Dietary supplements

Vitamins: There are no recommendations for vitamin therapy when treating dyslipidemia. This could be due to lack of adequate understanding regarding the underlying cellular mechanisms of LDL oxidation.18 No vitamins or supplements, except for fish oil, are approved for hyperlipidemia therapy. 

Omega-3 polyunsaturated fatty acids: Omega-3 ester is the only FDA-approved supplement for treatment of dyslipidemia, specifically for lowering serum triglyceride levels.19 Prescription ethyl esters of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (Omacor) decrease hepatic production of triglycerides and very low-density lipoproteins (VLDL). Little effect is seen on HDL levels, and LDL concentrations increase marginally. However, LDL size changes to the less atherogenic, large, buoyant particles, suggesting some mitigation of LDL effect. Prescribing Omacor for the treatment of high VLDL is not recommended because no data support VLDL reduction to limit clinical CV events. Note that the FDA has approved this preparation only to lower triglycerides >500 in patients at risk for pancreatitis; Omacor is not currently approved for CV risk reduction.


Continue Reading

The Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-Prevenzione trial illustrated a reduction in death, nonfatal MI, and nonfatal stroke at nine months as well as a reduction in the risk of sudden cardiac death after four months with omega-3 ester 850 mg/day, suggesting an additional antiarrythmic effect.20 Furthermore, in 2002, the American Heart Association (AHA) recommended that patients with known CHD consume 1 g EPA plus DHA per day, preferably from oily fish.21 This is easily achieved by consuming two fatty fish meals per week (i.e., salmon, herring, mackerel, swordfish, albacore tuna, sardines, lake trout) and by using liquid vegetable oils containing α-linolenic acid (flaxseed, canola, and soybean oils).4,21 However, commercially prepared fried fish products should be avoided because they are low in omega-3 polyunsaturated fatty acids and high in trans-fatty acids.

Lifestyle changes

Currently, no clinical trials have evaluated the long-term effects of weight reduction, exercise, diet, or alcohol intake as single treatments for secondary prevention of coronary events. However, several observational studies support the use of these lifestyle changes for primary prevention of CHD because these measures have demonstrated significant reductions in risk markers for CHD. 

Weight loss: Modest weight loss (5%-10% body weight) lowers BP, prevents type 2 diabetes or improves its control, and improves lipid profiles, specifically lowering triglycerides, LDL, and total cholesterol while increasing HDL.4 The AHA recommends patients reduce their weight by 10% in the first year of a comprehensive risk-reduction program.22 Goal BMI is 18.5-24.9 kg/m2, with a goal waist circumference of ≤40 in (men) or ≤35 in (women).22 

Exercise: More than 40 observational studies have demonstrated an inverse relationship between amount of exercise and all-cause mortality in men and women with CHD or CHD risk factors.4 The AHA recommends a minimum of 30 minutes of moderate-intensity exercise at least four days per week, but preferably every day.22 This includes activities that increase the heart rate to 40%-60% of maximum capacity.22 

Diet: AHA guidelines regarding diet and primary prevention of CHD and stroke recommend a total cholesterol intake of <300 mg/day, limiting saturated fats to <10% of total caloric intake, and reducing trans-fatty acids by substituting grains and unsaturated fats from fish, vegetables, legumes, and nuts.22 NCEP ATP-III recommendations for dietary changes in patients with elevated LDL levels consist of limiting cholesterol and saturated fats to <200 mg/day and <7% of total daily caloric intake, respectively.

Alcohol: More than 100 prospective studies have shown an inverse relationship between moderate alcohol consumption and increased risk of heart attack, stroke, peripheral vascular disease, sudden cardiac death, and all-cause CVD mortality, both in primary and secondary CHD prevention in men and women.4 Moderate alcohol consumption raises HDL levels; low levels are an independent risk factor for CHD. The AHA recommends limiting alcohol consumption to two or fewer drinks per day in men and no more than one drink per day in women.22

Ms. Stubbs is a family nurse practitioner specializing in cardiology at the G.V. Montgomery VA Medical Center in Jackson, Miss., where Dr. Geraci is chief of medical service.

References

1. 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. 2001;285:2486-2497.
2. American Heart Association. High blood cholesterol and other lipids: heart disease and stroke statistics — 2005 update. Available at: www.americanheart.org/downloadable/heart/1105390918119HDSStats2005Update
.pdf. Accessed July 17, 2006.
3. 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. 2004;110;227-239.
4. Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed. St Louis, Mo: WB Saunders; 2005:1024-1025, 1048, and 1073-1074.
5. Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004;350:1495-1504.
6. LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352:1425-1435.
7. Colhoun HM, Betteridge DJ, Durrington PN, et al. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet. 2004;364:685-696.
8. Pedersen TR, Faergeman O, Kastelein JJ, et al. High-dose atorvastatin vs. usual-dose simvastatin for secondary prevention after myocardial infarction: the IDEAL study: a randomized controlled trial. JAMA. 2005;294:2437-2445.
9. The Lipid Research Clinics Coronary Primary Prevention Trial results. I. Reduction in incidence of coronary heart disease. JAMA. 1984;251:351-364.
10. Birjmohun RS, Hutten BA, Kastelein JJ, Stroes ES. Efficacy and safety of high-density lipoprotein cholesterol-increasing compounds: a meta-analysis of randomized controlled trials. J Am Coll Cardiol. 2005;45:185-197.
11. Jacobson TA, Zimmerman FH. Fibrates in combination with statins in the management of dyslipidemia. J Clin Hypertens (Greenwich). 2006; 8:35-41.
12. Rubins HB, Robins SJ, Collins D, et al. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. N Engl J Med. 1999;341:410-418.
13. Frick MH, Elo O, Haapa K, et al. Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, and incidence of coronary heart disease. N Engl J Med. 1987;317:1237-1245.
14. Keech A, Simes RJ, Barter P, et al. Effects of long-term fenofibrate therapy on cardiovascular events in 9,795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet. 2005;366:1849-1861.
15. Brown BG, Zhao X-Q, Chait A, et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med. 2001;345:1583-1592.
16. Davidson MH, McGarry T, Bettis R, et al. Ezetimibe coadministered with simvastatin in patients with primary hypercholesterolemia. J Am Coll Cardiol. 2002;40:2125-2134.
17. Gagne C, Gaudet D, Bruckert E, Ezetimibe Study Group. Efficacy and safety of ezetimibe co-administered with atorvastatin or simvastatin in patients with homozygous familial hypercholesterolemia. Circulation. 2002;105:2469-2475.
18. Steinberg D, Witztum JL. Is the oxidative modification hypothesis relevant to human atherosclerosis? Do the antioxidant trials conducted to date refute the hypothesis? Circulation. 2002;105:2107-2111.
19. Abramowicz M, ed. Omega-3 polyunsaturated fatty acids (Omacor) for hypertriglyceridemia. Med Lett Drugs Ther. 2005;47:91-92.
20. Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002;105:1897-1903.
21. Kris-Etherton PM, Harris WS, Appel LJ. American Heart Association Nutrition Committee. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 2002;106:2747-2757.
22. Pearson TA, Blair SN, Daniels SR, et al. AHA Guidelines for Primary Prevention of Cardiovascular Disease and Stroke: 2002 Update: Consensus Panel Guide to Comprehensive Risk Reduction for Adult Patients Without Coronary or Other Atherosclerotic Vascular Diseases. American Heart Association Science Advisory and Coordinating Committee. Circulation. 2002;106:388-391.