Lipid Guidelines - Dr. Ajay Kantharia
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The document discusses lipids and lipoproteins, providing information on their structure, function, and roles in cardiovascular disease. It outlines guidelines for lipid profiling and therapeutic lifestyle changes and drug therapies to control lipid levels and reduce cardiovascular risk. Key points include classifications of lipoproteins and lipid levels, goals for lowering LDL and triglycerides, and drug classes like statins, fibrates, and niacin that are used to treat dyslipidemia.
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Lipid Guidelines - Dr. Ajay Kantharia
- 1. Consulting Physician & Cardiologist Critical Care Physician HON. PHYSICIAN : Saifee Hospital Sir H. N. Hospital Motiben Dalvi Hospital Lipids Guidelines
- 5. An adult ingests about 60-150 gm of lipids / day. 90% is Triglycerides (TG) The remaining 10% is cholesterol , cholesteryl esters , phospholipids and unesterified (free ) fatty acids.
- 9. What is a Lipoprotein? Protein Lipo (Lipid) + Lipoprotein is a macro-molecular complex in blood carrying protected lipids
- 10. Why are lipoproteins formed? Cholesterol is insoluble in water To transport it thro’ blood (92% water) it is combined with Protein to make Watersoluble Lipo proteins -Harper’s Biochemistry (2000),p 268 For utilization and storage in tissues,it is converted to water-insoluble Cholesterol ‘Ester’ -Krause’s (2000), Food,Nutrition and Diet Therapy, p 62
- 11. Structure of a Lipoprotein
- 12. What is a Apolipoprotein? -Harper’s Biochemistry (2000),p 270 Apo = ‘Derived from’ Apolipoprotein is the name given to ‘ Protein’ part of Lipoprotein (ie,Protein derived from Lipoprotein)
- 14. Which Lipoproteins have which Apolipoproteins ? -Harper’s Biochemistry (2000),p 270 Apolipoprotein Lipoprotein Apo A-I/II/IV HDL,Chylo Apo C-I/II/III VLDL,HDL,Chylo Apo D HDL Apo E VLDL,LDL,HDL,Chylo B-100 has the longest amino acidchain(4536) B-48 means 48 % of B 100 Apo B-100 LDL,VLDL,IDL Apo B-48 Chylo
- 21. Primary Prevention and Risk Factor assessment
- 34. LDL Cholesterol Goals and Cutpoints for Therapeutic Lifestyle Changes (TLC) and Drug Therapy in Different Risk Categories Risk Category LDL Goal (mg/dL) LDL Level at Which to Initiate Therapeutic Lifestyle Changes (TLC) (mg/dL) LDL Level at Which to Consider Drug Therapy (mg/dL) CHD or CHD Risk Equivalents (10-year risk >20%) <100 100 130 (100–129: drug optional) 2+ Risk Factors (10-year risk 20%) <130 130 10-year risk 10–20%: 130 10-year risk <10%: 160 0–1 Risk Factor <160 160 190 (160–189: LDL-lowering drug optional)
- 35. And –the latest As per July 13 th 2004 NCEP ATP III update, high risk patient needs to achieve LDL-C<70 mg/dL Risk LDL goal mg/dL(NCEP ATP III) 1 LDL goal (Recommendations for modifications to footnote ATP III) 2 CHD (10 yr risk>20%) < 100 < 70 2+ RF -10 yr risk 10-20% -10 yr risk < 10% < 130 < 130 < 100 Unchanged 0-1 RF < 160 Unchanged
- 47. HMG CoA Reductase Inhibitors 1.) LDL Uptake Cholesterol 2.) Synthesis HMG CoA Bile Acids Cholesterol HMG CoA Bile Acids
- 52. Comparative LDL Effects -70 -60 -50 -40 -30 -20 -10 0 10 40 20 80 10 10 20 20 20 20 80 40 40 40 40 1 5 20 Atorvastatin Simvastatin Pravastatin Lovastatin Fluvastatin Rosuvastatin Am J Cardiol 1998;81:582-7. Am J Cardiol 2001;88:504-8. J Int Med Res 2000;28:47-68. Clin Cardiol 2000;23:39-46. 80 80 80
- 53. Comparative HDL Effects -4 -2 0 2 4 6 8 10 12 Atorva Simva Prava Lova Rosuva 10 20 40 40 40 40 20 20 20 20 10 10 40 80 80 Adapted from Jones PH et al. Am J Cardiol 2003;92:152–160 & CURVES Study. Am J Cardiol 1998;81:582-7. 10
- 54. Comparative TG Effects -35 -30 -25 -20 -15 -10 -5 0 5 10 40 20 80 10 10 20 20 20 20 80 40 40 40 40 Atorvastatin Simvastatin Pravastatin Lovastatin Rosuvaastatin Adapted from Jones PH et al. Am J Cardiol 2003;92:152–160 & CURVES Study. Am J Cardiol 1998;81:582-7. 10
- 68. Common medications that increases levels of HDL and its subclasses Medication HDL HDL2 HDL3 Apo AI Statins +5 to 10% +5 + 30% -5 to +5% -5 to +5% Fibrates +10 to 15% -5% +5 to +30 -5 to +5 Niacin +25 to 50% +50 to 200% -5 to +5% +5 to +30%
- 74. Bile Acid Sequestrants 1.) LDL Uptake Cholesterol 2.) Synthesis HMG CoA Bile Acids Cholesterol HMG CoA Bile Acids Intestines Intestines
Notas do Editor
- Other dietary considerations include to limit trans fatty foods . Diets that lower cholesterol include plant stanols/sterols (2 g/day) and soluble fiber (10-25 g/day). The role of alcohol is not well-defined.
- The role and benefits of exercise is to be stressed: Aerobic exercise of > 20 minutes per activity for at least 3 days per week has been proved to be beneficial. Exercise also promotes weight loss and HDL
- Complete cessation of smoking c an lower oxidative stress, reverses endothelial dysfunction and HDL.
- Weight loss by exercise and dieting increases HDL, i mproves glycemic control and reduces blood pressure
- Cholesterol lowering drug therapy includes : HMG CoA Reductase Inhibitors: Lovastatin,Pravastatin,Simvastatin,Fluvastatin,Atorvastatin and Rosuvastatin Cholesterol Absorption Inhibitors: Ezetimibe Fibrates: Gemfibrozil,Micronized Fenofibrate and Clofibrate Bile Acid Sequestrants: Cholestyramine ,Colestipol and Colesevelam And Niacin
- HMG CoA reductase acts directly on the cholesterol and bile acids .
- Dosage of statins depends on the level of LDL : Start with lower dose and increase as needed . Doses should be given in the evening or at bedtime (Atorva and Rosuva can be given any time) . May need to decrease dose occasionally by adding potentially interacting drug if a profound drop in LDL is noted.
- Side effects of statins include : Major toxicitieslike Hepatic transaminases , myalgias and rhabdomyolysis . Selected minor adverse effects like d yspepsia/heartburn , headache and taste disturbances
- Monitoring of the drug therapy must be done at regular intervals : Lipid Profiles Before initiation and at 6-12 weeks until stable Every 6 months thereafter Hepatic Transaminases Baseline and every 6-12 weeks until stable Every 6 months thereafter Creatine Kinase (CK) Only as needed Glucose and Uric Acid .
- Signs and symptoms of myotoxicity include : Symptoms consist primarily of gradually decreased muscle strength and localized or generalized muscle weakness. Symptoms can occur within days or may not occur for years after starting therapy. Symptoms involving other organ systems (such as fatigue, shortness of breath, decreased urine output, dark-colored/turbid urine).
- Graph shows the comparative LDL lowering effects of statins .
- Graph shows a comparative study of statins and the beneficial effects on the HDL levels
- Graph shows comparison of statins and their effect on lowering of TG levels
- Drug interactions of statins include risk of hepatotoxicity and/or myalgias or myopathy when combined with fibrates or niacin Statins absorption with bile acid sequestrants, inhibit or induce CYP-based metabolism and inhibit CYP activity
- Mechanism of action of fibrates include :Inhibition of cholesterol synthesis, decreased TG synthesis, inhibition of lipolysis in adipose tissue, decreased production of VLDL/ clearance and increased plasma and hepatic LPL activity. Effect on lipids includes TC, LDL, HDLand TG .
- Dosing of fibrates are : Gemfibrozil: 600mg BID Micronized Fenofibrate: 67mg QD; to 67-201mg QD Clofibrate: 2g daily in divided doses Adverse effects are Nausea, diarrhea, cholelithiasis, phototoxicity Drug interactions include Increased risk of hepatotoxicity and/or myalgias with concurrent statins and/or niacin and protein binding displacement (e.g., warfarin
- Niacin: The Mechanism of action includes inhibition of free fatty acid release from adipose tissue,inhibition of cAMP accumulation ,inhibition of VLDL and LDL synthesis and increased LPL activity. The effects on lipids are that it TC, LDL, HDL, TG , c onverts LDL phenotypic pattern B into pattern A and lowers Lp(a) .
- Niacin is immediately released in dose of 100mg TID; it may be by 100mg TID every week as tolerated and the ideal goal = 500-1000mg TID . Sustained release tablets are also available as 375mg QD; it maybe gradually as needed to an ideal goal = 500-2000mg QD.
- Precautions while adminstering niacin to be kept in mind are the adverse effects that include f lushing, pruritis, headache, fatigue (PG-mediated? -- ASA), gastritis, abdominal pain, aggravation of PUD, hepatotoxicity ,impaired glucose control and uric acid concentrations. The drug interactions include with alcohol: risk of hepatotoxicity , with Statins, fibrates: risk of hepatotoxicity and/or myalgias. Contra-Indication are a H/o gout,peptic ulcer disease, liver disease.
- Bile acids reaches the gut and bile acid sequestrants prevent re-entry into the liver.
- Ezetimibe is the first member of a new class of lipid-lowering drugs that target intestinal absorption by inhibiting absorption of dietary and biliary cholesterol across the intestinal wall. Ezetimibe, co-administered with a statin, at any dose, provides even greater plasma cholesterol reduction by controlling two sources of cholesterol through Dual Inhibition. Ezetimibe may also be useful as monotherapy in patients who cannot tolerate or do not respond to statins. Current data from controlled clinical trials indicate that ezetimibe has a favorable safety profile, alone it is similar to placebo and when co-administered with a statin, similar to the statin alone. Co-administration therapy with a statin and ezetimibe should decrease the need for statin dose adjustments, broaden lipid control, and facilitate achievement and maintenance of LDL-C goals.
- Ezetimibe is useful as monotherapy for patients intolerant or nonresponsive to statins or enhanced benefits in addition to statins. Favorable safety and tolerability profile shown in clinical trials reveal they are similar to placebo, similar to statin alone, in coadministration
- Certain herbs and natural products are found to be beneficial : Garlic Fish Oils Red Yeast Rice Dietary Fiber Oat Bran Plant Sterols Guggul CoEnzyme Q10