What Is Atorvastatin (Lipitor) and How Does It Work?Atorvastatin (Lipitor) is a medication prescribed by a doctor to lower cholesterol in people who have been diagnosed with high cholesterol (high levels of cholesterol in the blood). Doctors diagnose high cholesterol through a simple blood test. Cholesterol (and triglycerides) are fats that are made in your body. While some cholesterol is necessary for the body, too much cholesterol is dangerous to your health. Cholesterol, specifically, is made in the liver. Lowering "bad" cholesterol and triglycerides and raising "good" cholesterol decreases the risk of heart disease and helps prevent strokes and heart attacks This drug can also lower the risk for heart attack or stroke in patients with diabetes. Note: Some research has shown a possible relationship between the use of statins and the risk of diabetes, however, the risk of developing diabetes from the use of statins is very small. About Cholesterol and StatinsThis medication is used along with a proper diet to help people lower "bad" cholesterol and fats (such as LDL(low-density lipoprotein), triglycerides) and raise "good" cholesterol (HDL) in the blood. It belongs to a group of drugs known as "statins." Statins (also HMG-CoA reductase inhibitors) like this medication work by reducing the amount of cholesterol found in the blood. Statins are safe medication for most people. It is important to note that statins are not recommended for pregnant patients or people with active or chronic liver disease. Also, statins can cause serious muscle problems. Some statins interact negatively with other drugs, so it is important that your doctor knows all the medicines that you are taking. If you have problems (such as pain or other symptoms) with one particular prescription statin, you may have fewer side effects with an alternative statin drug. Your doctor may prescribe an alternative medication to see if you feel better or notice a difference. Doctors commonly prescribe statins like Lipitor because of their ability to lower cholesterol levels and risks of cardiovascular events. Patients should closely follow the instructions included on the prescription label to ensure the effectiveness of the medicine. Due to changes and updates, patients should read the health information that accompanies this medicine each and every time this prescription is filled. In addition to eating a proper diet for optimal health (such as low cholesterol and a low-fat diet), there are other lifestyle changes that people can make that may help this medication work better. These include exercising, weight loss, and stopping smoking. Consult your doctor for more details and medical information about this drug and for medical advice about your health while taking this drug. This medication is only available by prescription. Atorvastatin is available under the following different brand names: Lipitor. HMG-CoA reductase inhibitors (statins) are lipid-lowering medications used in the primary and secondary prevention of coronary heart disease. This activity reviews the indications, contraindications, and mechanism of action of atorvastatin to manage coronary heart disease and familial dyslipidemias, covering the indications, contraindications, activity, adverse events, and other key elements of atorvastatin therapy. This activity also highlights the critical role of the interprofessional team in the management of patients with clinically significant atherosclerotic cardiovascular disease or individuals with risk factors for heart disease who can benefit from statin therapy. Objectives:
In combination with dietary modifications, atorvastatin is FDA approved to prevent cardiovascular events in patients with cardiac risk factors and for patients with abnormal lipid profiles.[1] Primary prevention: For patients without coronary heart disease but with multiple risk factors, the FDA has approved atorvastatin to reduce the risk of myocardial infarction, stroke, revascularization procedures, and angina. For patients diagnosed with type 2 diabetes mellitus without coronary heart disease but with multiple risk factors, atorvastatin has FDA approval to reduce the risk of myocardial infarction and stroke. Secondary prevention: For patients with coronary heart disease, atorvastatin has approval as a therapy to reduce the risk of non-fatal myocardial infarction, fatal and non-fatal stroke, revascularization procedures, hospitalizations for congestive heart failure, and angina. Atorvastatin has FDA approval for the treatment of the following dyslipidemias:
Atorvastatin has not been studied in Fredrickson Type I and V dyslipidemias. Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase.[2] By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver. Atorvastatin also increases the number of LDL receptors on the surface of hepatic cells. In patients with homozygous or heterozygous familial hypercholesterolemia, mixed dyslipidemia, isolated hypertriglyceridemia, or nonfamilial hypercholesterolemia, atorvastatin has been shown to reduce total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (apo B), very-low-density lipoprotein (VLDL-C) and triglycerides (TGs) while increasing high-density lipoprotein cholesterol (HDL-C). In patients with dysbetalipoproteinemia, atorvastatin has been shown to decrease intermediate-density lipoprotein (IDL-C). Pharmacokinetics [3] Absorption Atorvastatin is rapidly absorbed after oral administration with a peak plasma concentration at 1 to 2 hours. The bioavailability is low at 14% due to extensive first-pass metabolism. Distribution Atorvastatin is highly plasma protein bound (over 98%) and has a volume of distribution of about 380 liters. Metabolism Atorvastatin is metabolized by cytochrome P450 3A4 (CYP3A4) to active ortho- and para-hydroxylated metabolites. Excretion Atorvastatin and its metabolites get eliminated in bile. Atorvastatin is not known to go through enterohepatic recirculation. The half-life of atorvastatin is about 14 hours, while its active metabolites have a half-life of about 20 to 30 hours. Atorvastatin is available as atorvastatin calcium tablets in strengths of 10, 20, 40, and 80 mg. This medication can be administered with or without food and should be taken at the same time every day. It is generally recommended to administer statins at bedtime since endogenous cholesterol synthesis is cyclical, with the highest production levels during fasting, as at night. However, the longer half-life of atorvastatin compared to other shorter half-life statins (e.g., lovastatin, fluvastatin, and simvastatin) offers greater flexibility regarding dosing times. Adult Dosing The dosing of atorvastatin can have its basis in LDL-C lowering ability (intensity), or doses are titratable to specific lipid goals. The American College of Cardiology/American Heart Association Guidelines recommends either moderate intensity (atorvastatin 10 to 20 mg) or high intensity (atorvastatin 40 to 80 mg) therapy depending on the statin benefit group to which a patient belongs. Moderate intensity statins should lower LDL-C by about 30 to 50%, while high-intensity statins should lower LDL-C by over 50 %.[4] Both the National Lipid Association and the American Association of Clinical Endocrinologists recommend utilizing statin therapy to reach specific lipid goals based on atherosclerotic cardiovascular disease risk.[5][6] Pediatrics Doses above 20 mg do not have study data for pediatric patients with heterozygous familial hypercholesterolemia. Doses up to 80 mg have been used in a limited number of pediatric patients with familial hypercholesterolemia. Studies have not evaluated atorvastatin use in pre-pubescent patients or those under ten years old. Geriatrics Patients over 65 years old may have higher plasma concentrations of atorvastatin when compared to young adults. Older patients may be at increased risk of statin-induced myopathies. Renal Impairment Atorvastatin and its metabolites do not undergo renal elimination, so no dose adjustments are required with reduced renal function. Hemodialysis will not likely remove atorvastatin due to plasma protein binding. Hepatic Impairment Increased plasma concentrations of atorvastatin have occurred in patients with chronic alcoholic liver disease. Drug exposure is four times higher in patients with Child-Pugh Class A and 11x higher in patients with Child-Pugh Class B. Atorvastatin is contraindicated in patients with active liver disease.[7] Drug Interactions [8] The use of atorvastatin with potent CYP3A4 inhibitors can lead to increased plasma concentrations, which may enhance adverse events, including myopathies. OATP1B1 inhibitors can increase the bioavailability of atorvastatin.[9] CYP3A4 inducers may cause decreased plasma concentrations of atorvastatin. Patients taking digoxin should undergo monitoring when starting atorvastatin as plasma concentrations of digoxin may increase. Atorvastatin may also increase drug exposure of norethindrone and ethinyl estradiol. Common adverse effects for patients taking atorvastatin include arthralgia, dyspepsia, diarrhea, nausea, nasopharyngitis, insomnia, urinary tract infection, and pain in extremities. Myopathies have occurred in patients taking atorvastatin, including muscle aches, muscle tenderness, or muscle weakness, with elevated creatine phosphokinase greater than ten times the upper limit of normal. Rhabdomyolysis has been reported in patients using atorvastatin.[10] Patients with impaired renal function may be at increased risk of developing rhabdomyolysis. Using atorvastatin in combination with other medications that increase atorvastatin plasma concentrations increases the risk for myopathies and rhabdomyolysis.[11] Management of statin-induced myopathies includes temporarily holding therapy, switching to an alternative statin, or reducing the dose. Some data suggest that statins may increase the risk of developing diabetes mellitus. In 2012, the FDA added safety label changes to statin safety labeling, indicating that they have been shown to increase glycosylated hemoglobin and fasting serum glucose.[12] The ACC/AHA guidelines group and other experts state that the risk-reducing benefits of statin therapy outweigh the generally mild rise in serum glucose levels or new-onset diabetes.[13] Clinicians are encouraged to use this opportunity to discuss healthy lifestyle measures with their patients, including weight loss, engaging in an exercise program, and consuming a healthy diet. Atorvastatin can cause liver function test abnormalities.[7] If patients develop serum transaminases over three times the upper limit of normal, plasma concentrations require more frequent monitoring until normalized, or atorvastatin therapy should undergo dose reduction or be discontinued. Atorvastatin contraindications include patients with hypersensitivity to any of its components. While atorvastatin contraindications also include patients with active liver disease, the benefits of lipid-lowering therapy in chronic liver diseases, such as non-alcoholic fatty liver disease and hepatitis, likely outweigh the possible risks.[14] Atorvastatin is contraindicated during pregnancy or in female patients who may become pregnant. All female patients of childbearing age should receive counseling on the potential risks to a fetus should they become pregnant while on atorvastatin. This risk is most pronounced in the first trimester, so current guidelines recommend ceasing statin therapy for at least 3 months prior to becoming pregnant. The patient should discontinue this medication immediately if they become pregnant. However, a recent meta-analysis has called this restriction into question; more research will be necessary to accurately assess the risk-benefit ratio of using statins during pregnancy.[15] Female patients should also avoid atorvastatin if they are nursing. If a patient requires atorvastatin therapy, they should receive direction to discontinue breastfeeding. Patients starting atorvastatin should have liver function tests and a lipid panel performed at baseline, with a repeat lipid panel after six weeks on therapy. Liver function tests should be repeated as clinically indicated. Once the patient is stable, lipids can be checked every 6 to 12 months. It may also be prudent to periodically monitor serum blood glucose levels in patients with diabetes or at risk for diabetes. There are no antidotes available for atorvastatin overdose. Patients should be monitored for adverse events and provided with supportive care. The success of statins in lowering lipids or preventing cardiovascular events depends on the patient's medication adherence. Some of the barriers to successful statin therapy include experiencing adverse effects, lack of understanding of the importance of statin therapy, and cost; these factors may prevent patients from taking these medications as prescribed. It is also crucial for the interprofessional team to emphasize the importance of lifestyle modification in the treatment of their hyperlipidemia. This includes eating a proper, healthy diet, adding exercise or activity several times a week, and losing weight if necessary. A dietician or nutritionist may be a valuable addition to the healthcare team to help guide patients through the necessary dietary changes. All members of the interprofessional health care team can help identify barriers to adherence. Additional education and counseling around patient concerns and medication benefits may help improve adherence.[16] [Level 3] Healthcare team members need to communicate across disciplinary lines to optimize therapy. Clinicians (MDs, DOs, NPs, PAs) will make the initial assessment and prescribe statin therapy. Nursing can counsel the patients on how to take their medication, and check for adherence to treatment and adverse effects on subsequent visits and report back to the prescriber. Pharmacists can counsel the patients on optimal dosing (e.g., take the drug at bedtime) and check for drug-drug interactions, reporting back to the prescriber or nurse. Pharmacists can also inquire about the most common adverse effects since they often will see the patient more frequently and let nursing know so it can be relayed to the prescriber as well. These are but a few examples of how interprofessional team interaction can optimize atorvastatin therapy. [Level 5] Review Questions1. Raddino R, Della Pina P, Gorga E, Caretta G, Madureri A, Dei Cas L. [Indications for statin therapy in patients with acute coronary syndrome of ischemic origin]. G Ital Cardiol (Rome). 2010 Oct;11(10 Suppl 1):78S-83S. [PubMed: 21416832] 2.Dagli-Hernandez C, Zhou Y, Lauschke VM, Genvigir FDV, Hirata TDC, Hirata MH, Hirata RDC. Pharmacogenomics of statins: lipid response and other outcomes in Brazilian cohorts. Pharmacol Rep. 2022 Feb;74(1):47-66. [PubMed: 34403130] 3.Karvaly GB, Karádi I, Vincze I, Neely MN, Trojnár E, Prohászka Z, Imreh É, Vásárhelyi B, Zsáry A. A pharmacokinetics-based approach to the monitoring of patient adherence to atorvastatin therapy. Pharmacol Res Perspect. 2021 Oct;9(5):e00856. [PMC free article: PMC8415218] [PubMed: 34478238] 4.Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH, Goldberg AC, Gordon D, Levy D, Lloyd-Jones DM, McBride P, Schwartz JS, Shero ST, Smith SC, Watson K, Wilson PW, Eddleman KM, Jarrett NM, LaBresh K, Nevo L, Wnek J, Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Hochman JS, Kovacs RJ, Ohman EM, Pressler SJ, Sellke FW, Shen WK, Smith SC, Tomaselli GF., American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014 Jun 24;129(25 Suppl 2):S1-45. [PubMed: 24222016] 5.Jacobson TA, Ito MK, Maki KC, Orringer CE, Bays HE, Jones PH, McKenney JM, Grundy SM, Gill EA, Wild RA, Wilson DP, Brown WV. National lipid association recommendations for patient-centered management of dyslipidemia: part 1--full report. J Clin Lipidol. 2015 Mar-Apr;9(2):129-69. [PubMed: 25911072] 6.Jellinger PS, Handelsman Y, Rosenblit PD, Bloomgarden ZT, Fonseca VA, Garber AJ, Grunberger G, Guerin CK, Bell DSH, Mechanick JI, Pessah-Pollack R, Wyne K, Smith D, Brinton EA, Fazio S, Davidson M. AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY GUIDELINES FOR MANAGEMENT OF DYSLIPIDEMIA AND PREVENTION OF CARDIOVASCULAR DISEASE. Endocr Pract. 2017 Apr;23(Suppl 2):1-87. [PubMed: 28437620] 7.Filppula AM, Hirvensalo P, Parviainen H, Ivaska VE, Lönnberg KI, Deng F, Viinamäki J, Kurkela M, Neuvonen M, Niemi M. Comparative Hepatic and Intestinal Metabolism and Pharmacodynamics of Statins. Drug Metab Dispos. 2021 Aug;49(8):658-667. [PubMed: 34045219] 8.Hirota T, Fujita Y, Ieiri I. An updated review of pharmacokinetic drug interactions and pharmacogenetics of statins. Expert Opin Drug Metab Toxicol. 2020 Sep;16(9):809-822. [PubMed: 32729746] 9.Božina N, Ganoci L, Simičević L, Gvozdanović K, Domjanović IK, Fistrek Prlić M, Križ T, Borić Bilušić A, Laganović M, Božina T. Drug-drug-gene interactions as mediators of adverse drug reactions to diclofenac and statins: a case report and literature review. Arh Hig Rada Toksikol. 2021 Jun 28;72(3):114-128. [PMC free article: PMC8265195] [PubMed: 34187111] 10.Nemati M, Srai M, Rudrangi R. Statin-Induced Autoimmune Myopathy. Cureus. 2021 Feb 26;13(2):e13576. [PMC free article: PMC8007198] [PubMed: 33815984] 11.Jayatilaka S, Desai K, Rijal S, Zimmerman D. Statin-Induced Autoimmune Necrotizing Myopathy. J Prim Care Community Health. 2021 Jan-Dec;12:21501327211028714. [PMC free article: PMC8255573] [PubMed: 34219515] 12.Chogtu B, Magazine R, Bairy KL. Statin use and risk of diabetes mellitus. World J Diabetes. 2015 Mar 15;6(2):352-7. [PMC free article: PMC4360430] [PubMed: 25789118] 13.Keni R, Sekhar A, Gourishetti K, Nayak PG, Kinra M, Kumar N, Shenoy RR, Kishore A, Nandakumar K. Role of Statins in New-onset Diabetes Mellitus: The Underlying Cause, Mechanisms Involved, and Strategies to Combat. Curr Drug Targets. 2021;22(10):1121-1128. [PubMed: 33494673] 14.Tandra S, Vuppalanchi R. Use of statins in patients with liver disease. Curr Treat Options Cardiovasc Med. 2009 Aug;11(4):272-8. [PubMed: 19627660] 15.Zarek J, Koren G. The fetal safety of statins: a systematic review and meta-analysis. J Obstet Gynaecol Can. 2014 Jun;36(6):506-509. [PubMed: 24927189] 16.Maningat P, Gordon BR, Breslow JL. How do we improve patient compliance and adherence to long-term statin therapy? Curr Atheroscler Rep. 2013 Jan;15(1):291. [PMC free article: PMC3534845] [PubMed: 23225173] |
A nurse is teaching a client who is taking atorvastatin daily. which of the following statements
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