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69 Year Old Male with Dyslipidemia and Abnormal CIMT

69 Year Old Male with Dyslipidemia and Abnormal CIMT. C ase category: Low HDL History of present illness: 69 year old male with dyslipidemia, history of low HDL and abnormal CIMT. Currently on simvastatin 40, metformin 1500 and Niaspan 1500. LDL-P remains high. Case Categories

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69 Year Old Male with Dyslipidemia and Abnormal CIMT

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  1. 69 Year Old Male with Dyslipidemia and Abnormal CIMT Case category: Low HDL History of present illness: 69 year old male with dyslipidemia, history of low HDL and abnormal CIMT. Currently on simvastatin 40, metformin 1500 and Niaspan 1500. LDL-P remains high. Case Categories Primary Prevention Secondary Prevention Pediatric Case Familial Hypertriglyceridemia Diabetes Metabolic Syndrome Low HDL Familial Combined Hyperlipidemia Familial Hypercholesterolemia Elevated Lipoprotein (a) Statin Intolerance

  2. Patient Information

  3. Patient History

  4. Current Medications

  5. Labs Worth Noting Simvastatin 40, Metformin 1500 and Niaspan 1500

  6. Questions to Consider • Question 1: Have diet and exercise efforts been maximized? (Yes, he is normal body weight and following low carb, low glycemic diet. Exercises 4 times/week.) • Question 2: Tolerating medications and compliant with therapy? (Yes)

  7. Labs on Simvastatin 40, Metformin 1500 and Niaspan 1500 (1 of 5)

  8. Labs on Simvastatin 40, Metformin 1500 and Niaspan 1500 (2 of 5) Diet and exercise maximized. Stable on meds but LDL-P remains high.

  9. Labs on Simvastatin 40, Metformin 1500 and Niaspan 1500 (3 of 5)

  10. Labs on Simvastatin 40, Metformin 1500 and Niaspan 1500 (4 of 5)

  11. Labs on Simvastatin 40, Metformin 1500 and Niaspan 1500 (5 of 5) Taking 4 grams EPA/DHA over the counter omega 3 fish oil.

  12. NMR LipoProfile • Insert NMR Lipoprofile 11302011 TN42 Insert

  13. Initial Treatment & Management • Switch from simvastatin 40 to Crestor 20 which provides greater LDL-P reduction. • Continue metformin 1500 for insulin resistance syndrome. • Hypertension is currently stable on Metoprolol. Continue therapy. • For low omega 3 Index, increase OTC omega 3 fish oil to 5 gor take more potent EPA/DHA product.

  14. Discussion (1 of 2)

  15. Discussion (2 of 2)

  16. Follow Up on Crestor 20, Metformin 1500 and Niaspan 1500 (1 of 2) • Dyslipidemia (history of low HDL) – Improved. • At last visit, switched from simvastatin 40 to Crestor 20. Also taking Niaspan 1500 and OTC omega 3 fish oil 5. • Excellent response to change in statin. LDL-P lowered from 1543 to 1005. Total cholesterol dropped to 122 from 180. LDL-C lowered to 63 from 108. Triglycerides reduced to 76 from 88. Apo B lowered from 95 to 62. Non-HDL-C lowered from 130 to 80. HDL did lower to 42 from 50. • It’s reassuring that all inflammatory markers are normal. • Sterol testing showed some hyperabsorption, but LDL-P and other labs are normal so no need for additional medication. Advised patient to avoid any supplements that contain phytosterols due to fact he absorbs these and would be potentially dangerous to consume as when absorbed is more toxic than his own cholesterol. • Continue therapy. • Insulin Resistance Syndrome – Stable. • Currently taking metformin 1500. • HbA1c is stable at 5.3. IR-score is 30.

  17. Follow Up on Crestor 20, Metformin 1500 and Niaspan 1500 (2 of 2) • Hypertension – Stable. • Stable on Metoprolol. • Continue therapy. • Low Omega 3 Index – Unchanged. • Omega 3 index remains low at 7.1%. • Continue supplements. • Homocystinemia – New. • Homocystinemia is an independent risk factor for premature CVD caused by deficiencies in folate, B12, and B6. Increased risk is >10. • Will need to work up secondary causes before treatment with folic acid supplementation. Need to determine if levels are high due to Niaspan therapy or MTHFR mutation. He has normal B12, and normal folate. Could do an Methyl malonic acid level and if high suspect B12 deficiency and supplement accordingly. May be reasonable to just have him take 500 mg oral B12. • We do not know if treatment of elevated homocysteine will reduce CV events.

  18. Follow Up Labs on Crestor 20, Metformin 1500 and Niaspan 1500 (1 of 6)

  19. Follow Up Labs on Crestor 20, Metformin 1500 and Niaspan 1500 (2 of 6)

  20. Follow Up Labs on Crestor 20, Metformin 1500 and Niaspan 1500 (3 of 6)

  21. Follow Up Labs on Crestor 20, Metformin 1500 and Niaspan 1500 (4 of 6)

  22. Follow Up Labs on Crestor 20, Metformin 1500 and Niaspan 1500 (5 of 6)

  23. Follow Up Labs on Crestor 20, Metformin 1500 and Niaspan 1500 (6 of 6)

  24. NMR LipoProfile • Insert NMR Lipoprofile 01242012 TN42 Insert

  25. Case Summary

  26. Clinical Pearls • When LDL-C and LDL –P are discordant, risk tracks with LDL-P. (See MESA data slide) • When patients have residual risk based on elevated LDL–P and are already on combination drug therapy (in this case simvastatin plus niacin), options are to add therapy or to simply change to more potent statin. Rosuvastatin (Crestor) is most potent for LDL-P reduction. If he had evidence of insulin resistance on NMR could titrate to higher dose of metformin and adjust diet further. His IR score and HbA1C are normal. • Statins reduce LDL-C more effectively than they reduce LDL-P in part by lowering the cholesterol content of the particles vs optimizing the total LDL–P concentration. The most “bang for the buck” comes from initial statin dose. Doubling dose will not likely improve LDL-P more then 6 %. Its more effective to add another agent or change to more potent statin.

  27. LDL-P and LDL-C Discordance in MESA CVD Event Rates in Subgroups with Low LDL Residual Risk Otvos et al. J ClinLipidol 2011;5:105-13

  28. COMETS: Percent LDL Lowering by Statin Monotherapy in Metabolic Syndrome Patients LDL-C (mg/dL) LDL-P (nmol/L) Rosuvastatin Atorvastatin 0 0 1960 1870 168 171 10 10 20 20 1300 Percent Reduction 1260 30 30 1260 33% 1210 38% 40 40 105 44% 93 95 50 50 50% 84 60 60 Baseline 6 weeks 12 weeks Baseline 6 weeks 12 weeks (10 mg) (20 mg) (10 mg) (20 mg) Less cholesterol per LDL particle Less cholesterol per LDL particle Fewer LDL particles Less cholesterol per particle Rosenson RS and Otvos J, unpublished data

  29. References (1 of 2) • Dyslipidemia • Cromwell WC, Otvos JD, Keyes MJ, et al. LDL particle number and risk of future cardiovascular disease in the Framingham offspring study – implications for LDL management. J ClinLipidol. 2007 Dec;1(6):583-92. • El Harchaoui K, van der Steeg WA, Stroes ES, et al. Value of low-density lipoprotein particle number and size as predictors of coronary artery disease in apparently healthy men and women: the EPIC-Norfolk Prospective Population Study. J Am CollCardiol. 2007 Feb 6;49(5):547-53. • Ballantyne C, Herd JA, Stein E, et al. Apolipoprotein E genotypes and response of plasma lipids and progression-regression of coronary atherosclerosis to lipid-lowering drug therapy. J Am CollCardiol2000;36:1572-8. • Nicholls SJ, Ballantyne CM, Barter PJ, et al. Effect of two intensive statin regimens on progression of coronary disease. N Engl J Med. 2011 Dec 1;365(22):2078-87. • Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008 Nov 20;359(21):2195-207. • Otvos JD, Mora S, Shalaurova I, et al. Clinical implications of discordance between low-density lipoprotein cholesterol and particle number. J ClinLipidol. 2011 Mar-Apr 5(2):105-13. • Rosenson RS, Otvos JD and Hsia J. Effects of rosuvastatin and atovastatin on LDL and HDL particle concentrations in patients with metabolic syndrome: a randomized, double-blind, controlled study. Diabetes Care. 2009 Jun;32(6):1087-91.

  30. References (2 of 2) • Insulin Resistance Syndrome • ADA Standards of Medical Care in Diabetes - 2012. Diabetes Care. Jan 2012 35(1)11-63. • Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002 Feb 7;346(6):393-403. • Omega 3 • Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Lancet. 1999 Aug 7;354(9177):447-55. • Homocystinemia • Bos MJ, Heijer M, Willems H, et al. Homocysteine lowering by B vitamins and the secondary prevention of deep vein thrombosis and pulmonary embolism: a first randomized, placebo-controlled, double-blind trial. Blood. 2004; 104: 142a. • Toole JF, Malinow MR, Chambless LE, et al. Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death. JAMA. 2004; 291: 565–575. • Wald DS, Law M, Morris JK. Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis. BMJ. 2002 Nov 23;325(7374):1202.

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