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C ase category: Elevated Lipoprotein(a)

52 Year Old Female with Hyperlipidemia, Elevated Lipoprotein(a), Elevated Homocysteine, Hypercoagulable State and Abnormal CIMT. C ase category: Elevated Lipoprotein(a)

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C ase category: Elevated Lipoprotein(a)

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  1. 52 Year Old Female with Hyperlipidemia, Elevated Lipoprotein(a), Elevated Homocysteine, Hypercoagulable State and Abnormal CIMT Case category: Elevated Lipoprotein(a) History of present illness: 52 year old female with hyperlipidemia, elevated lipoprotein(a), elevated homocysteine, hypercoagulable state and abnormal CIMT >75th%. Seen a year ago, her hyperlipidemia had improved on Simcor (Niacin-Simvastatin) 1000-40 with LDL-P at 805, triglycerides at 46, LDL-C at 88, total cholesterol at 172, HDL at 75 and IR score at 9. She is here for a routine follow-up appointment.

  2. Patient Information

  3. Patient History

  4. Current Medications

  5. Labs Worth Noting on Simcor 1000/40 and Lovaza 3

  6. Questions to Consider • Question 1: Always assess medication compliance. She is tolerating Simcor (Niacin-Simvastatin) well and taking consistently. • Question 2: Assess diet, exercise and weight management goals and motivation to improve further. • Question 3: Assess sleep. Any evidence of sleep apnea? • Question 4: Mental health? Any stressors that may be contributing to abnormal labs?

  7. Labs on Simcor 1000/40 and Lovaza 3 (1 of 5) She has normal traditional lipids on combination therapy. With history of known disease based on abnormal CIMT in past and treatment goal of plaque stabilization and regression, it is important all risk factors have been aggressively managed. Next slide shows she has elevated LDL-P > 1000. Also with high lipoprotein(a) we try to lower LDL –P even further (<700) as we recognize it will be difficult to normalize Lp (a) even with niacin. If LDL-P/Apo B are very low, much less likely to see risk associated with high lipoprotein(a).

  8. Labs on Simcor 1000/40 and Lovaza 3 (2 of 5)

  9. Labs on Simcor 1000/40 and Lovaza 3 (3 of 5)

  10. Labs on Simcor 1000/40 and Lovaza 3 (4 of 5)

  11. Labs on Simcor 1000/40 and Lovaza 3 (5 of 5) Assess compliance with taking Lovaza 3/day. Typically omega 3 index should be normal with high dose omega 3 prescription supplement. She admits to using over the counter on occasion. This is a good marker of compliance with therapy.

  12. NMR LipoProfile • Insert NMR Lipoprofile 08032011 LW59 Insert

  13. Other Labs on Simcor 1000/40 and Lovaza 3

  14. Initial Treatment & Management • Increase dose of Simcor (Niacin-Simvastatin) to 1500/40 with 750/20 Simcor 2/day to lower Lp(a) and decrease LDL-P. • Continue to take folic acid for homocystinemia and hypercoagulable state. With MTHFR mutation may need to supplement with active methylfolate or betainesupplementation. • Increase dose of Lovaza to 4 g/day for low omega 3 index or consume more omega 3. Highest sources come from Atlantic salmon, herring, mackerel, or Bluefin tuna.

  15. Discussion (1 of 3)

  16. Discussion (2 of 3)

  17. Discussion (3 of 3)

  18. Follow Up on Simcor 1500/40 and Lovaza 4 • Hyperlipidemia – Improved. • Currently on Simcor (Niacin-Simvastatin) 1500/40 (higher dose) and Lovaza 4. LDL lowered from 1179 to 674. Total cholesterol dropped from 188 to 172. LDL-C lowered to 60 from 82. Triglycerides reduced to 47 from 68. Non-HDL-C dropped from 115 to 87. HDL increased from 73 to 85. • Continue therapy. • Elevated Lipoprotein(a) – Improved. • With increase in niacin, Lp(a) lowered from 117 to 108. L(p) a cholesterol is still too high. Will be difficult to normalize Lp(a) even with high dose niacin therapy as typically only 20-30 % reduction expected. • Homocystinemia and Hypercoagulable State – Unchanged. • Currently taking folic acid. • Homocysteine decreased from 13 to 12. • Has MTHFR mutation. Consider methylfolate which will be more effective due to this mutation. No clinical trials support need to treat this elevation. Homocysteine may be mildly increased from use of niacin as well. Fibrates are more likely to elevate homocysteine but niacin does have small effect as well. • Low omega 3 Index – Unchanged. • Currently taking Lovaza 4. • Continue therapy.

  19. Labs on Simcor 1500/40 and Lovaza 4 (1 of 5)

  20. Labs on Simcor 1500/40 and Lovaza 4 (2 of 5)

  21. Labs on Simcor 1500/40 and Lovaza 4 (3 of 5)

  22. Labs on Simcor 1500/40 and Lovaza 4 (4 of 5)

  23. Labs on Simcor 1500/40 and Lovaza 4 (5 of 5)

  24. NMR LipoProfile • Insert NMR Lipoprofile 02142012 LW59 Insert

  25. Case Summary

  26. Clinical Pearls • Increases in homocysteine concentration can occur with aging, menopause, hypothyroidism, low plasma levels of vitamin (B6, B12 and folate), certain drugs, and chronic renal insufficiency. • She is heterozygous (C/T) for MTHFR mutation. This indicates that a portion of her MTHFR enzyme is not as effective at methylatingfolate. Methylfolateis the active form of folate. In most cases heterozygosity of the MTHFR polymorphism will not result in elevated homocysteine, but these individuals may have a greater sensitivity to folate deficiency, and in the absence of adequate folate intake, homocysteine values may increase to higher levels. Patients with high homocysteine values who are heterozygous for the MTHFR polymorphism will respond to folate supplementation with folic acid, but should consider supplementation with active methylfolate. • Although homocysteine is an independent risk factor for CVD events, treatment of elevated homocysteine with folic acid and B vitamins (B6 and B12) has not been shown to decrease events. Consideration should be given to more aggressive treatment of other CV risk factors in patients with elevated homocysteine. Other homocysteine lowering efforts which may be beneficial include methylfolate and/or betainesupplementation.

  27. Lp(a) and CHD Reykjavik Study (n=18 569) 2047 patients with first-ever MI or who died of CHD. vs. 3921 control participants Bennet et al. Lipoprotein(a) levels and risk of future coronary heart disease: large-scale prospective data. Arch Intern Med. 2008 Mar 24;168(6):598-608.

  28. Lp(a) Proven as Causal Factor for MI Copenhagen Heart Study Kamstrup PR, Tybjaerg-Hansen A, Steffensen R, et al. Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA. 2009 Jun 10;301(22):2331-9.

  29. References (1 of 2) Hyperlipidemia • 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. • Lyseng-Williamson KA. Niacin extended release (ER)/Simvastatin (Simcor): A guide to its use in lipid regulation. Drug R D. 2010;10(4):235-60. • Karas RH, Kashyap ML, Knopp RH, et al. Long-term safety and efficacy of a combination of niacin extended release and simvastatin in patients with dyslipidemia: the OCEANS study. Am J Cardiovasc Drugs. 2008;8(2):69-81. • Airan-Javia SL, Wolf RL, Wolfe ML, et al. Atheroprotective lipoprotein effects of a niacin-simvastatin combination compared to low- and high-dose simvastatin monotherapy. Am Heart J. 2009;157:687-688. Elevated Lipoprotein(a) • Nordestgaard B, Chapman M, Ray K, et al. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010 Dec;31(23):2844-53. • Marcovina SM, Kennedy H, Bittolo Bon G, et al. Fish intake, independent of apo(a) size, accounts for lower plasma lipoprotein(a) levels in Bantu fishermen of Tanzania: The Lugalawa Study. ArteriosclerThrombVasc Biol. May;19(5):1250–6. • Bennet A, Di Angelantonio E, Erqou S, et al. Lipoprotein(a) levels and risk of future coronary heart disease: large-scale prospective data. Arch Intern Med. 2008 Mar 24;168(6):598-608. • Kamstrup PR, Tybjaerg-Hansen A, Steffensen R, et al. Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA. 2009 Jun 10;301(22):2331-9.

  30. References (2 of 2) Homocystinemia and Hypercoagulable State • 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. • Klerk M, Verhoef P, Clarke R, et al. MTHFR 677C-T polymorphism and risk of coronary heart disease: a meta-analysis. JAMA. 2002; 288: 2023–2031. • Wald DS, Law M, Morris JK. Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis. BMJ. 2002 Nov23;325(7374):1202. • Saposnik G, Ray JG, Sheridan P, et al. Homocysteine-lowering therapy and stroke risk, severity, and disability: additional findings from the HOPE 2 trial. Stroke. 2009 Apr;40(4):1365-72. Low Omega 3 Index • 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.

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