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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.

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We have recently reported that pre-treatment, but not the post-treatment with atorvastatin showed survival benefit and improved hemodynamic functions in cecal ligation and puncture (CLP) model of sepsis in mice. Here we examined whether combined treatment with atorvastatin and imipenem after onset of sepsis can prolong survival and improve vascular functions. At 6 and 18h after sepsis induction, treatment with atorvastatin plus imipenem, atorvastatin or imipenem alone or placebo was initiated. Ex vivo experiments were done on mouse aorta to examine the vascular reactivity to nor-adrenaline and acetylcholine and mRNA expressions of α1D AR, GRK2 and eNOS. Atorvastatin plus imipenem extended the survival time to 56.00±4.62h from 20.00±1.66h observed in CLP mice. The survival time with atorvastatin or imipenem alone was 20.50±1.89h and 27.00±4.09h, respectively. The combined treatment reversed the hyporeactivity to nor-adrenaline through preservation of α1D AR mRNA/protein expression and reversal of α1D AR desensitization mediated by GRK2/Gβγ pathway. The treatment also restored endothelium-dependent relaxation to ACh through restoration of aortic eNOS mRNA expression and NO availability. In conclusion, combined treatment with atorvastatin and imipenem exhibited survival benefit and improved vascular functions in septic mice.

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Pretreatment with atorvastatin significantly reduced the occurrence of postoperative AF after off-pump CABG.

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Myopathy is the most commonly reported adverse effect of statins. All statins are associated with myopathy, though with different rates. Rosuvastatin is a potent statin reported to induce myopathy comparable to earlier statins. However, in clinical practice most patients could tolerate rosuvastatin over other statins. This study aimed to evaluate the myopathic pattern of rosuvastatin in rats using biochemical, functional and histopathological examinations. The possible deleterious effects of rosuvastatin on muscle mitochondria were also examined. The obtained results were compared to myopathy induced by atorvastatin in equimolar dose. Results showed that rosuvastatin induced a rise in CK, a slight increase in myoglobin level together with mild muscle necrosis. Motor activity, assessed by rotarod, showed that rosuvastatin decreased rats' performance. All these manifestations were obviously mild compared to the prominent effects of atorvastatin. Parallel results were obtained in mitochondrial dysfunction parameters. Rosuvastatin only induced a slight increase in LDH and a minor decrease in ATP (∼14%) and pAkt (∼12%). On the other hand, atorvastatin induced an increase in LDH, lactate/pyruvate ratio and a pronounced decline in ATP (∼80%) and pAkt (∼65%). These findings showed that rosuvastatin was associated with mild myotoxic effects in rats, especially when compared to atorvastatin.

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The attempts to develop new treatments for acute ischemic stroke have been fraught with costly and spectacularly disappointing failures. Repurposing of safe, older drugs provides a lower risk alternative. Vascular protection is a novel strategy for improving stroke outcome. Promising targets for vascular protection after stroke have been identified, and several of these targets can be approached with "repurposed" old drugs, including statins, angiotensin receptor blockers (ARBs), and minocycline. We tested the vascular protection (ability to reduce hemorrhagic transformation) of three marketed drugs (candesartan, minocycline, and atorvastatin) in the experimental stroke model using three different rat strains [Wistar, spontaneously hypertensive rats (SHR) and type 2 diabetic Goto-Kakizaki (GK) rats]. All agents decreased the infarct size, improved the neurological outcome and decreased bleeding. Mechanisms identified include inhibition of MMP-9, activation of Akt, and increased expression of proangiogenic growth factors. Premorbid vascular damage (presence of either diabetes or hypertension) increased the likelihood of vascular injury after ischemia and reperfusion and improved the response to vascular protection.

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Atorvastatin 10 mg/day increases HDL-C more in patients with low pretreatment HDL-C levels, an effect that seems to be related to the hypotriglyceridemic activity of the drug.

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We investigated the effect of atorvastatin on cyclooxygenase (COX) contribution to endothelial dysfunction in spontaneously hypertensive rat (SHR) mesenteric resistance arteries. Atorvastatin (10 mg/kg per day, oral gavage) or its vehicle was administered for 2 weeks to male SHR or Wistar-Kyoto rats. Endothelial function of mesenteric arteries was assessed by pressurized myograph. In Wistar-Kyoto rats, relaxation to acetylcholine was inhibited by N(G)-nitro-L-arginine methyl ester and unaffected by SC-560 (COX-1 inhibitor), DuP-697 (COX-2 inhibitor), or ascorbic acid. In SHRs, the response to acetylcholine was attenuated, less sensitive to N(G)-nitro-L-arginine methyl ester, unaffected by SC-560, and enhanced by DuP-697 or SQ-29548 (thromboxane-prostanoid receptor antagonist) to a similar extent. Endothelium-dependent relaxation was normalized by ascorbic acid or apocynin (NADPH oxidase inhibitor), which also restored the inhibition by N(G)-nitro-L-arginine methyl ester. In atorvastatin-treated SHRs, relaxation to acetylcholine was normalized, fully sensitive to N(G)-nitro-L-arginine methyl ester, and not affected by SC-560, DuP-697, SQ 29548, or antioxidants. Dihydroethidium assay showed an increased intravascular superoxide generation in SHRs, which was abrogated by atorvastatin. RT-PCR revealed a COX-2 induction in SHR arteries, which was downregulated by atorvastatin. The release of prostacyclin and 8-isoprostane was higher from SHR than Wistar-Kyoto mesenteric vessels. COX-2 inhibition and apocynin decreased 8-isoprostane without affecting prostacyclin levels. Atorvastatin increased phosphorylated extracellular signal-regulated kinase 1/2, pAkt, peNOS(1177), and inducible NO synthase levels in SHR mesenteric vessels and decreased 8-isoprostane release. In conclusion, COX-2-derived 8-isoprostane contributes to endothelial dysfunction in SHR mesenteric arteries. Atorvastatin restores NO availability by increasing phosphorylated extracellular signal-regulated kinase 1/2, pAkt, peNOS(1177), and inducible NO synthase levels and by abrogating vascular NADPH oxidase-driven superoxide production, which also results in a downregulation of COX-2-dependent 8-isoprostane generation.

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Glycaemic control deteriorated in patients with diabetes following high-dose statin therapy. Future controlled studies are needed to verify these findings and, if confirmed, determine whether such changes represent a true decline in glycaemic control. Presently, it appears that, based on the overwhelming prospective trial data available, the preventive effect of statin therapy supersedes that of the slight increase in HbA(1c).

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The pharmacokinetic parameters of ATV were determined in Wistar rats after per-oral pre-treatment with CLZ for 7 days in order to assess the interaction potential between ATV and CLZ. In-vitro metabolic inhibition and everted gut sac studies were conducted to elucidate the mechanism of this interaction. Biochemistry analyser was used to estimate lipid profiles in Wistar rats. A validated LC-MS/MS method was employed to simultaneously quantify both ATV and CLZ in rat plasma matrix.

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The mean levels of total cholesterol, triglyceride, LDL-cholesterol, MDA and AuAb-oxLDL were decreased while HDL-cholesterol and TAS were increased significantly after lipid-lowering therapy in patients with dyslipidemia. On the other hand, PON activities in serum and HDL were increased significantly. The percentage increase in serum PON activity was associated significantly with the percentage decrease in serum AuAb-oxLDL (r=-0.32, P=0.047) and that of HDL PON activity was associated with the percentage increase in HDL-cholesterol level after atorvastatin therapy (r=0.52, P=0.001). The therapy was more effective in increasing PON activity in patients with HDL levels above 35 mg/dl.

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Four hundred and fifty-nine English and Scottish general practices contributing EHRs to a research database, of which 17 participated in the trials.

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Some recent clinical trials have concluded the following: Patients who need noncardiac surgery and who are at risk of major cardiac events should not undergo revascularization with the aim of achieving a better perioperative outcome. They should have an office evaluation only and be prescribed a beta-blocker, if indicated. Except for unusual, high-risk cases, patients at risk of stroke due to atherosclerotic carotid artery stenosis should undergo carotid endarterectomy rather than carotid stenting. Because the technology is still developing, however, carotid stenting may still be appropriate as part of a clinical trial. Although drug-eluting coronary stents reduce the risk of restenosis in the short-term, they pose a small but significant risk of in-stent thrombosis. Clopidogrel (Plavix) should be prescribed for at least a year following drug-eluting stent placement, and perhaps indefinitely. Patients with known coronary heart disease have better outcomes if they receive aggressive statin therapy (eg, atorvastatin [Lipitor] 80 mg/day) to lower their serum levels of low-density lipoprotein cholesterol to less than 70 mg/dL.

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We did a randomised, double-blind clinical trial in 325 patients with familial hypercholesterolaemia. Patients were given either atorvastatin 80 mg (n=160) or simvastatin 40 mg (n=165) daily, on an intent-to-treat basis. The primary endpoint was the change of carotid intima media thickness (IMT), as measured by quantitative B-mode ultrasound, over 2 years.

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lipitor 8 mg 2016-09-14

Until recently, the role of statin therapy in diabetic patients without clinical signs or symptoms of coronary heart disease had been inadequately defined. The Collaborative Atorvastatin Diabetes Study (CARDS) is a prospective, randomized, placebo-controlled trial designed to compare the effects of atorvastatin with placebo in preventing primary coronary events in diabetic patients. After a median of only 3.9 years (the study was terminated approximately 2 years early due to the magnitude of benefit attributable to atorvastatin therapy), risk for major cardiovascular events was decreased by 37%, acute coronary heart disease-related events were also reduced by 36%, coronary revascularizations by 31%, and stroke by 48%. Benefit emerged within 1 year of initiating Cefixime Dose Uses therapy.

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The PON1 phenotype may be a novel predictive factor for the effectiveness of statin treatment on PON1 activity and serum lipid levels; however, different types of statins may exert different effects on these parameters. Celebrex High Dose

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While waiting for data from ongoing large clinical randomized trials to definitively outline the role of aspirin in Suprax Tab 400mg primary prevention, our study shows that among diabetic patients without previous vascular events, statins but not aspirin reduce thrombotic risk assessed by TG.

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Hypercholesterolaemia exacerbated LV remodelling and dysfunction in post-MI rat hearts and upregulated cardiac AT1 receptors. All these effects were effectively prevented by atorvastatin. Thus, the pleiotropic statin effects may include interference with the renin-angiotensin system through Deltasone Drug Information downregulation of AT1 receptors.

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Statin therapy in HC patients with normal endothelial function does Norvasc Pill Identifier not augment endothelial function.

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Lipid abnormalities, and especially hypertriglyceridaemia, are a prominent feature of peritoneal dialysis (PD) patients. The results from several studies have shown that statins are effective and safe lipid-lowering agents in these individuals. Besides lipid lowering, current evidence suggests that these agents Cleocin 450 Mg exert multiple beneficial effects on PD patients. Statins may maintain residual kidney function by altering the response of the kidneys to dyslipidaemia and, thus, slow the progression of renal failure in PD patients. Also, statins may reduce the incidence of cardiovascular events, as well as morbidity and mortality rates in this high-risk group. However, despite the multiple beneficial effects, PD patients receive suboptimal statin treatment. Apart from the German Dialysis and Diabetes (4D) study, no other prospective, randomised controlled trial has investigated the effects of statin treatment on dialysis patients. The results of large-scale, multi-centre randomised controlled studies (such as AURORA and SHARP) are expected to define the role of statin therapy in this high-risk population.

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This retrospective database study included patients with Cytoxan Tablets a prescription for atorvastatin monotherapy between November 30, 2008, and November 30, 2011, with the index date defined as the first atorvastatin prescription during this period. Eligible high-risk patients with evidence of coronary heart disease (CHD), atherosclerotic vascular disease (AVD), diabetes mellitus (DM), or familial hypercholesterolemia (FH) were required to have ≥1 TC and LDL-C measurement between 3 and 12 months after the index date, and continuous enrollment 1 year before and 1 year after the index date. Cholesterol levels were assessed using the National Institute for Health and Care Excellence (NICE) guidelines: TC <4.0 mmol/L or LDL-C <2.0 mmol/L.

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A total of 10,001 patients with CHD were randomized to double-blind therapy with atorvastatin 80 mg/day Buy Generic Cialis Online Australia or 10 mg/day. Patients with CKD were identified at baseline on the basis of an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m(2) using the Modification of Diet in Renal Disease equation. The primary efficacy outcome was time to first major cardiovascular event.

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BACKGROUND Is the timing of dosing for amlodipine and atorvastatin important with regard to therapeutic efficacy? To answer this question, we designed an outpatient, practice-based, case-control study lasting 8 weeks. MATERIAL AND METHODS Two hundred patients were Arava Tablet divided into 2 groups: in Group I, patients were provided with a single pill containing amlodipine/atorvastatin (5/20 mg) to be taken each night at 10 pm, and in Group II, patients were taking amlodipine (5 mg) and atorvastatin (20 mg) each morning at 7 am. RESULTS Our results indicated no obvious difference in blood pressure control between the 2 groups. Taking amlodipine at night not only lowered blood pressure, but it also provided better control during the peak blood pressure in the morning. Hypercholesterolemia control in the 2 groups was also not significantly different, taking atorvastatin in the morning was as effective as dosing at night in patients with hypercholesterolemia. While the carotid IMT, hs-CRP, and LVMI were significantly lower after treatment, no differences were found between the 2 groups. Although no obvious difference was found in adverse drug reactions between the 2 groups, compliance was much better in the single-pill group than in patients taking the 2 medications separately. CONCLUSIONS In conclusion, single-pill amlodipine-atorvastatin taken at night can lower blood pressure and reduce the morning peak blood pressure levels the next day. Additionally, this dosing method could improve patient adherence to the therapy.

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Across Europe there was a significant reduction in the Compare Buspar Prices cost of maintaining patients at their appropriate LDL-C levels with simvastatin versus atorvastatin. The results of this analysis, along with the proven clinical benefits of simvastatin, support the use of this drug as the treatment of choice in the secondary prevention of CHD.

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CFR increased significantly in both groups during the 8-month follow-up. The 8-month increases from baseline in CFR were significantly greater in the ATOR40 group than in the ATOR10 group (0.99+/-0.69 vs 0.55+/-0.47, p=0.017, respectively). The serial increases in the absolute number of CD34+ and CXCR4+ cells were significantly greater in the ATOR40 group, especially at 24 h after the procedure (two-way repeated-measures analysis of variance: p=0.046 and p=0.022, respectively). Decreases from baseline for interleukin 6 (-2.94+/-3.31 vs -1.52+/-2.82 pg/ml), tumour necrosis factor alpha (-1.31+/-2.96 vs -0.01+/- Zyrtec D Dosage Child 1.29 pg/ml), soluble intercellular adhesion molecule-1 (-71+/-95 vs 37+/-83 ng/ml) and soluble vascular cell adhesion molecule-1 (-51+/-364 vs 190+/-204 ng/ml) were significantly greater in the ATOR40 group.