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Lipitor (Atorvastatin)

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Generic Lipitor is an extremely strong medical preparation which is taken in treatment of high cholesterol diseases. Generic Lipitor can also be helpful for patients with heart complications caused by type 2 diabetes or coronary heart disease. Generic Lipitor acts as an anti-high cholesterol remedy.

Other names for this medication:

Similar Products:
Atorlip-10, Atorlip-20, Atorlip-5


Also known as:  Atorvastatin.


Generic Lipitor is made by highly educated specialists to combat high cholesterol diseases (heart attack, stroke). Target of Generic Lipitor is to control and decrease level of cholesterol.

Generic Lipitor acts as an anti-high cholesterol remedy. Generic Lipitor operates by reducing decrease level of cholesterol.

Lipitor is also known as Atorvastatin, Atorbest, Agitor, Attor, Atorlip, Lipvas, Sortis, Torvast, Torvacard, Totalip, Tulip.

Generic Lipitor is HMG-CoA reductase inhibitor (statin).

Generic name of Generic Lipitor is Atorvastatin.

Brand name of Generic Lipitor is Lipitor.


Generic Lipitor can be taken in tablets. You should take it by mouth.

It is better to take Generic Lipitor once a day at the same time with meals or without it.

If you want to achieve most effective results do not stop taking Generic Lipitor suddenly.


If you overdose Generic Lipitor and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 20 to 25 degrees C (68 to 77 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Lipitor are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Lipitor if you are allergic to Generic Lipitor components.

Be careful with Generic Lipitor if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Lipitor can ham your baby.

Be careful with Generic Lipitor usage in case of having liver disease.

Be careful with Generic Lipitor in case of taking erythromycin (E.E.S., E-Mycin, Erythrocin); cimetidine (Tagamet); ketoconazole (Nizoral) and itraconazole (Sporanox); spironolactone (Aldactone); oral contraceptives (birth control pills); cyclosporine (Neoral, Sandimmune); digoxin (Lanoxin); cholesterol-lowering medications as fenofibrate (Tricor), gemfibrozil (Lopid), and niacin (nicotinic acid, Niacor, Niaspan).

Use Generic Lipitor with great care in case you want to undergo an operation (dental or any other).

If you experience drowsiness and dizziness while taking Generic Lipitor you should avoid any activities such as driving or operating machinery.

Avoid alcohol.

Elderly people should be very careful with Generic Lipitor.

Keep low-cholesterol and low-fat diet.

Do not stop taking Generic Lipitor suddenly.

lipitor user reviews

There is extensive but controversial evidence on the diverse effects of statins on the level of high-density lipoprotein cholesterol (HDL-C). Some of these effects may limit the benefits of statins in terms of cardiovascular risk reduction. To identify the conditions for beneficial effects, this study investigated the response to atorvastatin and simvastatin treatment in type 2 diabetic patients with elevated low-density lipoprotein cholesterol (LDL-C).

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Chronic subdural haematoma (CSDH) is a common neurosurgical condition. Burr-hole for drainage is an effective treatment. However, recurrence can be up to 8-33% and is associated with morbidities and mortalities. The underlying pathogenesis was postulated to be localised inflammation and pathological aberrant vessels formation. Atorvastatin, an HMG-CoA reductase inhibitor, is a type of lipid-lowering medication. In animal studies and a preliminary clinical trial, Atorvastatin was shown to be effective in the treatment of CSDH. It was found to inhibit inflammation and promote vascular maturation at the neomembrane of CSDH. Our study aimed to investigate the efficacy of Atorvastatin in CSDH. During the study period from January to December 2014, Atorvastatin was used in 12 CSDH patients with Glasgow Coma Scale (GCS) 13-15 or Markwalder's Grading Scale (MGS) Grade 0-2. They were retrospectively compared with GCS- and MGS-matched controls who had not used statin. Improvement with haematoma resolution at 3 months was 75% (9/12) for the Atorvastatin group, versus 42% (5/12) for the Control group (p = 0.0977). The risk of deterioration requiring burr-hole drainage was 16.7% (2/12) in the Atorvastatin group, versus 58.3% (7/12) in the Control group (p = 0.0447). The Odds Ratio (OR) of deterioration requiring burr-hole drainage with Atorvastatin was 0.143 (95%CI: 0.021-0.958), which favours the use of Atorvastatin in CSDH (p = 0.0451). The Number needed to treat (NNT) was 2.4 (p = 0.0447; 95%CI: 1.31-14.93). In conclusion, this retrospective cohort comparison study has shown that CSDH with Atorvastatin had a lower rate of deterioration and burr-hole drainage.

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This study assessed atorvastatin safety among Asian patients enrolled in 58 randomized clinical trials.

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A progressive reduction in the benefit of intensive LLT with atorvastatin 80 mg over pravastatin 40 mg occurred in statin-naïve ACS patients as baseline LDL-C declined. (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 [PROVE IT-TIMI 22]; NCT00382460).

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Statins are used for treatment of hypercholestremia. Common adverse reports associated with use of statins are generalized bodyache, rhabdomyolysis, muscles weakness and gastrointestinal disorders. The current work is an attempt to explain how smooth muscles of gastrointestinal tissues are affected by the current statins (Simvastatin, atorvastatin, fluvastatin and rosuvastatin).

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The addition of low-dose sirolimus to enalapril and statin is safe, stabilizes renal function and reduces glomerular proliferative lesions in patients with poor prognosis IgA nephropathy.

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NCB-02 had a favourable effect, comparable to that of atorvastatin, on endothelial dysfunction in association with reductions in inflammatory cytokines and markers of oxidative stress. Further studies are needed to evaluate the potential long-term effects of NCB-02 and its combination with other herbal antioxidants.

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The ATP-binding-cassette transporter A1 (ABCA1) plays an essential role in cellular cholesterol efflux and helps prevent macrophages from becoming foam cells. The statins are widely used as cholesterol-lowering agents and have other anti-atherogenic actions. We tested the effects of four different statins (fluvastatin, atorvastatin, simvastatin, and lovastatin) on ABCA1 expression in macrophages in vitro. The statins suppressed ABCA1 mRNA expression in RAW246.7 and THP-1 macrophage cell lines and in mouse peritoneal macrophages. The effect was time- and dose-dependent and was abolished by the addition of the post-reductase product, mevalonate. These findings imply that there is a possible modulation of the well-known beneficial effects of the statins on the reverse cholesterol transport pathway.

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Cardiovascular event risk and mortality risk were used as outcomes. Statin efficacy at LDL-c and cardiovascular events levels lowering data was obtained from a systematic review of literature. A decision analytic model was developed to perform a cost-effectiveness analysis comparing atorvastatin 10mg/day and simvastatin 40 mg/day to placebo treatment in patients with dyslipidemia in Brazil. The target population of this study was a hypothetic cohort of men and women with a mean age of 50 years old and high risk of cardiovascular disease. The model includes only direct costs obtained from Ambulatory and Hospital Information System and Price Database of Brazilian Ministry of Health. The comparative cost-effectiveness analysis itself was done through Excel spreadsheets covering a 5 -years time horizon.

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The expected 5-yr decline in renal function was not observed. Estimated GFR improved in both treatment groups but was significantly greater with 80 mg than with 10 mg, suggesting this benefit may be dosage related.

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Three large secondary prevention studies have shown that, in patients with a history of cardiovascular disease, statin treatment reduces the risk of further events and lowers overall mortality. In these studies, total mortality was reduced by as much as 30% in high-risk groups and 22% in average-risk groups. However, these studies did not include patients immediately after the coronary event. There are many benefits to early intervention with statin therapy in patients with acute coronary syndromes, including reduction of the risk of a subsequent event, which is highest immediately after the index event. Early treatment may reduce this likelihood in the first months after a coronary event by stabilizing atherosclerotic plaques and improving endothelial function in addition to lowering low-density lipoprotein cholesterol levels. This article reviews the case for early statin therapy in patients with a history of coronary heart disease. Results of clinical studies have now shown early statin therapy to be safe and cost-effective in reducing in-hospital and 6-month mortality.

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The focus of lipid-lowering therapy with drugs is prevention of complications of atherosclerosis. Landmark clinical trials have demonstrated that lowering low density lipoprotein cholesterol (LDL-C) may not only reduce coronary artery disease (CAD) risk but also may slow the progression and even induce regression of atherosclerosis in the coronary arteries. In addition, much attention has been given in recent years to the importance of triglyceride-rich lipoprotein (TRL) as a CAD risk factor, and the benefit of reducing plasma triglyceride levels and raising high density lipoprotein cholesterol (HDL-C) levels to prevent the recurrence of coronary events. Lipid-lowering drugs should be used within the framework of a systematic approach to treatment. Consideration must be given to the lipoprotein abnormality, the severity of disease, the role of combination therapy, and the spectrum of action of the drug and its pleiotropic effects (ie, effects beyond the expected action on lipoproteins). Five major agents have been used for the treatment of dyslipidemias. Three (resins, probucol and statins) target LDL-C, and two (fibrates and niacin) target primarily TRL and HDL-C. Fibrates and statins are the drugs of choice. Fibrates correct many abnormalities of lipoprotein metabolism in addition to having beneficial pleiotropic effects such as reducing fibrinogen and plasma viscosity. They inhibit the transcription of apolipoprotein (apo) CIII and enhance that of apoAI and lipoprotein lipase. Statins are safe and potent drugs for reducing LDL-C levels, and their efficacy in primary and secondary prevention of CAD has been amply demonstrated. They share a modes effect of raising HDL-C levels. Their pleiotropic effects, which include improvement of endothelial dysfunction, are numerous and may contribute to their spectacular beneficial effect of reducing CAD risk. They have effects that are complementary to those of fibrates, but the two drugs should be combined with caution because of the danger of myopathy. Atorvastatin is a major addition to this class of drugs because of its high efficacy and large spectrum of action. It lowers LDL-C levels effectively, not only in patients with severe forms of hypercholesterolemia but also in those with homozygous familial hypercholesterolemia. The effect of atorvastatin on LDL-C may be further enhanced by combining it with a resin. The ability of atorvastatin to lower triglyceride levels as well as LDL-C levels indicates that combined hyperlipidemia, a condition that, in the past, was best controlled with combination therapy, can now be treated with a single drug. It is also effective in patients with isolated hypertriglyceridemia and, although less potent than fenofibrate at reducing TRL and increasing HDL-C, it has a greater impact on the atherogenic risk ratios such as LDL-C:HDL-C. The profile of its pleiotropic effects is promising.

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Statins, HMG-CoA reductase inhibitors, are used widely in the treatment of hypercholesterolemia. Apart from lowering lipid levels, statins have been shown to have anti-inflammatory effects. Previously we showed that atorvastatin inhibits NF-kappaB activation, dose and time dependently, in LPS-TLR4 signaling pathway. In this study, we investigated the anti-inflammatory mechanism of atorvastatin via Toll-like receptor 4 (TLR4) in murine pro-B cell lines transfected with TLR4. Co-treatment of LPS-stimulated cells with both atorvastatin and mevalonate rescued NF-kappaB activation and TLR4 blockade demonstrated that atorvastatin does not exert its inhibitory effect via TLR4 receptor-ligand binding mechanism. Further investigation into the anti-inflammatory mechanism has shown that atorvastatin causes an impairment of TLR4 recruitment into the lipid raft thereby affecting anti-inflammatory responses. In contrast, mevalonate repaired lipid raft function leading to TLR4 clustering in the lipid raft. Together, these data suggest that atorvastatin exerts its anti-inflammatory effect via lipid raft modification. This novel finding offers another insight into the pleiotropic effects of atorvastatin and may be applicable to other pattern recognition receptors that utilize membrane lipid raft as a platform for signal transduction.

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In these 2 large, randomized clinical trials, carriers of the KIF6 719Arg allele were not at increased cardiovascular risk and did not obtain consistent cardiovascular benefit from high-dose statin therapy compared with noncarriers.

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Hematologic parameters such as mean platelet volume (MPV), red cell distribution width (RDW), and neutrophil to lymphocyte (N/L) ratio are associated with increased cardiovascular risk. We investigated the effect of atorvastatin on hematologic parameters in patients with hypercholesterolemia. A total of 79 patients with hypercholesterolemia and 47 normocholesterolemic healthy participants were included. Patients with hypercholesterolemia received 10 to 80 mg/d atorvastatin during a 24-week period. Hematologic parameters were measured at baseline and after 6 months. Atorvastatin treatment produced a significant decrease in MPV levels (9.3 ± 1.3 vs 9.1 ± 1.2 fL, P = .008) and platelet count (259 ± 61 vs 248 ± 51 10(9)/L, P = .005). The N/L ratio decreased significantly after atorvastatin treatment from 2.9 ± 1.2 to 2.6 ± 1.1, (P = .014). The RDW and platelet distribution width levels were not different among the study groups, before and after treatment. Atorvastatin may beneficially reduce MPV levels and N/L ratio. This antiplatelet and anti-inflammatory effect of atorvastatin treatment could play a role in reducing cardiovascular risk.

lipitor 300 mg

This was a post hoc analysis of a randomized, double-blind, 6-week study of adults 18-79 years with cardiovascular disease and diabetes mellitus with low-density lipoprotein cholesterol (LDL-C) ≥70 and ≤160 mg/dl. The percent change in LDL-C and other lipids was estimated within each subgroup separately. Safety and tolerability were assessed.

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The aim of this study was to compare the effect of atorvastatin treatment on high-grade yellow coronary plaques (grade ≥ 2, group H) vs. low-grade yellow plaques (grade ≤ 1, group L).

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Twenty three patients (mean age 61.4 ± 7.4 years, 87.0% men) were included in the study, of which 12 received high-dose atorvastatin prior to PCI. The mean number of EPC-CFUs before PCI was higher in patients treated with high-dose atorvastatin vs. low-dose statins (165.8 ± 58.8 vs. 111.7 ± 38.2 CFUs/plate, respectively, p < 0.001). However, 24 h after the PCI, the number of EPC-CFUs was similar (188.0 ± 85.3 vs. 192.9 ± 66.5 CFUs/plate in patients treated with high-dose atorvastatin vs. low- dose statins, respectively, p = 0.15). There were no statistical significant differences in FACS analyses between the 2 groups.

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Currently the apolipoprotein B:AI ratio integrates information about the potential for cardiovascular disease (CVD) risk reduction better than any other lipid or lipoprotein index. Certainly it could, with benefit, replace serum cholesterol and HDL cholesterol in the estimation of CVD risk. Defining the therapeutic target of statin therapy in terms of serum apolipoprotein B (apo B) rather than LDL cholesterol could also help to optimize statin treatment. Deciding whether a therapeutic response is adequate also requires knowledge of whether there is persisting hypertriglyceridaemia, because this gives an indication of whether small dense LDL is likely to have been satisfactorily reduced. Raising low levels of HDL, probably best measured as apo AI, may also prove to be an important aim of treatment. This is, however, a more complex issue and also depends on the mechanism by which a particular therapy alters HDL levels and on whether the capacity of HDL to perform its anti-inflammatory and antioxidative functions is restored. A meta-analysis of randomized clinical trials of statins in which apo B and apo AI have been reported could provide valuable information.

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Relative to non-2/2 haplotype (n = 23), subjects with the 2/2 haplotype (n = 14) had significantly increased plasma concentrations of total, LDL-cholesterol, and total apoB (P < 0.05). The fractional catabolic rate (FCR) of LDL-apoB was significantly lower in 2/2 subjects compared with non-2/2 subjects (P < 0.05), with an associated increase in LDL-apoB pool size in the former group. Sixteen subjects were then treated with 40 mg atorvastatin (6 weeks): 2/2 subjects (n = 8) had a significantly greater reduction in plasma concentrations of cholesterol and total apoB and in LDL-apoB pool size, as well as a greater increase in LDL-apoB FCR compared with non-2/2 subjects. There were no significant treatment-related between-haplotype differences in VLDL-apoB kinetics or in plasma concentrations of lathosterol and campesterol.

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Statins inhibit endogenous cholesterol synthesis, up-regulate low-density lipoprotein (LDL) receptor expression in mammalian liver cells, and thus decrease circulating LDL-cholesterol concentrations. As cholesterol seems to play a role in the development of neurodegenerative diseases, it is of interest to evaluate the effect of high dosages of statins (eg, atorvastatin or simvastatin) on brain cholesterol metabolism. Plasma samples from 44 participants (aged 30-69 years, 16 men and 18 women) of an earlier randomized, placebo-controlled, double-blind trial, who took 40 mg atorvastatin or 80 mg simvastatin daily for 2 months, were used to analyze total cholesterol, its precursor lathosterol, and its metabolites 24(S)-hydroxycholesterol and 27-hydroxycholesterol. Despite a significant decrease in absolute plasma concentrations of oxysterols, total cholesterol, and its endogenous synthesis rate, indicated by a decreased ratio of lathosterol to cholesterol, the plasma 24(S)-hydroxycholesterol to cholesterol ratio, a surrogate marker of brain cholesterol homeostasis, remained unchanged. Short-term high-dose atorvastatin and simvastatin treatment does not seem to influence brain cholesterol metabolism in patients with moderately elevated plasma cholesterol levels.

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Results from the PROVE IT trial suggest that patients with acute coronary syndrome (ACS) treated with atorvastatin 80 mg/day (A80) have significantly lower rates of cardiovascular events compared with patients treated with pravastatin 40 mg/day (P40). In a genetic post hoc substudy of the PROVE IT trial, the rate of event reduction was greater in carriers of the Trp719Arg variant in kinesin family member 6 protein (KIF6) than in noncarriers. We assessed the cost effectiveness of testing for the KIF6 variant followed by targeted statin therapy (KIF6 Testing) versus not testing patients (No Test) and treating them with P40 or A80 in the USA from a payer perspective.

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Between April 1991 and December 2003, we retrospectively evaluated 336 heart transplant patients (including 55 women) with regard to the occurrence of possible adverse effects of statins (rhabdomyolysis, myalgia, hepatotoxicity, high CK without muscle symptoms, and others). Resolution on reduction of dosage or discontinuance and/or change of statin were deemed to constitute confirmation of cause. Relations were sought between adverse effects and age, sex, immunosuppressive therapy, kidney failure, body mass index (BMI), arterial hypertension, and diabetes mellitus.

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Among the 16 860 patients, the mean age was 63 years and 74% were male. Overall, 78% of the patients had documented CHD, 40% had CVD, 5% had PAD and 21% reported more than one condition. The median time from initial diagnosis of vascular disease to screening was 18 months. At screening, the proportions who took various treatments were 83% for antiplatelet agents, 49% for beta-blockers, 47% for statins and 28% for angiotensin-converting enzyme inhibitors. The proportion treated with statin was much higher in CHD than in CVD or PAD patients (61% vs. 10% vs. 22% respectively) and decreased significantly with time from initial diagnosis. Simvastatin (mainly 20 mg) and atorvastatin (mainly 10 mg) each accounted for about 40% of total statin use.

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To examine how pharmacy bargaining activities affect reimbursement rates in Medicare Part D prescription drug plan (PDP) contracts, controlling for pharmacy quality attributes, market structures, and area socioeconomic status.

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The recently identified lipid-regulated group of ATP-binding cassette (ABC) transporters acts in various cells and tissues that are important for total body lipid homeostasis. ABCA1 and ABCG1 are key regulators of high-density lipoprotein (HDL) metabolism, acting as protective factors against the development of atherosclerosis. Recent data regarding how these ABC transporters control cholesterol and phospholipid homeostasis have provided valuable insights into the mechanisms of mRNA and protein expression, intracellular trafficking, surface membrane localization and interaction with binding partners and lipoproteins. These studies have identified several potential new targets, including nuclear receptors, ABCA1-interactive proteins and apolipoprotein A-I mimetics, which could be promising tools for raising HDL levels and improving the pharmacological treatment of cardiovascular disease.

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Exposure to ticagrelor and its active metabolite, AR-C124910XX, was generally unchanged by a single dose of either statin, except for a minor increase in ticagrelor C(max) in the presence of simvastatin. Effects of ticagrelor on atorvastatin pharmacokinetics were modest and unlikely clinically relevant, while with simvastatin, changes were slightly larger, and simvastatin doses >40 mg with ticagrelor should be avoided.

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lipitor 300 mg 2015-05-12

Pilot multicenter open-label prospective clinical study of 26 patients with diagnosis of AMD and the presence of many large, soft drusenoid deposits. Patients received 80 mg of atorvastatin daily and were monitored at baseline and every 3 buy lipitor online months with complete ophthalmologic exam, best corrected visual acuity (VA), fundus photographs, optical coherence tomography (OCT), and blood work (AST, ALT, CPK, total cholesterol, TSH, creatinine, as well as a pregnancy test for premenopausal women).

lipitor drug 2017-03-27

Compared with patients who had very short statins coverage (less than 6 months), those on 7-24, 25-48, and >48 months of coverage respectively had risk reductions of 15% (OR: 0.85; 95% CI: 0.74 to 0.98), 28% (OR: 0.72; 95% CI: 0.61 to 0.85), and 25% (OR: 0.75; 95% CI: 0.61 buy lipitor online to 0.94). Simvastatin and atorvastatin were both associated with a reduced risk of dementia, while no similar evidence was observed for fluvastatin and pravastatin.

lipitor 4 mg 2016-10-16

There is little information available on the benefits of selection of statins as upstream therapy for the prevention of paroxysmal atrial fibrillation (AF). We compared the efficacy and safety of atorvastatin (A-group, n = 43) and pravastatin (P-group, n = 41) as upstream therapy in patients with paroxysmal AF and dyslipidemia. A total of 84 patients (45 men, mean age, 66 ± 9 years, mean follow-up, 49 ± 32 months) were retrospectively assigned to receive atorvastatin (n = 41;10 mg/day) or pravastatin (n = 43 ; 10 mg/day). Survival rates free from AF recurrence at 1, 6, 12, and 24 months were 93%, 74%, 60%, and 53% in A-group, and 88%, 49%, 37%, and 29%, respectively, in P-group (P = 0.029, A-group versus P-group). Survival rates free from conversion to permanent AF at 12, 36, 60, and 90 months were 100%, 100%, 98%, and 95% in A-group, and 100%, 95%, 88%, and 83%, respectively, in P-group (P = 0.063, A-group versus P-group). Using a logistic regression model, atorvastatin was found to be associated with a significantly reduced risk of AF recurrence in comparison to pravastatin (unadjusted odds ratio [OR] = 0.27, 95% confidence interval 0.11-0.68, P = 0.005). This association remained significant after adjustment for potentially confounding variables (OR = 0.26, 95% CI 0.08-0.86, P buy lipitor online = 0.027). Using a logistic regression model, atorvastatin was not associated with a significantly reduced risk of converting to permanent AF in comparison to pravastatin (unadjusted OR = 0.29, 95% CI 0.05-1.50, P = 0.138), but this association did show a significant difference after adjustment for potentially confounding variables in a multivariate model (OR = 0.08, 95% CI 0.06-0.96, P = 0.046). Adverse effects requiring discontinuation of statins were observed in 1 case (2%, myalgia) in A-group, and 1 case (2%, elevation in CPK level ≥ 500 IU/L) in P-group, respectively (P = NS, A-group versus P-group). Atorvastatin, a lipophilic statin, was considered to be more effective in preventing recurrence of paroxysmal AF and conversion to permanent AF than pravastatin, a hydrophilic statin.

lipitor reviews webmd 2017-09-18

Recent evidence suggests that treatment of mild-to-moderate Alzheimer's disease (AD) with atorvastatin provides significant benefit on the Alzheimer Disease Assessment Scale-Cognitive ( buy lipitor online ADAS-cog) after 6 months.

lipitor missed dose 2017-01-20

Twenty-seven patients (mean age 61 +/- 8 years) with chronic cerebrovascular disease and hyperlipidaemia were included in the study. Serum lipid levels, haemorrheological parameters (haematocrit, plasma fibrinogen levels, plasma and whole blood viscosity [WBV] and red blood cell [RBC] aggregation and deformability) and platelet aggregation were assessed at baseline and after 1 and 3 months of treatment with buy lipitor online atorvastatin (Sortis) 10 mg/day. von Willebrand factor (vWF) activity (a measure of endothelial function) was measured at baseline and after 1 month of treatment. Adverse events were recorded at each visit. Physical examinations, haematological assessments and serum and urine chemistry assays were performed during the study.

lipitor brand name 2016-03-04

Along with a decrease in LDL level, the levels of DHEAS, testosterone, and estradiol decreased in both groups (p<0.001). While cortisol levels were maintained in the group given 10 mg of atorvastatin plus 10 mg of ezetimibe, it decreased significantly after the crossover to 80 mg of atorvastatin ( buy lipitor online p<0.001). The group initially given 80 mg of atorvastatin measured a lower level of cortisol for the first 3 months and it returned to normal levels after switching to 10 mg of atorvastatin plus 10 mg of ezetimibe.

lipitor reviews 2015 2017-01-08

The study included 31 men with LOH who had been treated for at least 6 months with atorvastatin (20-40mg daily). On the basis of patient preference, atorvastatin-treated patients were divided into two matched groups of patients: receiving intramuscular testosterone enanthate (100mg weekly, n=16) and not treated with this hormone (n=15). Plasma lipids, glucose homeostasis markers, as well as plasma levels of androgens, uric acid, high-sensitivity C-reactive protein (hsCRP), homocysteine, and fibrinogen were assessed before and after 4 months buy lipitor online of therapy.

lipitor 20mg dosage 2017-03-20

3-Hydroxy-3-methylglutaryl coenzyme-A reductase (HMGR) is generally regarded as targets for the treatment of hypercholesterolemia. HMGR inhibitors (more commonly known as statins) are discovered as plasma cholesterol lowering molecules. In this work, 120 atorvastatin analogues were studied using a combination of molecular modeling techniques including three-dimensional quantitative structure-activity relationship (3D-QSAR), molecular docking and molecular dynamics (MD) simulation. The results show that the best CoMFA (comparative molecular field analysis) model has q(2)=0.558 and r(2)=0.977, and the best CoMSIA (comparative molecular similarity indices analysis) model has q(2)=0.582 and r(2)=0.919. Molecular docking and MD simulation explored the binding relationship of the ligand and the receptor protein. The calculation results indicated that the hydrophobic and electrostatic fields play key roles in QSAR model. After MD buy lipitor online simulation, we found four vital residues (Lys735, Arg590, Asp690 and Asn686) and three hydrophobic regions in HMGR binding site. The calculation results show that atorvastatin analogues obtained by introduction of F atoms or gem-difluoro groups could obviously improve the inhibitory activity. The new HMGR inhibitor analogues design in this Letter had been submitted which is being currently synthesized by our laboratories.

lipitor medication 2015-01-25

These data indicate that patients with coronary heart disease and metabolic syndrome derive incremental benefit from buy lipitor online high-dose atorvastatin therapy, irrespective of the presence of diabetes.

lipitor 25 mg 2015-05-18

We evaluated 85 labels after excluding 11 ibuprofen buy lipitor online prescriptions that were filled with over-the-counter containers that lacked labels printed at the pharmacy. The pharmacy name or logo was the most prominent item on 71 (84%) of the labels, with a mean font size of 13.6 point. Font sizes were smaller for medication instructions (9.3 point), medication name (8.9 point), and warning and instruction stickers (6.5 point). Color, boldfacing, and highlighting were most often used to identify the pharmacy and items most useful to pharmacists. While the content of the main label was generally consistent, there was substantial variability in the content of instruction and warning stickers from different pharmacies, and independent pharmacies were less likely to use such stickers (P < .001). None of the ibuprofen containers were delivered with Food and Drug Administration-approved medication guides, as required by law.

lipitor dosage information 2017-03-15

Prospective studies indicate that baseline levels of C-reactive protein (CRP), the prototypic marker of inflammation, are associated with an increased risk for cardiovascular events. Limited studies have examined therapies that influence high-sensitive CRP (hs-CRP) levels, especially in hyperlipidemic patients. Thus, we tested the effects of 3 hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins), simvastatin (20 mg/d), pravastatin ( buy lipitor online 40 mg/d), and atorvastatin (10 mg/d), on levels of hs-CRP in a randomized, double-blind, crossover trial of 22 patients with combined hyperlipidemia (LDL cholesterol >130 mg/dL and triglycerides of 200 to 600 mg/dL).

lipitor dosage forms 2016-05-20

A tissue-based approach to in vitro drug screening allows for determination of the cumulative positive and negative effects of a drug at the tissue rather than the cellular or subcellular level. Skeletal muscle myoblasts were tissue-engineered into three-dimensional muscle with parallel myofibers generating directed forces. When grown buy lipitor online attached to two flexible micro-posts (mu posts) acting as artificial tendons in a 96-well plate format, the miniature bioartificial muscles (mBAMs) generated tetanic (active) forces upon electrical stimulation measured with a novel image-based motion detection system. mBAM myofiber hypertrophy and active force increased in response to insulin-like growth factor 1. In contrast, mBAM deterioration and weakness was observed with a cholesterol-lowering statin. The results described in this study demonstrate the integration of tissue engineering and biomechanical testing into a single platform for the screening of compounds affecting muscle strength.

lipitor normal dosage 2016-01-11

Statin initiators without a statin prescription during the 365 days preceding the initiation from 1 January 1998 through 31 December 2004 were captured from the nation-wide Prescription Register in Finland. Associations of demographic factors and morbidities with atorvastatin versus simvastatin at initiation of statin treatment were analysed by a logistic regression model adjusted for significant Trandate Drug Classification covariates separately for each year.

cut lipitor tablets 2015-12-05

There was no difference in CoQ10 levels from baseline to post-drug therapy for either P or A (0.61 +/- 0.14 vs 0.62 +/- 0.2 microg/mL and 0.65 +/- 0.22 vs 0.6 +/- 0.12 microg/mL, respectively; P >.05). There Neurontin Yellow Pill was a significant difference in low-density lipoprotein (LDL) levels from baseline to post-drug therapy for both P and A (97 +/- 21 vs 66 +/- 19 mg/dL and 102 +/- 21 vs 52 +/- 14 mg/dL, respectively; P <.01). There was no significant correlation between LDL and CoQ10.

lipitor 5mg dose 2016-12-01

A 41-year-old man presented with severe gastric ulceration 3 mo Anafranil 50 Mg after beginning treatment with atorvastatin 20 mg once daily for hypercholesterolemia. The patient was not taking any ulcerogenic drugs and had no evidence of Helicobacter pylori infection. Proton pump inhibitor therapy was initiated and atorvastatin was replaced by simvastatin with complete resolution of gastrointestinal symptoms. To our knowledge, this is the first report of atorvastatin-induced gastric ulceration, which should be looked for in patients who develop abdominal pain while on this drug.

lipitor 5 mg 2015-09-10

Periostin can promote rat VSMC migration and proliferation. Atorvastatin inhibition of periostin expression induced by TGF-β1 in VSMCs may be exerted by inhibition of the production of MVA and other isoprene compounds and by blocking the Rho/ Tegretol Iv Dose Rho kinase signaling pathway.

lipitor and alcohol 2015-11-17

Participants were randomly assigned to receive either atorvastatin 10 mg/day or matching placebo. Toddler Zantac Dosage Cognitive testing was performed in two sessions occurring 12 weeks apart and involved three repeated measures of attention and concentration.

lipitor drug interactions 2015-10-24

Patients with cardiovascular death or MI after 30 days (cases) had higher median [25th, 75th percentile] MRP-8 Cordarone 100 Tablet /14 levels than patients who remained free of recurrent events (5.6 [2.8, 13.5] mg/L vs 4.0 [1.9, 10.1] mg/L, P = .020). The risk of a recurrent cardiovascular event increased with each increasing quartile of MRP-8/14 (P-trend = 0.007) such that patients with the highest levels had a 2.0-fold increased odds (95% CI 1.1-3.6, P = .029) of a recurrent event after adjusting for standard risk indicators, randomized treatment, and C-reactive protein. Patients with elevated levels of MRP-8/14 and high-sensitivity C-reactive protein showed significantly increased risk of cardiovascular death or MI compared with patients with the lowest levels of both markers (adjusted odds ratio 2.1, 95% CI 1.2-3.8).

lipitor with alcohol 2017-06-14

The concentrations of Lopid Maximum Dose crospovidone (CP), maltodextrin and microcrystalline cellulose (MCC) have been optimized in the development of self-microemulsified tablets (SMET) to improve the oral bioavailability of an anti-hyperlipidemic drug, atorvastatin, and the in-vivo pharmacokinetic parameters of the optimized SMET were compared with those of a commercial tablet in rabbits.

lipitor 10mg tablet 2016-10-15

We conducted a post-hoc analysis of the St. Francis Heart Study treatment trial, a double-blind, placebo-controlled randomized controlled trial of atorvastatin (20 mg), vitamin C (1 g), and vitamin E (1000 U) daily, versus placebos in 990 asymptomatic individuals with CAC ≥ 80th percentile for age and gender. Primary cardiovascular outcomes included non-fatal Seroquel Bipolar Dosage myocardial infarction or coronary death, coronary revascularization, stroke, and peripheral arterial revascularization. We further stratified the treatment and placebo groups by eligibility (eligible when statin indicated) for statin therapy based on 2013 ACC/AHA guidelines and based on CAC categories.

lipitor 10mg dosage 2015-11-03

We conducted a randomized, double-blind, placebo-controlled study at a tertiary care setting in United Kingdom.