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Statins in acute coronary syndrome
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
A multi-centre, randomised, double-blind, placebo-controlled trial studied the effect of fluvastatin therapy initiated as first-line therapy of ACS (Fluvastatin in the Therapy of Acute Coronary Syndrome [FACS] trial) [11]. 156 hospitalised ACS patients were randomised to fluvastatin 80 mg or placebo. Fluvastatin therapy was associated with a significant reduction in the cardiovascular event rate at 1 year (11.5% vs. 24.4%; OR 0.40 [95% CI 0.17–0.95]; p = 0.038).
Cardiovascular Drugs
Published in Radhwan Nidal Al-Zidan, Drugs in Pregnancy, 2020
Risk Summary: The use of Fluvastatin is contraindicated during pregnancy due to the fact that Cholesterol and products synthesized by cholesterol are essential during fetal development. Moreover, the discontinuation of Fluvastatin during pregnancy should have no influence on the long-term treatment of hyperlipidemia.
Commonly prescribed drugs
Published in Alistair Burns, Michael A Horan, John E Clague, Gillian McLean, Geriatric Medicine for Old-Age Psychiatrists, 2005
Alistair Burns, Michael A Horan, John E Clague, Gillian McLean
The statins (atorvastatin, fluvastatin, pravastatin, rosuvastatin and simvas- tatin) inhibit one of the enzymes involved in cholesterol synthesis in the liver and are the most effective class of drugs in reducing low-density lipoproteins (LDLs) and cholesterol. There is good evidence that taking statins reduces myocardial infarction, cardiovascular episodes and mortality. They are now very widely used for the primary and secondary prevention of all cerebrovascular and cardiovascular events.
Statins-induced hepatotoxicity: still more questions than answers
Published in Expert Opinion on Drug Safety, 2020
Rubina Mulchandani, Tanica Lyngdoh, Ashish Kumar Kakkar
Clinically apparent liver injury is a rare adverse effect of statins [3,4] and elevations in serum transaminases are temporary, often occur during early stages of treatment, and resolve over time despite continued treatment in a majority of the cases [5,6]. At the same time, it is true that in rare cases, idiosyncratic hepatic injury could be severe and even lead to liver failure. However, evidence from recent systematic reviews and meta-analyses regarding hepatic effects of statins seems to be inconclusive so far. A few meta-analyses have concluded that statins when used in patients with pre-cirrhotic conditions and cirrhosis, can lower the risk of disease progression, decompensation, and hepatocellular carcinoma and may improve survival rates. They have also been shown to reduce portal hypertension and variceal hemorrhage in patients with cirrhosis [7–9]. On the contrary, another meta-analysis has demonstrated an increased risk of liver injury in statin users, especially among users of fluvastatin. It was shown that an increase in transaminases was higher among patients on a 40 mg daily dose. Additionally, negative effects were observed during the initial period of the intervention and evidence to describe long-term toxicity was not substantial [10].
Niosomal delivery of simvastatin to MDA-MB-231 cancer cells
Published in Drug Development and Industrial Pharmacy, 2020
Iman Akbarzadeh, Anita Saremi Poor, Soheila Yaghmaei, Dariush Norouzian, Hassan Noorbazargan, Samaneh Saffar, Reza Ahangari Cohan, Haleh Bakhshandeh
Statins including lovastatin, fluvastatin, atorvastatin, and simvastatin are a class of drugs that popularly used to decrease the cholesterol level in patients by inhibiting HMG-COA reductase enzyme, which plays a key role in the production of cholesterol in the liver [1]. Besides its role in cholesterol-lowering, statins have known as potential antitumor agents in colon, lung, and breast cancers [2,3]. Previous in vitro and in vivo studies have shown antitumor activity of simvastatin in different types of cancers such as breast, colon, and lung. Simvastatin inhibits cancer cells proliferation through cell cycle arrest, apoptosis, and necrosis induction [4]. Statins by competitively inhibiting HMG-COA reductase, the rate limiting enzyme of mevalonate pathway, simultaneously inhibit the production of both cholesterol and specific prenylated proteins [5]. This inhibition leads to a decreased level of mevalonate and various downstream intermediates such as dolichol, ubiquinone, farnesyl-pyrophosphate (FPP), and geranyl pyrophosphate (GPP) proteins [6,7]. GPP and FPP are essential for the post translational modifications of intracellular G-proteins including Ras and RhoA which promotes cellular functions such as cell signaling, protein synthesis, and cell cycle progression [8,9]. Therefore, HMG-COA reductase inhibition leads to a decrease in the proliferation of tumor cells [8–10].
Statin use and safety concerns: an overview of the past, present, and the future
Published in Expert Opinion on Drug Safety, 2020
Rubina Mulchandani, Tanica Lyngdoh, Ashish Kumar Kakkar
While lovastatin, simvastatin, and atorvastatin are metabolized mainly by CYP3A4 and CYP3A5, fluvastatin, rosuvastatin and to a lesser extent pitavastatin undergo oxidation through CYP2C9. Pravastatin, however, is largely excreted unchanged in the urine. Drugs that either inhibit or compete for CYP3A4 can, therefore, raise plasma concentration of corresponding statins viz. azole antifungals, macrolides, antiretroviral protease inhibitors, cyclosporine, nefazodone, amiodarone, cobicistat and its related formulations. Rosuvastatin, pravastatin, fluvastatin, and pitavastatin are therefore preferred when concomitant therapy with these agents cannot be avoided. The risk of statin-induced myopathy is also exacerbated when used with gemfibrozil or niacin. While the former inhibits hepatic uptake as well as metabolism of statins, niacin acts by greater inhibition of cholesterol biosynthesis in skeletal muscles. Fenofibrate is considered to be the preferred fibrate for combining with statin therapy. Calcium channel blockers – verapamil and diltiazem, when co-administered with simvastatin or lovastatin can result in moderate increase in statin exposure, and such combinations should be considered when potential benefits outweigh the risks in the opinion of the prescriber. However, for lovastatin and simvastatin, doses greater than 20 mg per day are not recommended when used along with amlodipine [118,119].