ATORVAST-NATRAPHARM Atorvastatin Calcium 80mg Film-Coated Tablet 1's
RXDRUG-DR-XY40119-1pc
Discreet Packaging
FDA-registered Products
FDA-licensed Pharmacies
Indications/Uses
An adjunct to lifestyle changes, including diet for the reduction of elevated total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) and apolipoprotein B (apo B), the total cholesterol: high-density lipoprotein cholesterol (TC:HDL-C) ratio and for increasing HDL-C; in hyperlipidemic and dyslipidemic conditions including: Primary hypercholesterolemia (type IIa); combined (mixed) hyperlipidemia (type IIb), including familial combined hyperlipidemia, regardless of whether cholesterol or TG are the lipid abnormality of concern; dysbetalipoproteinemia (type III); hypertriglyceridemia (type IV); familial hypercholesterolemia (homozygous and heterozygous).
For homozygous familial hypercholesterolemia, atorvastatin should be used as an adjunct to treatments eg, LDL apheresis or as monotherapy if such treatments are not available.
An adjunct to diet to reduce total-C, LDL-C and apo B levels in boys and postmenarchal girls 10-17 years with heterozygous familial hypercholesterolemia, if after an adequate trial of diet therapy the following findings are still present: LDL-C remains ≥4.9 mmol/L (190 mg/dL) or ≥4.1 mmol/L (160 mg/dL), and there is a positive family history of premature cardiovascular disease (CVD) or ≥2 other CVD risk factors are present in the pediatric patient.
Prior to initiating therapy with atorvastatin, secondary causes should be excluded for elevations in plasma lipid levels (eg, poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver disease and alcoholism) and a lipid profile performed to measure total-C, LDL-C, HDL-C and TG.
For homozygous familial hypercholesterolemia, atorvastatin should be used as an adjunct to treatments eg, LDL apheresis or as monotherapy if such treatments are not available.
An adjunct to diet to reduce total-C, LDL-C and apo B levels in boys and postmenarchal girls 10-17 years with heterozygous familial hypercholesterolemia, if after an adequate trial of diet therapy the following findings are still present: LDL-C remains ≥4.9 mmol/L (190 mg/dL) or ≥4.1 mmol/L (160 mg/dL), and there is a positive family history of premature cardiovascular disease (CVD) or ≥2 other CVD risk factors are present in the pediatric patient.
Prior to initiating therapy with atorvastatin, secondary causes should be excluded for elevations in plasma lipid levels (eg, poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver disease and alcoholism) and a lipid profile performed to measure total-C, LDL-C, HDL-C and TG.
Dosage/Direction for Use
Patients should be placed on a standard cholesterol-lowering diet before receiving atorvastatin and should continue on this diet during treatment with atorvastatin. If appropriate, a program of weight control and physical exercise should be implemented.
Prior to initiating therapy with atorvastatin, secondary causes for elevations in plasma lipid levels should be excluded. A lipid profile should also be performed.
Primary Hypercholesterolemia and Combined (Mixed) Dyslipidemia, Including Familial Combined Hyperlipidemia: Recommended Starting Dose: 10 or 20 mg once daily, depending on patient's LDL-C reduction required. Patients who require a large reduction in LDL-C (>45%) may be started at 40 mg once daily. The dosage range of atorvastatin is 10-80 mg once daily. A significant therapeutic response is evident within 2 weeks and the maximum response is usually achieved within 2-4 weeks. The response is maintained during chronic therapy. Adjustments of dosage, if necessary, should be made at intervals of 2-4 weeks. The maximum dose is 80 mg/day.
The dosage of atorvastatin should be individualized according the baseline LDL-C, TC:HDL-C ratio and/or TG levels to achieve the recommended desired lipid values at the lowest dose needed to achieve LDL-C desired level. Lipid levels should be monitored periodically and if necessary, the dose of atorvastatin adjusted based on desired lipid levels recommended by guidelines.
Severe Dyslipidemias: In patients with severe dyslipidemias including homozygous and heterozygous familial hypercholesterolemia and dysbetalipoproteinemia (type III), higher dosages (up to 80 mg/day) may be required (see Precautions and Interactions).
Heterozygous Familial Hypercholesterolemia in Pediatric Patients (10-17 years): Recommended Starting Dose: 10 mg/day. Maximum Recommended Dose: 20 mg/day (doses >20 mg/day have not been studied in this patient population). Doses should be individualized according to the recommended goal of therapy (see Pharmacology: Pharmacodynamics under Actions and Indications). Adjustments should be made at intervals of ≥4 weeks.
Prevention of Cardiovascular Disease: Clinical trials conducted that evaluated atorvastatin in the primary prevention of myocardial infarction used a dose of atorvastatin 10 mg once daily. For secondary prevention of myocardial infarction, optimal dosing may range from 10-80 mg atorvastatin once daily, to be given at the discretion of the prescriber, taking into account the expected benefit and safety considerations relevant to the patient to be treated.
Concomitant Therapy: See Interactions.
Renal Impairment: See Precautions.
Missed Dose: Take it as soon as possible. But if it is almost time for the next dose, skip the missed dose and just take the next dose. Don't take a double dose.
Administration: Doses can be given at any time of the day with or without food, and should preferably be given in the evening.
Prior to initiating therapy with atorvastatin, secondary causes for elevations in plasma lipid levels should be excluded. A lipid profile should also be performed.
Primary Hypercholesterolemia and Combined (Mixed) Dyslipidemia, Including Familial Combined Hyperlipidemia: Recommended Starting Dose: 10 or 20 mg once daily, depending on patient's LDL-C reduction required. Patients who require a large reduction in LDL-C (>45%) may be started at 40 mg once daily. The dosage range of atorvastatin is 10-80 mg once daily. A significant therapeutic response is evident within 2 weeks and the maximum response is usually achieved within 2-4 weeks. The response is maintained during chronic therapy. Adjustments of dosage, if necessary, should be made at intervals of 2-4 weeks. The maximum dose is 80 mg/day.
The dosage of atorvastatin should be individualized according the baseline LDL-C, TC:HDL-C ratio and/or TG levels to achieve the recommended desired lipid values at the lowest dose needed to achieve LDL-C desired level. Lipid levels should be monitored periodically and if necessary, the dose of atorvastatin adjusted based on desired lipid levels recommended by guidelines.
Severe Dyslipidemias: In patients with severe dyslipidemias including homozygous and heterozygous familial hypercholesterolemia and dysbetalipoproteinemia (type III), higher dosages (up to 80 mg/day) may be required (see Precautions and Interactions).
Heterozygous Familial Hypercholesterolemia in Pediatric Patients (10-17 years): Recommended Starting Dose: 10 mg/day. Maximum Recommended Dose: 20 mg/day (doses >20 mg/day have not been studied in this patient population). Doses should be individualized according to the recommended goal of therapy (see Pharmacology: Pharmacodynamics under Actions and Indications). Adjustments should be made at intervals of ≥4 weeks.
Prevention of Cardiovascular Disease: Clinical trials conducted that evaluated atorvastatin in the primary prevention of myocardial infarction used a dose of atorvastatin 10 mg once daily. For secondary prevention of myocardial infarction, optimal dosing may range from 10-80 mg atorvastatin once daily, to be given at the discretion of the prescriber, taking into account the expected benefit and safety considerations relevant to the patient to be treated.
Concomitant Therapy: See Interactions.
Renal Impairment: See Precautions.
Missed Dose: Take it as soon as possible. But if it is almost time for the next dose, skip the missed dose and just take the next dose. Don't take a double dose.
Administration: Doses can be given at any time of the day with or without food, and should preferably be given in the evening.
Overdosage
There is no specific treatment for atorvastatin overdosage. Should an overdose occur, the patient should be treated symptomatically and supportive measures instituted as required. Due to extensive drug binding to plasma proteins, hemodialysis is not expected to significantly enhance atorvastatin clearance (see Adverse Reactions).
Administration
May be taken with or without food: Avoid excessive consumption (>1 L/day) of grapefruit juice.
Contraindications
Hypersensitivity to atorvastatin calcium or to any component of Atorvast-Natrapharm (see Description).
Active liver disease or unexplained persistent elevations of serum transaminases exceeding 3 times the upper limit of normal (ULN) (see Precautions).
Use in pregnancy: Atorvastatin is contraindicated during pregnancy. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Atorvastatin should be administered to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the possible harm. If the patient becomes pregnant while taking atorvastatin, the drug should be discontinued immediately and the patient apprised of the potential harm to the fetus. Atherosclerosis being a chronic process, discontinuation of lipid metabolism regulating drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia.
Active liver disease or unexplained persistent elevations of serum transaminases exceeding 3 times the upper limit of normal (ULN) (see Precautions).
Use in pregnancy: Atorvastatin is contraindicated during pregnancy. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Atorvastatin should be administered to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the possible harm. If the patient becomes pregnant while taking atorvastatin, the drug should be discontinued immediately and the patient apprised of the potential harm to the fetus. Atherosclerosis being a chronic process, discontinuation of lipid metabolism regulating drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia.
Special Precautions
Monitor lipid levels periodically. Discontinue use if markedly elevated creatine kinase levels & hypersensitivity occurs, if myopathy is diagnosed or suspected, during fusidic acid therapy & having risk factor predisposing to development of renal failure secondary to rhabdomyolysis. Patients w/ predisposing factors for myopathy/rhabdomyolysis. Concomitant use w/ CYP3A4 inhibitors; digoxin; drugs that may decrease endogenous steroid hormone levels (eg, ketoconazole, spironolactone, cimetidine). Consider risk of hemorrhagic stroke prior to treatment in patients w/ recent (1-6 mth) stroke or transient ischemic attack. Decrease in myocardial ubiquinone (CoQ10) levels may lead to impaired cardiac function in CHF patients. Severe renal impairment. Perform liver function test prior to treatment & periodically thereafter. Ped patients except childn 10-17 yr w/ heterozygous familial hypercholesterolemia. Elderly ≥70 yr.
Use In Pregnancy & Lactation
Use in pregnancy: Atorvastatin is contraindicated during pregnancy. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Atorvastatin should be administered to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the possible harm. If the patient becomes pregnant while taking atorvastatin, the drug should be discontinued immediately and the patient apprised of the potential harm to the fetus. Atherosclerosis being a chronic process, discontinuation of lipid metabolism regulating drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia.
Use in lactation: In rats, milk concentrations of atorvastatin are similar to those in plasma. It is not known whether this drug is excreted in human milk. Because of the potential for adverse reactions in nursing infants, women taking atorvastatin should not breastfeed.
Use in lactation: In rats, milk concentrations of atorvastatin are similar to those in plasma. It is not known whether this drug is excreted in human milk. Because of the potential for adverse reactions in nursing infants, women taking atorvastatin should not breastfeed.
Adverse Reactions
Adverse reactions with atorvastatin have usually been mild and transient. In the atorvastatin placebo-controlled clinical trial database of 16,066 (8,755 atorvastatin vs 7,311 placebo) patients treated for a median period of 53 weeks, 5.2% of patients on atorvastatin discontinue due to adverse reactions compared to 4% of the patients on placebo.
Adverse experiences occurring at an incidence ≥1% in patients participating in placebo-controlled clinical studies of atorvastatin and reported to be possibly, probably or definitely drug.
Adverse experiences occurring at an incidence ≥1% in patients participating in placebo-controlled clinical studies of atorvastatin and reported to be possibly, probably or definitely drug.
The following additional adverse events were reported in placebo-controlled clinical trials during atorvastatin therapy: Muscle cramps, myositis, muscle fatigue, myopathy, paresthesia, peripheral neuropathy, pancreatitis, hepatitis, cholestatic jaundice, cholestasis, anorexia, vomiting, abdominal discomfort, alopecia, pruritus, rash, urticaria, erectile dysfunction, nightmare, blurred vision, tinnitus, eructation, neck pain, malaise, pyrexia and white blood cells urine positive.
In summary, the adverse events occurring at a frequency <1% are listed as follows: General Disorders and Administration Site Conditions: Malaise, pyrexia.
Gastrointestinal Disorders: Abdominal discomfort, eructation.
Hepatobiliary Disorders: Hepatitis, cholestasis.
Musculoskeletal and Connective Tissue Disorders: Muscle fatigue, neck pain.
Psychiatric Disorders: Nightmare.
Skin and Subcutaneous Tissue Disorders: Urticaria.
Eye Disorders: Blurred vision.
Ear and Labyrinth Disorders: Tinnitus.
Investigations: White blood cells urine positive.
Heterozygous Familial Hypercholesterolemia in Pediatric Patients (10-17 years): In a 26-week controlled study in boys and postmenarchal girls (n=187, where 140 patients received atorvastatin), the safety and tolerability profile of atorvastatin 10-20 mg daily was similar to that of placebo. The adverse events reported in ≥1% of patients were as follows: Abdominal pain, depression and headache (see Pharmacology: Pharmacodynamics under Actions and Use in children under Precautions).
Laboratory Changes and Adverse Events: The criteria for clinically significant laboratory changes were >3 x ULN for liver enzymes and >5 x ULN for CK. A total of 8 unique subjects met ≥1 of these criteria during the double-blind phase. Hence, the incidence of patients who experienced abnormally high enzymatic levels (AST/ALT and CK) was >4% (8/187).
Five (5) atorvastatin and 1 placebo subjects had increases in CK >5 x ULN during the double-blind phase; 2 of the 5 atorvastatin-treated subjects had increases in CK >10 x ULN.
There were 2 subjects who had clinically significant increases in ALT.
Abnormal Hematologic and Clinical Chemistry Findings: Laboratory Tests: Increases in serum transaminase levels and serum glucose have been noted in clinical trials (see Precautions).
Post-Market Adverse Drug Reactions: The following adverse events have also been reported during post-marketing experience with atorvastatin, regardless of causality assessment: Rare Reports: Severe myopathy with or without rhabdomyolysis (see Precautions and Interactions).
Isolated Reports: Gynecomastia, thrombocytopenia, arthralgia and allergic reactions including urticaria, angioneurotic edema, anaphylaxis and bullous rashes (including erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis); fatigue, back pain, chest pain, malaise, dizziness, amnesia, peripheral edema, weight gain, abdominal pain, insomnia, hypoesthesia, tinnitus, tendon rupture and dysgeusia.
Ophthalmologic Observations: see Precautions.
Cases of erectile dysfunction have been reported in association with the use of statins.
The following adverse events have been reported with some statins: Sleep disturbances including insomnia and nightmares; mood related disorders including depression; very rare cases of interstitial lungs disease, especially with long-term therapy. If it is suspected a patient has developed interstitial lung disease, statin therapy should be discontinued.
In summary, the adverse events occurring at a frequency <1% are listed as follows: General Disorders and Administration Site Conditions: Malaise, pyrexia.
Gastrointestinal Disorders: Abdominal discomfort, eructation.
Hepatobiliary Disorders: Hepatitis, cholestasis.
Musculoskeletal and Connective Tissue Disorders: Muscle fatigue, neck pain.
Psychiatric Disorders: Nightmare.
Skin and Subcutaneous Tissue Disorders: Urticaria.
Eye Disorders: Blurred vision.
Ear and Labyrinth Disorders: Tinnitus.
Investigations: White blood cells urine positive.
Heterozygous Familial Hypercholesterolemia in Pediatric Patients (10-17 years): In a 26-week controlled study in boys and postmenarchal girls (n=187, where 140 patients received atorvastatin), the safety and tolerability profile of atorvastatin 10-20 mg daily was similar to that of placebo. The adverse events reported in ≥1% of patients were as follows: Abdominal pain, depression and headache (see Pharmacology: Pharmacodynamics under Actions and Use in children under Precautions).
Laboratory Changes and Adverse Events: The criteria for clinically significant laboratory changes were >3 x ULN for liver enzymes and >5 x ULN for CK. A total of 8 unique subjects met ≥1 of these criteria during the double-blind phase. Hence, the incidence of patients who experienced abnormally high enzymatic levels (AST/ALT and CK) was >4% (8/187).
Five (5) atorvastatin and 1 placebo subjects had increases in CK >5 x ULN during the double-blind phase; 2 of the 5 atorvastatin-treated subjects had increases in CK >10 x ULN.
There were 2 subjects who had clinically significant increases in ALT.
Abnormal Hematologic and Clinical Chemistry Findings: Laboratory Tests: Increases in serum transaminase levels and serum glucose have been noted in clinical trials (see Precautions).
Post-Market Adverse Drug Reactions: The following adverse events have also been reported during post-marketing experience with atorvastatin, regardless of causality assessment: Rare Reports: Severe myopathy with or without rhabdomyolysis (see Precautions and Interactions).
Isolated Reports: Gynecomastia, thrombocytopenia, arthralgia and allergic reactions including urticaria, angioneurotic edema, anaphylaxis and bullous rashes (including erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis); fatigue, back pain, chest pain, malaise, dizziness, amnesia, peripheral edema, weight gain, abdominal pain, insomnia, hypoesthesia, tinnitus, tendon rupture and dysgeusia.
Ophthalmologic Observations: see Precautions.
Cases of erectile dysfunction have been reported in association with the use of statins.
The following adverse events have been reported with some statins: Sleep disturbances including insomnia and nightmares; mood related disorders including depression; very rare cases of interstitial lungs disease, especially with long-term therapy. If it is suspected a patient has developed interstitial lung disease, statin therapy should be discontinued.
Drug Interactions
Overview: Pharmacokinetic interaction studies conducted with drugs in healthy subjects may not detect the possibility of a potential drug interaction in some patients due to differences in underlying diseases and use of concomitant medications (see Precautions).
Concomitant Therapy with Other Lipid Metabolism Regulators: Based on post-marketing surveillance, gemfibrozil, fenofibrate, other fibrates and lipid-modifying doses of niacin (nicotinic acid) may increase the risk of myopathy when given concomitantly with HMG-CoA reductase inhibitors, probably because they can produce myopathy when given alone (see Precautions). Therefore, combined drug therapy should be approached with caution; lower starting and maintenance doses of atorvastatin should be considered.
Cytochrome P-450-Mediated Interactions: Atorvastatin is metabolized by the CYP450 isoenzyme, CYP3A4. Erythromycin, a CYP3A4 inhibitor, increased atorvastatin plasma levels by 40%. Co-administration of CYP3A4 inhibitors eg, grapefruit juice, some macrolide antibiotics (ie, erythromycin, clarithromycin), immunosuppressants (cyclosporine), azote antifungal agents (ie, itraconazole, ketoconazole), protease inhibitors or the antidepressant, nefazodone, have the potential to increase plasma concentrations of HMG-CoA reductase inhibitors, including atorvastatin (see Interactions). Concomitant use of strong inhibitors of CYP3A4 with atorvastatin should be used with caution. If such use must be instituted, lower starting and maintenance doses of atorvastatin should be considered and patients should be monitored closely for musculoskeletal effects (see Dosage & Administration and Precautions).
Transporter Inhibitors: Atorvastatin and atorvastatin-metabolites are substrates of the organic anion-transporting polypeptide (OATP1B1) transporter. Inhibitors of the OATP1B1 (eg, cyclosporine) can increase the bioavailability of atorvastatin (see Pharmacology: Pharmacokinetics under Actions).
Inducers of Cytochrome P-450 3A: Concomitant administration of atorvastatin with inducers of CYP3A4 (eg, efavirenz, rifampin) can lead to variable reductions in plasma concentrations of atorvastatin. Due to the dual interaction mechanism of rifampin, (CYP3A4 induction and inhibition of hepatocyte uptake transporter OATP1B1), simultaneous co-administration of atorvastatin with rifampin resulted in a mean increase in Cmax and AUC of atorvastatin of 12% and 190%, respectively. In contrast, a delayed administration of atorvastatin after administration of rifampin has been associated with a significant reduction (approximately 80%) in atorvastatin plasma concentrations.
Drug-Drug Interactions: The drugs listed in Table 2a an 2b are based on either drug interactions studies, case reports or potential interactions due to the expected magnitude and seriousness of the interaction (ie, those identified as contraindicated). Interactions with other drugs have not been established.
Concomitant Therapy with Other Lipid Metabolism Regulators: Based on post-marketing surveillance, gemfibrozil, fenofibrate, other fibrates and lipid-modifying doses of niacin (nicotinic acid) may increase the risk of myopathy when given concomitantly with HMG-CoA reductase inhibitors, probably because they can produce myopathy when given alone (see Precautions). Therefore, combined drug therapy should be approached with caution; lower starting and maintenance doses of atorvastatin should be considered.
Cytochrome P-450-Mediated Interactions: Atorvastatin is metabolized by the CYP450 isoenzyme, CYP3A4. Erythromycin, a CYP3A4 inhibitor, increased atorvastatin plasma levels by 40%. Co-administration of CYP3A4 inhibitors eg, grapefruit juice, some macrolide antibiotics (ie, erythromycin, clarithromycin), immunosuppressants (cyclosporine), azote antifungal agents (ie, itraconazole, ketoconazole), protease inhibitors or the antidepressant, nefazodone, have the potential to increase plasma concentrations of HMG-CoA reductase inhibitors, including atorvastatin (see Interactions). Concomitant use of strong inhibitors of CYP3A4 with atorvastatin should be used with caution. If such use must be instituted, lower starting and maintenance doses of atorvastatin should be considered and patients should be monitored closely for musculoskeletal effects (see Dosage & Administration and Precautions).
Transporter Inhibitors: Atorvastatin and atorvastatin-metabolites are substrates of the organic anion-transporting polypeptide (OATP1B1) transporter. Inhibitors of the OATP1B1 (eg, cyclosporine) can increase the bioavailability of atorvastatin (see Pharmacology: Pharmacokinetics under Actions).
Inducers of Cytochrome P-450 3A: Concomitant administration of atorvastatin with inducers of CYP3A4 (eg, efavirenz, rifampin) can lead to variable reductions in plasma concentrations of atorvastatin. Due to the dual interaction mechanism of rifampin, (CYP3A4 induction and inhibition of hepatocyte uptake transporter OATP1B1), simultaneous co-administration of atorvastatin with rifampin resulted in a mean increase in Cmax and AUC of atorvastatin of 12% and 190%, respectively. In contrast, a delayed administration of atorvastatin after administration of rifampin has been associated with a significant reduction (approximately 80%) in atorvastatin plasma concentrations.
Drug-Drug Interactions: The drugs listed in Table 2a an 2b are based on either drug interactions studies, case reports or potential interactions due to the expected magnitude and seriousness of the interaction (ie, those identified as contraindicated). Interactions with other drugs have not been established.
Storage
Store at room temperatures not exceeding 30°C. Keep away from warm and damp places eg, bathroom or kitchen.
Action
Pharmacology: Pharmacodynamics: The lowering of total cholesterol (total-C), low-density lipoprotein-cholesterol (LDL-C) and apolipoprotein B (apo B) have been shown to reduce the risk of cardiovascular events and mortality.
Atorvastatin is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. In both subjects and in patients with homozygous and heterozygous familial hypercholesterolemia, nonfamilial forms of hypercholesterolemia, mixed dyslipidemia, hypertriglyceridemia and dysbetalipoproteinemia, atorvastatin has been shown to reduce levels of total-C, LDL-C, apo B and total triglycerides (TG), and raises high-density lipoprotein-cholesterol (HDL-C) levels.
Epidemiologic and clinical studies have associated the risk of coronary artery disease (CAD) with elevated levels of total-C, LDL-C and decreased levels of HDL-C. These abnormalities of lipoprotein metabolism are considered as major contributors to the development of the disease. Like LDL, cholesterol-enriched lipoproteins, including VLDL, intermediate-density lipoproteins (IDL) and remnants can also promote atherosclerosis. Elevated plasma TG are frequently found in a triad with low HDL-C levels and small LDL particles, as well as in association with nonlipid metabolic risk factors for coronary heart disease (CHD) (metabolic syndrome). Clinical studies have also shown that serum TG can be an independent risk factor for CAD. Coronary artery disease risk is especially increased if the hypertriglyceridemia is due to increased IDL or associated with decreased HDL or increased LDL-C. In addition, high TG levels are associated with an increased risk of pancreatitis. Although epidemiological and preliminary clinical evidence link low HDL-C levels and high TG levels with CAD and atherosclerosis, the independent effect of raising HDL or lowering TG on the risk of coronary and cerebrovascular morbidity and mortality has not been demonstrated in prospective, well-controlled outcome studies. Other factors eg, interactions between lipids/lipoproteins and endothelium, platelets and macrophages, have also been incriminated in the development of human atherosclerosis and of its complications. Regardless of the intervention used (low fat/low-cholesterol diet, partial ileal bypass surgery or pharmacologic therapy), effective treatment of hypercholesterolemia/dyslipidemia has consistently been shown to reduce the risk of CAD.
Atorvastatin is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. In both subjects and in patients with homozygous and heterozygous familial hypercholesterolemia, nonfamilial forms of hypercholesterolemia, mixed dyslipidemia, hypertriglyceridemia and dysbetalipoproteinemia, atorvastatin has been shown to reduce levels of total-C, LDL-C, apo B and total triglycerides (TG), and raises high-density lipoprotein-cholesterol (HDL-C) levels.
Epidemiologic and clinical studies have associated the risk of coronary artery disease (CAD) with elevated levels of total-C, LDL-C and decreased levels of HDL-C. These abnormalities of lipoprotein metabolism are considered as major contributors to the development of the disease. Like LDL, cholesterol-enriched lipoproteins, including VLDL, intermediate-density lipoproteins (IDL) and remnants can also promote atherosclerosis. Elevated plasma TG are frequently found in a triad with low HDL-C levels and small LDL particles, as well as in association with nonlipid metabolic risk factors for coronary heart disease (CHD) (metabolic syndrome). Clinical studies have also shown that serum TG can be an independent risk factor for CAD. Coronary artery disease risk is especially increased if the hypertriglyceridemia is due to increased IDL or associated with decreased HDL or increased LDL-C. In addition, high TG levels are associated with an increased risk of pancreatitis. Although epidemiological and preliminary clinical evidence link low HDL-C levels and high TG levels with CAD and atherosclerosis, the independent effect of raising HDL or lowering TG on the risk of coronary and cerebrovascular morbidity and mortality has not been demonstrated in prospective, well-controlled outcome studies. Other factors eg, interactions between lipids/lipoproteins and endothelium, platelets and macrophages, have also been incriminated in the development of human atherosclerosis and of its complications. Regardless of the intervention used (low fat/low-cholesterol diet, partial ileal bypass surgery or pharmacologic therapy), effective treatment of hypercholesterolemia/dyslipidemia has consistently been shown to reduce the risk of CAD.
MedsGo Class
Dyslipidaemic Agents
Features
Brand
Atorvast-Natrapharm
Full Details
Dosage Strength
80mg
Drug Ingredients
- Atorvastatin
Drug Packaging
Film-Coated Tablet 1's
Generic Name
Atorvastatin Calcium
Dosage Form
Film-Coated Tablet
Registration Number
DR-XY40119
Drug Classification
Prescription Drug (RX)
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