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53 Year Old Female with Premature CAD and Elevated Lp (a)

53 Year Old Female with Premature CAD and Elevated Lp (a). Case category: Familial Combined Hyperlipidemia; Secondary Prevention

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53 Year Old Female with Premature CAD and Elevated Lp (a)

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  1. 53 Year Old Female with Premature CAD and Elevated Lp(a) Case category: Familial Combined Hyperlipidemia; Secondary Prevention History of present illness: 53 year old female being treated for CAD with premature family history of heart disease/stoke, elevated lipoprotein(a), and hyperlipidemia.

  2. Patient Information

  3. Patient History

  4. Current Medications

  5. Labs worth noting

  6. Questions to Consider • Question 1: Any secondary causes of high LDL-P? Possible hypothyroidism? Ask about symptoms of fatigue, constipation, dry skin, muscle aches, depression, hair loss, and weight gain. • Question 2: Any prior use of Zetia or Bile acid sequestrants? Treatment response? • Question 3: Elevated lipoprotein (a) in setting of premature heart disease may warrant more aggressive treatment. • Question 4: Clear discordance between LDL-C and LDL-P. What agents will be more effective than statin monotherapy?

  7. Labs on Lipitor 40 mg Discordance between LDL-C and Apo B/LDL-P

  8. Labs

  9. Labs on Lipitor 40 mg: Sterol Absorption/Synthesis On Lipitor 40 mg: this suggests no longer oversynthesizing cholesterol in the liver based on normal desmosterol levels. But statin may have caused increase in absorption of sterols in gut and this is at least one potential cause of elevated LDL-P. We see this in the abnormal campesterol and cholestanol levels.

  10. Labs

  11. Labs

  12. NMR LipoProfile • Insert NMR LipoProfile 10122011 AZ58 Insert

  13. Other Labs

  14. Initial Treatment & Management • Stop Lipitor 40 mg • Start Crestor 20mg 1/day • Start Zetia 10mg 1/day • Start Niaspan 500mg for 1 month then increase to 1000 mg

  15. Discussion

  16. Discussion

  17. Discussion

  18. Follow Up • Familial Combined Hyperlipidemia, low Apo A1, and low HDL-P– change from Lipitor 40 last visit to Crestor 20, Niaspan 1000, and Zetia 10; Total cholesterol lowered from 169 to 143; LDL-C down to 57 from 92; HDL-C increased from 40 to 54; Non-HDL-C lowered to 89 from 129; Apo B also improved from 96 to 62; LDL-P reduced to 720 from 1634 (goal is <700). Responded well to Zetia, as she is a hyperabsorber of sterols. Lp(a) is still high which is expected not likely normalize even with Niaspan, she is responding well to combination therapy. • Elevated Lipoprotein(a) – unchanged. Level is still high (>225) as well as high Lp(a) cholesterol; Continue to lower LDL-P with statin and Niacin therapy; Consider additional dietary strategies. • Vitamin D Deficiency – has worsened to 25 from 30 on 1000 mg/day; Will increase to 5000 mg/day. • Elevated TSH – improved but still high. May consider addition of thyroid hormone if levels remain high next visit. Currently only mildly symptomatic with fatigue.

  19. Clinical Pearls Recognize the importance of discordance between LDL –C and LDL –Particle concentration (NMR) /Apo B in the setting of known coronary disease. The risk is carried in the LDL-Particles not the cholesterol. Lipoprotein(a) may be a contributor to premature disease, consider Niaspan or more aggressive control of LDL –P and Apo B to reduce risk. Understand the significance of adding sterol supplements without knowing whether patients are Hyperabsorbing. Without use of sterol testing it is best to avoid sterols as effect on LDL-C is minimal and may not be worth the risk. There are no outcomes data available to support benefit of sterols beyond small reductions in LDL-C.

  20. Case Summary

  21. References • Nicholls SJ, Ballantyne CM, Barter PJ, et al. Effect of two intensive statin regimens on progression of coronary disease. N Engl J Med 2011; DOI: 10.1056/NEJMoa1110874. • Rosenson, RS and Hsia Otvos. 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. • Sudhop T, Gottwald BM, and von Bergmann K. Serum plant sterols as a potential risk factor for coronary heart disease. Metabolism 2002;51:1519-1521. • Brown AJ and Jessup W. Oxysterols and atherosclerosis. Atherosclerosis 199;142:1-28. • Miettinen TA and Gylling H. et al. Relation of non-cholesterol sterols to coronary risk factors and carotid intima-media thickness: the Cardiovascular Risk in Young Finns Study. Atherosclerosis 2010 Apr;209(2):592-7. Epub 2009 Oct 20. • Assmann, Gerd; Cullen, Paul; Erbey, John; Ramey, Dena R.; Kannenberg, Frank; Schulte, Helmut (2006). "Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: Results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study". Nutrition, Metabolism and Cardiovascular Diseases16: 13–21 • Rajaratnam, Radhakrishnan A; Gylling, Helena; Miettinen, Tatu A (2000). "Independent association of serum squalene and noncholesterol sterols with coronary artery disease in postmenopausal women". Journal of the American College of Cardiology35 (5): 1185–91.

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