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HMG-CoA Reductase InhibitorAka: 3-Hydroxy-3-Methyl-Glutaryl Coenzyme A Reductase, Rosuvastatin, Zocor, Lipitor, Crestor, Statin, Lovastatin, Simvastatin, Pravastatin, Atorvastatin, Fluvastatin

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  1. Effects
    1. Lipid-related effects
      1. LDL decreased (20-40%)
      2. HDL Increased (5-15%)
      3. Triglycerides decreased
        1. Atorvastatin (40%)
        2. Simvastatin (30%)
        3. Other Statins (10-20%)
    2. Other effects (related to decreased coronary events)
      1. Antiproliferation effect on smooth muscle cells
      2. Antioxidant and anti-inflammatory effects
  2. Contraindications
    1. Active or Chronic Liver Disease
    2. Drug Interactions (see below): Myopathy or hepatitis
  3. Efficacy
    1. Findings
      1. Reduces Myocardial Infarction risk (30%)
        1. Reduces need for Angioplasty (47 vs 20)
        2. Associated with regression on angiogram
      2. Reduces coronary death rate (42%)
      3. Reduces Cerebrovascular Accident risk (30%)
      4. Conflicting evidence on reducing Dementia risk
        1. Recent prospective articles do not suggest benefit
        2. Rea (2005) Arch Neurol 62:1047
      5. Reduces C-Reactive Protein
        1. Inflammatory factors related to ACS pathogenesis
        2. May explain benefit to normolipidemic patients
    2. References
      1. (1994) Lancet 344(8934):1383
      2. (1997) FDC Reports 59(46):T&G6
      3. (2004) Lancet 363:757
      4. Jick (2000) Lancet 356:1627
      5. Jukema (1995) Circulation 91:2528
      6. Ridker (2001) N Engl J Med 344:1959
      7. Sacks (1996) N Engl J Med 335:1001
  4. Precautions
    1. Do not stop statins abruptly (worse CAD outcomes)
  5. Adverse Effects
    1. Mild Gastrointestinal upset
    2. Rash
    3. Insomnia (seen more with lipophilic agents)
      1. May be reduced with Pravastatin or Fluvastatin
    4. Liver Function Abnormalities (1-2% Incidence)
      1. AST and ALT increased 2-3x Normal
    5. Lupus-like syndrome
    6. Peripheral Neuropathy
    7. Concurrent use with Coumadin increases bleeding risk
    8. Myalgia or Muscle Weakness
      1. Myalgias are common (5%)
      2. Rhabdomyolysis is uncommon (0.1%)
      3. Creatine Phosphokinase (CPK) is a poor marker for Myositis
        1. Normal in most patients despite myalgias
        2. CPK may be increased 10 fold in patients with Rhabdomyolysis
      4. Risk factors for statin induced Myopathy
        1. Combination with Gemfibrozil
        2. Older patients
        3. Low body weight
        4. Female gender
        5. Acute illness or major surgery
      5. Patient should stop drug and contact physician if
        1. Severe myalgias
        2. Muscle Weakness
        3. Dark urine
      6. Symptomatic management
        1. Coenzyme Q10 (Ubiquinone) 100 mg orally daily
          1. Reduces myalgias by 40%
          2. Caso (2007) Am J Cardiol 99:1409
      7. References
        1. Phillips (2002) Ann Intern Med 137:581
  6. Adverse Effects: Possible
    1. Cognitive Impairment
      1. Subjective patient reports but not found in studies
      2. Statins may also protect cognitive function by affecting atherosclerosis
      3. Consider a water soluble statin (e.g. Pravastatin) that does not cross blood-brain barrier
      4. Wagstaff (2003) Pharmacotherapy 23(7):871
  7. Compliance/Tolerance
    1. Discontinuation rate with statins: 15%
    2. Discontinuation rate with other medications: 35%
  8. Pharmacokinetics
    1. First-pass metabolism in all statins except Pravastatin
    2. Protein binding
      1. Most statins are 90% protein bound
      2. Pravastatin is 50% protein bound
    3. Cytochrome P450 Metabolism
      1. CYP3A4 isoenzyme metabolizes most statins
      2. CYP2C9 isoenzyme metabolizes Fluvastatin
      3. Pravastatin is not metabolized by P450 system
        1. Safer to use in combination with other drugs
    4. Renal elimination occurs most with Pravastatin
  9. Preparations (from least to most potent)
    1. Fluvastatin (Lescol)
      1. Dose 20 mg lowers LDL 17% (recommended starting dose)
      2. Dose 40 mg lowers LDL 23%
      3. Dose 80 mg lowers LDL 33%
    2. Pravastatin (Pravachol)
      1. Dose 10 mg lowers LDL 19%
      2. Dose 20 mg lowers LDL 24% (recommended starting dose)
      3. Dose 40 mg lowers LDL 34%
      4. Dose 80 mg lowers LDL 40%
    3. Lovastatin (Mevacor)
      1. Starting Dose: 20 mg qd
      2. Dose 20 mg lowers LDL 29% (recommended starting dose)
      3. Dose 40 mg lowers LDL 31%
      4. Dose 80 mg lowers LDL 48%
    4. Cerivastatin (Baycol, not available in US)
      1. Cerivastatin recalled in United States (August 2001)
      2. Dose 0.2 mg lowers LDL 25% (start if Renal Failure)
      3. Dose 0.3 mg lowers LDL 30% (recommended start dose)
      4. Dose 0.4 mg lowers LDL 36%
      5. Dose 0.8 mg lowers LDL 44%
    5. Simvastatin (Zocor)
      1. Dose 10 mg lowers LDL 28%
      2. Dose 20 mg lowers LDL 35% (recommended starting dose)
      3. Dose 40 mg lowers LDL 40%
      4. Dose 80 mg lowers LDL 48%
    6. Atorvastatin (Lipitor)
      1. Dose 10 mg lowers LDL 38% (recommended starting dose)
      2. Dose 20 mg lowers LDL 46%
      3. Dose 40 mg lowers LDL 51%
      4. Dose 80 mg lowers LDL 54%
      5. Triglycerides lowered 40%
    7. Rosuvastatin (Crestor)
      1. Dose 5 mg lowers LDL 45%
      2. Dose 10 mg lowers LDL: 52%
      3. Dose 20 mg lowers LDL 55%
      4. Dose 40 mg lowers LDL: 63%
      5. Indications to start at lower dose (5 mg)
        1. Asians
          1. Higher drug levels leads to higher toxicity risk
        2. Renal insufficiency (max 10 mg if CrCl < 30 ml/min)
        3. Hypothyroidism (uncontrolled)
        4. Age over 65 years
        5. Cyclosporine use (max dose 5 mg daily)
        6. Concurrent Gemfibrozil (max dose 10 mg daily)
  10. Management: Statin choices if special concerns
    1. Preferred agents if risk of drug interactions
      1. Pravastatin (no CYP 450 METABOLISM)
      2. Fluvastatin
    2. Preferred agents if Renal Function impaired
      1. Atorvastatin
      2. Fluvastatin
      3. Avoid Pravastatin if Creatinine Clearance <60 ml/min
        1. If used, start dosing at 10 mg and titrate slowly
  11. Monitoring: Liver transaminase testing (AST,ALT)
    1. No history of liver disease
      1. Stop statin if >3x over baseline
      2. Liver Transaminase testing (AST, ALT) schedule
        1. Baseline
        2. Week 6
        3. Month 3
        4. Every 6 months to yearly
    2. Chronic Liver Disease history
      1. Start with lower initial statin dose
      2. Stop statin if transaminase >2x over baseline
      3. Liver Transaminase testing (AST, ALT) schedule
        1. Baseline
        2. Two weeks
        3. One month
        4. Two months
        5. Three months
  12. Drug Interactions (See Contraindications above)
    1. Mibefradil (Posicor)
    2. Itraconazole
    3. Macrolides (Erythromycin, Azithromycin, Clarithromycin)
      1. Stop statin while on Macrolide antibiotic
    4. Cyclosporine
    5. Gemfibrozil
    6. Niacin
    7. Grapefruit juice increases some statin levels
      1. Drugs affected: Lipitor, Zocor, Mevacor
      2. Drugs not affected: Pravachol, Crestor, Lescol
      3. Limit Grapefruit juice to 8 ounces daily
      4. Limit juice timing to opposite statin dose
        1. Take juice at night, if statin taken in morning
      5. Refernces
        1. Reamy (2007) Am Fam Physician 76:190
    8. Alcohol
      1. Increases risk of liver enzyme elevations
  13. References
    1. Chong (2001) Am J Med 111:390
    2. Crouch (2001) Am Fam Physician 63(2):309
    3. Jones (1998) Am J Cardiol 81:582
    4. Sasaki (1998) Clin Ther 20:539

Lovastatin (C0024027)

Definition (MSH)A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.
Definition (CSP)HMG coA reductase inhibitor which inhibits cholesterol biosynthesis and thus lowers blood cholesterol levels; also blocks isoprenylation of protein CAAX motifs.
Definition (PDQ)A lactone metabolite isolated from the fungus Aspergillus terreus with cholesterol-lowering activity and potential antineoplastic activity. Lovastatin is hydrolyszed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxyl-3-methylgutarylcoenzyme A (HMG-CoA) reductase, an enzyme involved in the cholesterol biosynthesis. In addition, this agent may inhibit tumor cell proliferation and reduce tumor cell invasiveness, thereby decreasing tumor metastatic potential; induce tumor cell apoptosis, possibly by inhibiting protein geranylgeranylation and; arrest cells in the G1 phase of the cell cycle, an effect that sensitizes tumor cells to the cytotoxic effects of ionizing radiation. Check for "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=41658&idtype=1" active clinical trials or "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=41658&idtype=1&closed=1" closed clinical trials using this agent. ("http://nciterms.nci.nih.gov:80/NCIBrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&code=C620" NCI Thesaurus)
Definition (NCI)A lactone metabolite isolated from the fungus Aspergillus terreus with cholesterol-lowering activity and potential antineoplastic activity. Lovastatin is hydrolyszed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxyl-3-methylgutarylcoenzyme A (HMG-CoA) reductase, an enzyme involved in the cholesterol biosynthesis. In addition, this agent may inhibit tumor cell proliferation and reduce tumor cell invasiveness, thereby decreasing tumor metastatic potential; induce tumor cell apoptosis, possibly by inhibiting protein geranylgeranylation and; arrest cells in the G1 phase of the cell cycle, an effect that sensitizes tumor cells to the cytotoxic effects of ionizing radiation. (NCI04)
ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121)
MSHD008148
English6 Methylcompactin, 6-Methylcompactin, Lovastatin, Lovastatin -RETIRED-, LOVASTATIN PREPARATION, mevinolin, Monacolin K
Spanishlovastatina, lovastatina-RETIRADO-, mevinolina, monacolina K
Parent ConceptsAnticholesteremic Agents (C0003277), Naphthalenes (C0027378), Hydroxymethylglutaryl-CoA Reductase Inhibitors (C0360714), Naphthalene Compound (C1881986), Antilipemic Agents (C0003367), Duplicate concept (C1274013)
SourcesCSP, MSH, MTH, MTHSPL, NCI, NDFRT, PDQ, RXNORM, SCTSPA, SNOMEDCT, USPMG, VANDF
Derived from the NIH UMLS (Unified Medical Language System)


Simvastatin (C0074554)

Definition (CSP)a derivative of lovastatin and inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG coA reductase), a rate limiting enzyme in the biosynthesis of cholesterol.
Definition (MSH)A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.
Definition (PDQ)A lipid-lowering agent derived synthetically from a fermentation product of the fungus Aspergillus terreus. Hydrolyzed in vivo to an active metabolite, simvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. Check for "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=455226&idtype=1" active clinical trials or "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=455226&idtype=1&closed=1" closed clinical trials using this agent. ("http://nciterms.nci.nih.gov:80/NCIBrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&code=C29454" NCI Thesaurus)
Definition (NCI)A lipid-lowering agent derived synthetically from a fermentation product of the fungus Aspergillus terreus. Hydrolyzed in vivo to an active metabolite, simvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. (NCI04)
ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121)
MSHD019821
EnglishSimvastatin, SIMVASTATIN PREPARATION, Synvinolin, Velastatin
Spanishsimvastatin, simvastatina
Parent ConceptsLovastatin (C0024027), Hydroxymethylglutaryl-CoA Reductase Inhibitors (C0360714), Antilipemic Agents (C0003367)
SourcesCSP, MSH, MTHSPL, NCI, NDFRT, PDQ, RXNORM, SCTSPA, SNOMEDCT, USPMG, VANDF
Derived from the NIH UMLS (Unified Medical Language System)


fluvastatin (C0082608)

Definition (NCI)A synthetic lipid-lowering agent with antilipidemic and potential antineoplastic properties. Fluvastatin competitively inhibits hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses through the suppression of MHC II (major histocompatibility complex II) on interferon gamma-stimulated antigen-presenting cells such as human vascular endothelial cells. Due to its anti-inflammatory effects mediated by alterations of lipid metabolism, fluvastatin may possess chemopreventive and therapeutic antineoplastic properties.
ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121)
MSHC065180
Englishfluindostatin, fluvastatin, FLUVASTATIN PREPARATION
Spanishfluvastatina
Parent ConceptsHydroxymethylglutaryl-CoA Reductase Inhibitors (C0360714), Antilipemic Agents (C0003367), Fatty Acids, Monounsaturated (C0015687), Indoles (C0021242)
SourcesMSH, NCI, NDFRT, RXNORM, SCTSPA, SNOMEDCT, USPMG, VANDF
Derived from the NIH UMLS (Unified Medical Language System)


Pravastatin (C0085542)

Definition (MSH)An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).
Definition (NCI)A synthetic lipid-lowering agent. Pravastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. Pravastatin lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. (NCI04)
Definition (PDQ)A synthetic lipid-lowering agent. Pravastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. Pravastatin lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. Check for "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=424450&idtype=1" active clinical trials or "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=424450&idtype=1&closed=1" closed clinical trials using this agent. ("http://nciterms.nci.nih.gov:80/NCIBrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&code=C29375" NCI Thesaurus)
ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121)
MSHD017035
EnglishEptastatin, PRAV, Pravastatin, PRAVASTATIN PREPARATION
Spanishpravastatin, pravastatina
Parent ConceptsNaphthalenes (C0027378), Hydroxymethylglutaryl-CoA Reductase Inhibitors (C0360714), Antilipemic Agents (C0003367)
SourcesCSP, MSH, NCI, NDFRT, PDQ, RXNORM, SCTSPA, SNOMEDCT, USPMG, VANDF
Derived from the NIH UMLS (Unified Medical Language System)


atorvastatin (C0286651)

Definition (CSP)a synthetic lipid-lowering agent; an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase that catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis.
Definition (PDQ)A synthetic lipid-lowering agent. Atorvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. Atorvastatin also increases the number of LDL receptors on hepatic cell surfaces to enhance uptake and catabolism of LDL and reduces LDL production and the number of LDL particles. This agent lowers plasma cholesterol and lipoprotein levels and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. Check for "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=460239&idtype=1" active clinical trials or "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=460239&idtype=1&closed=1" closed clinical trials using this agent. ("http://nciterms.nci.nih.gov:80/NCIBrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&code=C28837" NCI Thesaurus)
Definition (NCI)A synthetic lipid-lowering agent. Atorvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. Atorvastatin also increases the number of LDL receptors on hepatic cell surfaces to enhance uptake and catabolism of LDL and reduces LDL production and the number of LDL particles. This agent lowers plasma cholesterol and lipoprotein levels and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. (NCI04)
ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121)
MSHC065179
Englishatorvastatin, Atorvastatin - chemical, ATORVASTATIN PREPARATION
Spanishatorvastatina
Parent ConceptsAnticholesteremic Agents (C0003277), Pyrroles (C0034325), Hydroxymethylglutaryl-CoA Reductase Inhibitors (C0360714), Antilipemic Agents (C0003367), Heptanoic Acids (C0019227), Duplicate concept (C1274013)
SourcesCSP, MSH, NCI, NDFRT, PDQ, RXNORM, SCTSPA, SNOMEDCT, USPMG, VANDF
Derived from the NIH UMLS (Unified Medical Language System)


Hydroxymethylglutaryl-CoA Reductase Inhibitors (C0360714)

Definition (MSH)Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121)
MSHD019161
English3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, HMG COA REDUCTASE INHIB, HMG COA reductase inhibitor, HMG CoA Reductase Inhibitors, HMG-CoA Reductase Inhibitor, HMG-CoA Reductase Inhibitors, HMG-CoA Statins, HYDROXYMETHYLGLUTARYL COA REDUCTASE INHIB, Hydroxymethylglutaryl CoA Reductase Inhibitors, Hydroxymethylglutaryl CoenzymeA Reductase Inhibitors, Hydroxymethylglutaryl-CoA Inhibitors, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hydroxymethylglutaryl-Coenzyme A Inhibitors, INHIB HMG COA REDUCTASE, INHIB HYDROXYMETHYLGLUTARYL COA, statin, Statins
Spanishestatina, inhibidor de 3-hidroxi-3-metilglutaril coenzima A reductasa, inhibidor de la 3-hidroxi-3-metilglutaril coenzima A reductasa, inhibidor de la HMG - CoA reductasa, inhibidor de la HMG-CoA reductasa
Parent ConceptsAnticholesteremic Agents (C0003277), Enzyme Inhibitors (C0014432), Enzyme Inhibitor Drugs (C0919438), Antilipidemic Agent (C1516000), Antilipemic Agents (C0003367), Drug allergen (C1320237), Dyslipidemics (C1579440)
SourcesCSP, MSH, MTH, NCI, NDFRT, SCTSPA, SNOMEDCT, USPMG
Derived from the NIH UMLS (Unified Medical Language System)


Lipitor (C0593906)

ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121)
MSHC065179
EnglishLipitor
SourcesCSP, MSH, NCI, PDQ, RXNORM
Derived from the NIH UMLS (Unified Medical Language System)


Zocor (C0678181)

ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121)
MSHD019821
EnglishZocor
SourcesCSP, MSH, NCI, PDQ, RXNORM
Derived from the NIH UMLS (Unified Medical Language System)


rosuvastatin (C0965129)

ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121)
MSHC422923
Englishrosuvastatin, ROSUVASTATIN PREPARATION
Spanishrosuvastatina
Parent ConceptsHydroxymethylglutaryl-CoA Reductase Inhibitors (C0360714), Antilipemic Agents (C0003367), Unclassified Ingredients (C1372954)
SourcesMSH, NCI, NDFRT, RXNORM, SCTSPA, SNOMEDCT, USPMG, VANDF
Derived from the NIH UMLS (Unified Medical Language System)


Rosuvastatin calcium (C1101751)

ConceptsOrganic Chemical (T109) , Pharmacologic Substance (T121) , Biologically Active Substance (T123)
MSHC422923
EnglishCrestor, Rosuvastatin calcium
Spanishrosuvastatina calcica
Parent ConceptsHydroxymethylglutaryl-CoA Reductase Inhibitors (C0360714), rosuvastatin (C0965129)
SourcesMSH, MTH, MTHSPL, NCI, RXNORM, SCTSPA, SNOMEDCT, USPMG
Derived from the NIH UMLS (Unified Medical Language System)



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