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51 Year Old Male with Known CAD, Recent CABG and Low HDL

51 Year Old Male with Known CAD, Recent CABG and Low HDL. Case Categories: Secondary P revention and Low HDL

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51 Year Old Male with Known CAD, Recent CABG and Low HDL

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  1. 51 Year Old Male with Known CAD, Recent CABG and Low HDL Case Categories: Secondary Prevention and Low HDL History of present illness: 51 year old male with known coronary artery disease with previous stents placed at age 43. Now disease has progressed leading to need for quadruple bypass surgery. He has low HDL and high cardiovascular risk. In cardiac rehab, labs are post 20 pound weight loss.

  2. Patient Information

  3. Patient History

  4. Current Medications

  5. Labs Worth Noting

  6. Questions to Consider • Question 1: Assess medication compliance. • Question 2: Diet low carb or low fat? Low carb would be of benefit. • Question 3: Any other illness or source of inflammation (high CRP)?

  7. Labs

  8. Labs

  9. NMR LipoProfile • Insert NMR LipoProfile 06192011 JT59 Insert

  10. Other Labs

  11. Initial Treatment & Management High risk secondary prevention with low HDL-P, Apo A1 and HDL-C despite Niaspan 2000, Simvastatin 40 and Tricor; Also Elevated Lp(a) and high CRP. • Continue Niaspan 2000 mg/day • Consider Lovaza (prescription Omega 3 1-2 g/day or higher dose of diet supplement omega 3 • Start 5000 IU Vitamin D3 daily and 50,000 Vitamin D2/week due to severe deficiency • Stop Simvastatin 40 mg • Start Crestor 40 mg/day • Stop Tricor (no history of elevated triglycerides) • Continue Carvedilol and Altace for BP control • Advise low carb diet and exercise

  12. Discussion

  13. Discussion

  14. Follow Up • Elevated CRP – Improved; levels now normal from 10 to 0.5; LpPLA2 remained normal. • Elevated Lipoprotein (a) – Unchanged; not likely to lower much further; dietary changes and addition of Metformin and normalizing thyroid may reduce, but no indication at this time; Note: insulin was borderline high. • CAD – Treating all risk factors aggressively; taking aspirin 81 mg/day. • Vitamin D Deficiency – Improved; Levels increased from 23 to 47; continue therapy. • Low HDL – Improved as well as Apo A1, HDL-P and HDL-C; As omega 3 index is still low, increase Lovaza or add salmon to diet; LDL-P dropped from 1196 to 613; Sterol absorption is slightly up so may add Benecol or decrease Crestor dose. • Homocystinemia – Improved; almost at a normal level; previous high level most likely due to Tricor use.

  15. Follow-Up Labs

  16. Follow-Up Labs

  17. Follow-Up Labs

  18. Follow-Up Labs

  19. Dietary Supplementation With Omega-3 Fatty Acids After Myocardial Infarction GISSI-P Results Placebo (n = 2828) Omega-3 FA 1 g (n = 2836) 15% Reduction P=.023 20% Reduction P=.008 Event Rate, % Death/ Nonfatal MI/ Nonfatal Stroke CVD Death/ Nonfatal MI/ Nonfatal Stroke GISSI-P Investigators. Lancet. 1999;354(9177):447-455.

  20. Clinical Pearls Always think about secondary causes, are all current medications needed? In very high risk patients optimal LDL-P and Apo B important to assess. This case had normal non HDL-C but had aggressive recurrent CAD despite combination drug therapy. Isolated low HDL also associated with residual risk. Lipoprotein (a) is a genetic marker for premature CAD. Niaspan is best option for Lp (a) lowering but ideally dual target of low Apo B and low LDL –P important to reduce risk associated with high lipoprotein(a). Crestor is more potent statin for LDL –P lowering as well as HDL raising.

  21. Case Summary

  22. References • GISSI-P Investigators. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzion trial. Lancet. 1999;354(9177):447-455. • ShimabukuroM, Higa M, Tanaka H, et al. Distinct effects of pitavastatin and atorvastatin on lipoprotein subclasses in patients with Type 2 diabetes mellitus. Diabet Med. Jul 2011;28(7):856-64. • Marcovina SM, Kennedy H, Bittolo Bon G, Cazzolato G, Galli C, Casiglia E, Puato M, Pauletto P (May 1999). "Fish intake, independent of apo(a) size, accounts for lower plasma lipoprotein(a) levels in Bantu fishermen of Tanzania: The Lugalawa Study". Arteriosclerosis, Thrombosis, and Vascular Biology 19 (5): 1250–6. doi:10.1161/01.ATV.19.5.1250. PMID 10323776. • Saposnik G, Ray JG, Sheridan P, McQueen M, Lonn E. Homocysteine-lowering therapy and stroke risk, severity, and disability: additional findings from the HOPE 2 trial. Stroke. Apr 2009;40(4):1365-72. • Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. May 16 2001;285(19):2486-97. • Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III Final Report). US Department of Health and Human Services; May 2001. • Grundy SM, Cleeman JI, Merz CN, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. Jul 13 2004;110(2):227-39. • Singh VN. New ATP III lipid guidelines update for patients at high risk for cardiovascular events. eMedicine Feature Series - Lipid Newsletter [serial online]. Jul 21, 2005;series 1(9). • Vega GL, Grundy SM. Comparison of lovastatin and gemfibrozil in normolipidemic patients with hypoalphalipoproteinemia. JAMA. Dec 8 1989;262(22):3148-53. • HDL-Atherosclerosis Treatment Study (HATS). Cardiosource: American College of Cardiology. • Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol 2 (ARBITER 2). Cardiosource: American College of Cardiology.

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