Coronary heart disease primary prevention
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The LDL target in primary prevention depends upon the patient's risk factors. If the patient has CHD or its equivalent, then the LDL goal is under 100 mg/dl. If the patient has 2 risk factors, the LDL goal is 130 mg/dl. If the patient has < 2 risk factors, the LDL goal is < 160 mg/dl.
Risk Equivalents in Primary Prevention
If CHD or a risk equivalent is present, the LDL goal is < 100 mg/dl. You are essentially considered to have the equivalent of coronary heart disease if you have any of the following "risk equivalents":
- Aortic aneurysm
- Diabetes
- Framingham Risk Score (FRS) of > 20% (A 20% risk of death or MI over 10 years)
- Peripheral vascular disease (PVD) (defined as claudication, an Ankle Brachial Index (ABI) of < 0.9)
- Symptomatic carotid artery disease (defined as prior stroke or TIA)
CV Risk Factors in the Setting of Primary Prevention
If you have two or more of the following risk factors, the LDL goal is < 130 mg/dl:
- Cigarette smoking
- Family history of premature coronary artery disease (CAD)
- High LDL (defined as LDL > 130 mg /dl)
- Hypertension ( defined as a BP ≥140/90 mm Hg or if the patient is on antihypertensive drugs)
- Low HDL (defined as HDL < 40 mg/dL males, < 50 mg/dL in females)
- Older Age (men ≥45 years old; women ≥55 years old)
If you have < two risk factors, the goal is an LDL < 160 mg/dl.
Primary Prevention: LDL Goals for Various Categories of Risk[1]
| Risk Category | LDL-C Goal | Consider Drug Therapy |
| CHD or CHD risk equivalent | <100 mg/dl | >130 mg/dl* |
| > 2 Risk Factors | ||
| 10 yr risk 10-20% | <130 mg/dl | >130 mg/dl |
| 10 yr risk < 10% | <130 mg/dl | > 160 mg/dl |
| < 2 Risk Factors | <160 mg/dl | >190 mg/dl |
- After lifestyle modification, if LDL is 100-129, consider a statin, niacin, or fibrate therapy.[2]
Drug Interactions with the LDL-Lowering Agents Simvastatin, Atorvastatin or Lovastatin
The following LDL-Lowering Agents simvastatin, atorvastatin and lovastatin interact with the following agents and should be avoided. The patient should be switched to pravastatin.
- HIV protease inhibitors
- Itraconazole (Sporanox)
- Ketoconazole (Nizoral)
- Posaconazole (Noxafil)
- Erythromycin
- Clarithromycin
- Telithromycin (Ketek)
- Grapefruit juice
- Nefazodone
- Gemfibrozil
- Cyclosporine
- Danazol
Treat Underlying Causes of Hyperlipidemia
- Hypothyroidism can increase LDL and triglycerides.
- Obstructive liver disease can increase LDL and increase HDL.
- Uncontrolled diabetes may increase triglycerides and reduce HDL.
- Nephrotic syndrome markedly increases LDL.
- Renal failure increases LDL, increases triglycerides and decreases HDL.
Drugs that Cause Dyslipidemia
- Androgenic steroids (↑LDL ↓HDL)
- Progestogens/estrogens (↑HDL/TG)
- Retinoic acid (Accutane) (↑TG)
- Corticosteroids (↑LDL/TG)
- Protease inhibitors (↑TG ↓HDL ↑LDL)
- Thiazide diuretics (↑LDL/TG)
- Beta-blockers (↑LDL/TG)
Lifestyle Modification Goals
- Reduce obesity
- Treat hypertension
- Encourage smoking cessation
- Encourage exercise[3]
Aspirin in Primary Prevention
Aspirin, in doses of less than 75 to 81 mg/d[4], can reduce the incidence of cardiovascular events, but may increase the risk of intracranial hemorrhage in men.[5] The U.S. Preventive Services Task Force 'strongly recommends that clinicians discuss aspirin chemoprevention with adults who are at increased risk for coronary heart disease'.[6] The Task Force defines increased risk as 'Men older than 40 years of age, postmenopausal women, and younger persons with risk factors for coronary heart disease (for example, hypertension, diabetes, or smoking) are at increased risk for heart disease and may wish to consider aspirin therapy'. More specifically, high-risk persons are 'those with a 5-year risk ≥ 3%'. A risk calculator is available.[7]
Regarding healthy women, the more recent Women's Health Study randomized controlled trial found insignficant benefit from aspirin in the reduction of cardiac events; however there was a signficant reduction in stroke.[8] Subgroup analysis showed that all benefit was confined to women over 65 years old.[8] In spite of the insignficant benefit for women < 65 years old, recent practice guidelines by the American Heart Association recommend to 'consider' aspirin in 'healthy women' <65 years of age 'when benefit for ischemic stroke prevention is likely to outweigh adverse effects of therapy'.[9]
Modification of Risk Factors that do not have a Robust Evidence Base
Just because something has been identified as a risk factor, that does not mean that lowering the risk factor improves outcomes. This is because the risk factor may not lie in the causal pathway for CHD. Risk factors that when modified may not improve outcomes include the following:
- There is little evidence that aggressive blood sugar control actually improves cardiac risk.
- Lowering uric acid and homocysteine levels
- Omega-3 fatty acids. The benefit of fish oil is controversial with conflicting conclusions reached by a negative meta-analysis[10] of randomized controlled trials by the international Cochrane Collaboration and a partially positive systematic review[11] by the Agency for Healthcare Research and Quality. Since these two reviews, a randomized controlled trial reported a reduction on coronary events in Japanese hypercholesterolemic patients.[12] Omega-3 fatty acids are also found in some plant sources including flax seed oil, hemp seed oil, and walnuts. Plant sources may be safer as fish products have been shown to contain heavy metals and other fat soluble pollutants.
- Vitamin C
- The World Health Organization (WHO) recommends "low to moderate alcohol intake" to reduce risk of coronary heart disease.[13]
- Avoidance of fats that are readily oxidized (e.g., saturated fats and trans-fats). The consumption of trans fat (commonly found in hydrogenated products such as margarine) has been shown to cause the development of endothelial dysfunction, a precursor to atherosclerosis.[14]
- Limit carbohydrates and processed sugars to reduce production of Low density lipoproteins while increasing High density lipoproteins.
- It has been suggested that coronary heart disease is partially reversible using an intense dietary regimen coupled with regular cardio exercise.[15]
References
- ↑ Expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001; 285:2486-2497
- ↑ Expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001; 285:2486-2497
- ↑ Thompson PD, Buchner D, Pina IL; et al. (2003). "Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease: a statement from the Council on Clinical Cardiology (Subcommittee on Exercise, Rehabilitation, and Prevention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity)". Circulation. 107 (24): 3109–16. doi:10.1161/01.CIR.0000075572.40158.77. PMID 12821592. http://www.ngc.gov/summary/summary.aspx?ss=15&doc_id=5360&string=#s23
- ↑ Campbell CL, Smyth S, Montalescot G, Steinhubl SR (2007). "Aspirin dose for the prevention of cardiovascular disease: a systematic review". JAMA. 297 (18): 2018–24. doi:10.1001/jama.297.18.2018. PMID 17488967.
- ↑ Berger J, Roncaglioni M, Avanzini F, Pangrazzi I, Tognoni G, Brown D (2006). "Aspirin for the primary prevention of cardiovascular events in women and men: a sex-specific meta-analysis of randomized controlled trials". JAMA. 295 (3): 306–13. PMID 16418466.
- ↑ "Aspirin for the primary prevention of cardiovascular events: recommendation and rationale". Ann Intern Med. 136 (2): 157–60. 2002. PMID 11790071.
- ↑ http://www.med-decisions.com/
- ↑ 8.0 8.1 Ridker P, Cook N, Lee I, Gordon D, Gaziano J, Manson J, Hennekens C, Buring J (2005). "A randomized trial of low-dose aspirin in the primary prevention of cardiovascular disease in women". N Engl J Med. 352 (13): 1293–304. doi:10.1056/NEJMoa050613. PMID 15753114. Unknown parameter
|rul=ignored (help) - ↑ http://circ.ahajournals.org/cgi/content/abstract/CIRCULATIONAHA.107.181546v1
- ↑ Hooper L, Thompson RL, Harrison RA, Summerbell CD, Ness AR, Moore HJ, Worthington HV, Durrington PN, Higgins JP, Capps NE, Riemersma RA, Ebrahim SB, Davey Smith G (2006). "Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review". BMJ. 332 (7544): 752–60. doi:10.1136/bmj.38755.366331.2F. PMID 16565093.
- ↑ Wang C, Harris WS, Chung M, Lichtenstein AH, Balk EM, Kupelnick B, Jordan HS, Lau J (2006). "n-3 Fatty acids from fish or fish-oil supplements, but not alpha-linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: a systematic review". Am. J. Clin. Nutr. 84 (1): 5–17. PMID 16825676. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat1a.chapter.38290
- ↑ Yokoyama M, Origasa H, Matsuzaki M; et al. (2007). "Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis". Lancet. 369 (9567): 1090–8. doi:10.1016/S0140-6736(07)60527-3. PMID 17398308.
- ↑ http://www.who.int/nutrition/topics/5_population_nutrient/en/index12.html
- ↑ Lopez-Garcia E, Schulze MB, Meigs JB, Manson JE, Rifai N, Stampfer MJ, Willett WC, Hu FB. (2005). "Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction". J Nutr. 135 (3): 562–6. PMID 15735094.
- ↑ Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA, McLanahan SM, Kirkeeide RL, Brand RJ, Gould KL. (1990). "Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial". Lancet. 336 (8708): 129–33. PMID 1973470.