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Management of Elevated Lipoprotein(a) in a 73-Year-Old Female with Familial Hypercholesterolemia

This case study involves a 73-year-old female with familial hypercholesterolemia, elevated lipoprotein(a), and LpPLA2. Learn about her history, medications, lab results, and treatment plan for managing these conditions effectively.

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Management of Elevated Lipoprotein(a) in a 73-Year-Old Female with Familial Hypercholesterolemia

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  1. 73 Year Old Female with Familial Hypercholesterolemia and Elevated Lipoprotein(a) and LpPLA2. 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 Case category: Familial Hypercholesterolemia, Elevated Lipoprotein(a), Statin Intolerance History of present illness: 73 year old female with familial hypercholesterolemia, elevated lipoprotein(a) and LpPLA2. Currently taking Welchol and red rice yeast. Previous history of intolerance to statins and Niaspan. Here today for follow-up.

  2. Patient Information

  3. Patient History

  4. Current Medications

  5. Labs Worth Noting on Welchol and Red Rice Yeast

  6. Questions to Consider • Question 1 • Question 2 • Question 3 • Question 4

  7. Labs on Welchol and Red Rice Yeast (1 of 4)

  8. Labs on Welchol and Red Rice Yeast (2 of 4)

  9. Labs on Welchol and Red Rice Yeast (3 of 4)

  10. Labs on Welchol and Red Rice Yeast (4 of 4)

  11. NMR LipoProfile • Insert NMR Lipoprofile 062211 MR38 Insert

  12. Other Labs on Welchol and Red Rice Yeast

  13. Initial Treatment & Management • Continue Welchol and start Pravachol 40 mg/day to lower LDL-P. Stop taking red rice yeast. • Increase OTC fish oil from 1200 to 3000 mg/day to help lower Lp(a) and LpPLA2. • Continue taking vitamin D3 5000 IU/day.

  14. Discussion (1 of 3)

  15. Discussion (2 of 3)

  16. Discussion (3 of 3)

  17. Follow Up on Welchol and Pravachol 40 (1 of 2) • Familial Hypercholesterolemia – Improved. • Currently taking Welchol and Pravachol 40. Excellent improvement. • LDL-P lowered from 1712 to 954. LDL-C decreased from 169 to 84. Total cholesterol dropped to 198 from 320. • NMR shows normal risk pattern. • Continue therapy. • Elevated Lipoprotein(a) – Unchanged. • Due to niacin intolerance, Lp(a) is unlikely to change. • Additional less proven strategies to lower Lp(a) include aspirin 81-150 mg/day, Omega 3 fish oil high dose 3000/day; low carb diet, ground flax 2 tbsp/day, raw almonds ¼ cup/day, CO Q 10 150 mg/day. • Metformin and normalizing thyroid may also reduce Lp(a).

  18. Follow Up on Welchol and Pravachol 40 (2 of 2) • Elevated LpPLA2 – Improved. • Currently taking OTC fish oil 3000 mg/day. • Levels lowered from 234 to 179. • Continue supplements. • Vitamin D Deficiency – Improved. • Currently taking vitamin D3 5000 IU/day. • Levels increased from 47 to 78. • Continue supplements.

  19. Follow Up Labs on Welchol and Pravachol 40 (1 of 6)

  20. Follow Up Labs on Welchol and Pravachol 40 (2 of 6)

  21. Follow Up Labs on Welchol and Pravachol 40 (3 of 6)

  22. Follow Up Labs on Welchol and Pravachol 40 (4 of 6)

  23. Follow Up Labs on Welchol and Pravachol 40 (5 of 6)

  24. Follow Up Labs on Welchol and Pravachol 40 (6 of 6)

  25. NMR LipoProfile • Insert NMR Lipoprofile 100611 MR38 Insert

  26. Case Summary

  27. Clinical Pearls

  28. References (1 of 3) Familial Hypercholesterolemia • 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. • Mora S, Szklo M, Otvos JD, et al. LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA). Atherosclerosis. 2007 May;192(1):211-7. • Brunzell JD, Davidson M, Furberg CD, et al. Lipoprotein management in patients with cardiometabolic risk: consensus statement from the American Diabetes Association and the American College of Cardiology Foundation. Diabetes Care. 2008 Apr;31(4):811-22. • Genest J, Libby P. Lipoprotein disorders and cardiovascular disease In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 42. • Mahley RW, Weisgraber KH, Bersot TP. Disorders of lipid metabolism. In: Kronenberg HM, Melmed S, Polonsky KS, Larsen PR, eds. Williams Textbook of Endocrinology. 11th ed. Philadelphia, Pa: Saunders Elsevier; 2008:chap 36. • Semenkovich CF. Disorders of lipid metabolism. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 217.

  29. References (2 of 3) Elevated Lp(a) and LpPLA2 • Jenkins DJ, Kendall CW, Marchie A, et al. Dose response of almonds on coronary heart disease risk factors: blood lipids, oxidized low-density lipoproteins, lipoprotein(a), homocysteine, and pulmonary nitric oxide: a randomized, controlled, crossover trial. Circulation. 2002 Sep 10;106(11):1327-32. • Herrmann W, Biermann J, Kostner GM. Comparison of effects of N-3 to N-6 fatty acids on serum level of lipoprotein(a) in patients with coronary artery disease. Am J Cardiol. 1995 Sep 1;76(7):459-62. • 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. • 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. • 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. • Koenig W, Twardella D, Brenner H, et al. Lipoprotein-associated phospholipase A2 predicts future cardiovascular events in patients with coronary heart disease independently of traditional risk factors, markers of inflammation, renal function, and hemodynamic stress. ArteriosclerThrombVasc Biol. 2006;26:1586-1593. • Davidson MH, Corson MA, Alberts MJ, et al. Consensus panel recommendation for incorporating lipoprotein-associated phospholipase A2 testing into cardiovascular disease risk assessment guidelines. Am J Cardiol. 2008;101 suppl:51F-57F.

  30. References (3 of 3) Vitamin D Deficiency • Dobnig H, Pilz S, Scharnagl H, et al. Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality. Arch Intern Med. 2008;168(12):1340-1349. • Cannell J, Hollis B, Zasloff M, et al. Diagnosis and treatment of vitamin D deficiency. Pharmacotherapy. 2008;9(1):1-12. • Giovannucci E, Liu Y, Hollis B, Rimm E. 25-hydroxyvitamin d and risk of myocardial infarction in men. Arch Intern Med. 2008;168(11):1174-1180. • Holick M. Vitamin D Deficiency. N Engl J Med. 2007;357:266-81. • Michos E and Blumenthal R. Vitamin D Supplementation and Cardiovascular Disease Risk. Circulation. 2007;115(7):827-828. • Hathcock J, Shao A, Vieth R, et al. Risk assessment for vitamin D. Am J ClinNutr. 2007;85:6-18. • Jockers B. Vitamin D sufficiency: An approach to disease prevention. The American Journal for Nurse Practitioners. 2007;11(10):43-50. • Perez-Castrillon J, Vega G, Abad L, et al. Effects of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Am J Cardiol. 2007;99(7):903-4.

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