precontracted with NA (0.1 microM) and KCl (60 mM). In contrast, pravastatin did not have any effect on the contractions. 3. Endothelial denudation or pretreatment with L-NAME did not prevent the relaxation, but did reduce the relaxant activity of SV. 4. SV prevented Rho activation caused by ET-1 and KCl in aortic homogenates, as assessed by a Rho pulldown assay. 5. The Rho kinase inhibitor HA-1077 mimicked the effects of SV on tonic contractions induced by ET-1, NA and KCl. 6. Pretreatment with the Kv channels inhibitor, 4-aminopyridine, attenuated the ability of SV to relax contractions mediated by ET-1 and NA. 7. In quiescent VSM cells, SV significantly inhibited DNA synthesis and Rho translocation stimulated by ET-1, as assessed by [3H]thymidine incorporation and Western blot, respectively. 8. Inhibition of Rho geranylgeranylation by GGTI-297, or treatment with HA-1077, mimicked the effects of SV on DNA synthesis stimulated by ET-1. 9. The results show that the statin potently inhibits both ET-1-mediated contraction and DNA synthesis via multiple mechanisms. Clinical benefits of statins may result, in part, from their effects on vascular function of ET-1.

Animals↗
PubMed2007

Statins induce S1P1 receptors and enhance endothelial nitric oxide production in response to high-density lipoproteins.

BACKGROUND AND PURPOSE: Sphingosine 1-phosphate (S1P) is a serum-borne naturally occurring sphingolipid, specifically enriched in high-density lipoprotein (HDL) fractions. S1P binds to G-protein-coupled S1P1 receptors to activate endothelial NO synthase (eNOS) in vascular endothelial cells. We explored whether and how statins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, modulate expression of S1P1 receptors and endothelial responses for subsequent stimulation with S1P or with HDL. EXPERIMENTAL APPROACH: Protein expression and phosphorylation and mRNA expression in cultured bovine aortic endothelial cells (BAEC) were determined using immunoblots and reverse transcription PCR analyses, respectively. NO synthesis was assessed as nitrite production. KEY RESULTS: Stimulation of BAEC with pitavastatin or atorvastatin led to significant increases in S1P1-receptors, at levels of protein and mRNA, in a dose-dependent manner. When BAEC were treated with pitavastatin prior to stimulation with S1P or with normal human HDL, phosphorylation and activation of eNOS evoked by S1P or by HDL was enhanced. These effects of statins were counteracted by L-mevalonate and were mimicked by an inhibitor of geranylgeranyl transferase I, suggesting that inhibition of HMG-CoA reductase activity and subsequent decreases in protein geranylgeranylation may contribute to these actions of statins. Specific knock down of S1P1 receptors by small interfering RNA led to attenuation of eNOS responses to HDL. CONCLUSIONS AND IMPLICATIONS: Statins induce S1P1 receptors and potentiate responses of endothelial cells to HDL-associated sphingolipids, identifying a novel aspect of the pleiotropic actions of statins through which they may exert NO-dependent vascular protective effects.

Alkyl and Aryl Transferases↗
PubMed2005

Protective effects of statins involving both eNOS and tPA in focal cerebral ischemia.

Previous studies have shown that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) protect the brain against ischemic injury by upregulating endothelial nitric oxide synthase (eNOS). Here, we tested the hypothesis that statins provide additional beneficial effects by also upregulating endogenous tissue plasminogen activator (tPA) and enhancing clot lysis in a mouse model of embolic focal ischemia. Heterologous blood clots (0.2 mm) were injected into the distal internal carotid artery to occlude blood flow in the middle cerebral artery territory after long-term (14 days) simvastatin, atorvastatin or vehicle treatment. Ischemic lesion volume, neurologic deficits, as well as residual blood clots were measured at 22 h. Reverse transcription-polymerase chain reaction assessed mRNA levels of eNOS, tPA, and the endogenous plasminogen activator inhibitor PAI-1. Ischemic lesion volumes and neurologic deficits were significantly reduced in wild-type mice by both simvastatin and atorvastatin. Statins increased eNOS and tPA mRNA levels but did not change mRNA levels of PAI-1. In eNOS knockout mice, atorvastatin reduced the volume of ischemic tissue and improved neurologic outcomes after arterial occlusion by blood clot emboli. In contrast, statins did not have protective effects in tPA knockout mice after embolic focal ischemia, but only in a filament model where focal ischemia was achieved via mechanical occlusion. These results suggest that statins protect against stroke by multiple mechanisms involving both eNOS and tPA. The involvement of each pathway may be revealed depending on the choice of experimental stroke model.

Animals↗
PubMed2003

Statins and their role in vascular protection.

The statins reduce cholesterol synthesis through inhibition of HMG-CoA (3-hydroxy-3-methylglutaryl-CoA) reductase and are widely prescribed for hyperlipidaemia to reduce the risk of atherosclerotic complications. The beneficial effect of lipid lowering by statins in the treatment of coronary heart disease has been demonstrated in large clinical trials. However, statins appear to have additional benefits on vascular function above and beyond their lipid lowering effects. Through inhibition of L-mevalonate synthesis, statins also prevent the synthesis of isoprenoid intermediates, including farnesylpyrophosphate and geranylgeranylpyrophosphate. Isoprenylation is important in the post-translational modification of a variety of proteins, including the small GTPases Rho, Rac and Ras, and hence plays an integral role in cellular signalling. Moreover, interference with isoprenylation underlies many of the beneficial actions of the statins on vascular endothelium, which include increased endothelial nitric oxide synthase expression, pro-angiogenic effects, increased fibrinolytic activity, immunomodulatory and anti-inflammatory actions, including increased resistance to complement. This has led to interest in the use of this class of drugs outside the realm of cardiovascular disease.

Aged↗
PubMed2004

Statins reduce oxidized low-density lipoprotein levels, but do not alter soluble intercellular cell-adhesion molecule-1 and vascular cell-adhesion molecule-1 levels in subjects with hypercholesterolaemia.

ICAM-1 (intercellular cell-adhesion molecule-1) and VCAM-1 (vascular cell-adhesion molecule-1) are cell-adhesion molecules that have an essential role in monocyte recruitment. In the present study we have investigated (i) whether statins reduce soluble levels of ICAM-1 (sICAM-1) and VCAM-1 (sVCAM-1), and the relationship between resistance of LDL (low-density lipoprotein) to in vitro oxidation and sICAM-1 and sVCAM-1 levels. Whole blood samples were obtained from 55 healthy non-smoking adults (aged 35-65 years) with moderate (LDL-cholesterol, 3.4-4.9 mmol/l) hypercholesterolaemia participating in a randomized double-blinded, 8-week trial comparing pravastatin (40 mg), simvastatin (20 and 80 mg) and placebo. sICAM-1 levels (means+/-S.D.) increased slightly from 12.2+/-4.2 to 13.6+/-4.2 ng/ml with statin therapy, whereas, among placebo-assigned subjects, levels were unchanged (11.8+/-5.0 and 11.8+/-3.9 ng/ml). sVCAM-1 increased from 18.9+/-10.1 to 21.1+/-7.4 ng/ml among those on active therapy and slightly declined with placebo assignment (19.8+/-8.8 to 19.4+/-6.4 ng/ml). Lag times increased with statin therapy from 74.3+/-39.8 min to 98.3+/-57.8 min ( P =0.003), and were unchanged in the placebo group (from 103.1+/-61.1 to 90.8+/-65.9 min; P =0.48). There were no significant changes between statin and placebo therapy for sICAM-1, sVCAM-1 or lag times ( P =0.09, 0.16 and 0.067 respectively). Changes in sICAM-1 and sVCAM-1 were not correlated with the change in lag times. In contrast with the known effects of oxidized LDL on gene activation of ICAM-1 and VCAM-1, lag times did not correlate with sICAM-1 and sVCAM-1. Statin therapy improved lag times, but has no effect on sICAM-1 or sVCAM-1 levels.

Adult↗
PubMed2002

High persistence of statin use in a Danish population: compliance study 1993-1998.

AIMS: Several studies have found that compliance with lipid-lowering drug (LLD) treatment is low. However, the results of these studies were based on crude measures of compliance. The aim of this study was to describe compliance with statin treatment by analysing prescription patterns on an individual level in a population-based prescription database over a 6 year period. METHODS: For incident statin users, all prescriptions for statins and drugs indicating cardiovascular disease or diabetes were retrieved from the OPED prescription database covering a population of about 470,000 inhabitants. Treatment was considered discontinued if the interval between two prescriptions exceeded number of tablets prescribed, plus 30 days. Compliance was assessed in terms of persistence and continuity. Persistence was defined as the period from the first prescription date to the date of discontinuation. Continuity was defined as the number of days with treatment (=number of tablets) divided by the total number of days in the period of persistence. RESULTS: 11% of the study cohort only received a single statin prescription. Survival analyses revealed a median persistence of 41 months. Less than 15% of the patients had more than 20% days without therapy within the period of persistence. Patients under 45 years without drug indicators of cardiovascular disease or diabetes presented the lowest compliance. CONCLUSIONS: The study showed good compliance with statin treatment in terms of persistence and continuity. A high percentage of the youngest patients, however, seemed to discontinue treatment before obtaining the full benefit in terms of decreased risk of coronary heart morbidity and mortality.

Adolescent↗
PubMed2003

Developing prevalence-based prescribing units for analysing variations in general practitioner prescribing: a case study using statins.

OBJECTIVE: To develop regionally specific prevalence-, age- and sex-standardized prescribing units (PASS-PUs) and to relate these to statin prescribing. DESIGN: Cross-sectional. SETTING: Ninety-four general practitioner (GP) practices within one health authority in the north-west of England. MAIN OUTCOME MEASURES: Comparisons between specific therapeutic group age-sex-related prescribing units (STAR-PUs) and PASS-PUs for statin prescribing. RESULTS: STAR-PUs and PASS-PUs were calculated for all GP practices and there was a high degree of correlation (Spearman's rank coefficient 0.88; P < 0.001). Using actual prescribing data for statins for a 12-month period, a statistically significant correlation was found between net ingredient cost per patient and STAR-PUs per patient (Spearman's rank coefficient 0.36; P < 0.01). However, the correlation between average daily quantities per patient and PASS-PUs per patient was not statistically significant. A scatter plot revealed a pattern whereby GP practices with high proportions of patients aged over 75 years exhibited low statin prescribing in relation to the expected prevalence of treated coronary heart disease (CHD) in their patient population. CONCLUSIONS: Low weightings for patients aged over 75 years in calculating STAR-PUs lead to a much lower number of prescribing units within GP practice populations when compared with PASS-PUs. Current statin prescribing across GP practices in this study correlates with national prescribing cost patterns (as measured by STAR-PUs) although not with expected prevalence of treated CHD (as measured by PASS-PUs). PASS-PUs reflect prevalence of treated CHD and may therefore be used to monitor and predict GP prescribing arising from the implementation of the National Service Framework targets for CHD. In addition, PASS-PUs maybe derived for a wide range of therapeutic areas.

Adolescent↗
PubMed2003

[Non-lipid effects of statins: myth or fact?].

Hydroxy-methylglutaryl coenzyme A reductase-inhibitors (HMG-CoA [statins]) are currently the most effective method to pharmacologically decrease total plasma cholesterol levels. A number of multicenter studies have demonstrated, that statins administered for several years lead to a significant reduction of cardiovascular events and mortality compared with placebo. Apart from the well known LDL- and cholesterol lowering effect, statins have been postulated to exert beneficial effects on mortality due to so called 'non-lipid effects'. There is circumstantial evidence from a number of experimental studies that statins can improve endothelial function, exert anti-inflammatory and anti-oxidative effects, stabilize arteriosclerotic plaque and inhibit proliferation and activation of smooth muscle cells. However, the clinical implications of these beneficial 'non-lipid effects' are unclear, but appear to exert only a minor role in comparison to the lowering effect of statins on total plasma cholesterol levels.

Animals↗
PubMed2003

[Are statins of value in therapy of osteoporosis?].

The statins do not only lower cholesterol. They may have also many other positive effects. The effects beyond lipid reduction are called pleiotropic effects. One of the most interesting points is the relationship between the statins and osteoporosis. They may stimulate bone formation and as a consequence they may reduce the risk of fracture. In the past years several studies were published concerning this topic. A number of observational studies found a decreased incidence of fractures among patients who take statins, but other studies did not. Prospective randomized controlled studies are necessary to exclude the possibility of unmeasured confounding variables. At the moment we have not enough data to give an answer to the question, if statins are a usefull opportunity in the treatment of osteoporosis. What we know now is, that the statins may be an interesting drug in the future for the treatment of osteoporosis, although many things are unclear, such as the right dose or the duration of treatment.

Aged↗