Coronary heart disease primary prevention: Difference between revisions

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*Treat [[hypertension]]
*Treat [[hypertension]]
*[[Smoking cessation]]
*[[Smoking cessation]]
*Exercise


==Treat Underlying Causes of [[Hyperlipidemia]]==
==Treat Underlying Causes of [[Hyperlipidemia]]==

Revision as of 04:31, 1 October 2012

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Risk calculators and risk factors for Coronary heart disease primary prevention

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":

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

Lifestyle Modification Goals

Treat Underlying Causes of Hyperlipidemia

Drugs that Cause Dyslipidemia

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:

An increasingly growing number of other physiological markers and homeostatic mechanisms are currently under scientific investigation. Among these markers are low density lipoprotein and asymmetric dimethylarginine. Patients with CHD and those trying to prevent CHD are advised to avoid fats that are readily oxidized (e.g., saturated fats and trans-fats), limit carbohydrates and processed sugars to reduce production of Low density lipoproteins while increasing High density lipoproteins, keeping blood pressure normal, exercise and stop smoking. These measures limit the progression of the disease. Recent studies have shown that dramatic reduction in LDL levels can cause mild regression of coronary heart disease.

Exercise

Separate to the question of the benefits of exercise; it is unclear whether doctors should spend time counseling patients to exercise. The U.S. Preventive Services Task Force (USPSTF), based on a systematic review of randomized controlled trials, found 'insufficient evidence' to recommend that doctors counsel patients on exercise.[7] However, the American Heart Association, based on a non-systematic review, recommends that doctors counsel patients on exercise [8]

Preventive diets

It has been suggested that coronary heart disease is partially reversible using an intense dietary regimen coupled with regular cardio exercise.[9]

  • Vegetarian diet: Vegetarians have been shown to have a 24% reduced risk of dying of heart disease.[10]
  • Cretan Mediterranean diet: The Seven Country Study found that Cretan men had exceptionally low death rates from heart disease, despite moderate to high intake of fat. The Cretan diet is similar to other traditional Mediterranean diets: consisting mostly of olive oil, bread, abundant fruit and vegetables, a moderate amount of wine and fat-rich animal products such as lamb, sausage and goat cheese.[11][12][13] However, the Cretan diet consisted of less fish and wine consumption than some other Mediterranean-style diets, such as the diet in Corfu, another region of Greece, which had higher death rates.

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]

Aspirin

Aspirin, in doses of less than 75 to 81 mg/d[15], can reduce the incidence of cardiovascular events.[16] 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'.[17] 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.[18]

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.[19] Subgroup analysis showed that all benefit was confined to women over 65 years old.[19] 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'.[20]

References

  1. Expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001; 285:2486-2497
  2. Expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001; 285:2486-2497
  3. 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.
  4. 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
  5. 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.
  6. http://www.who.int/nutrition/topics/5_population_nutrient/en/index12.html
  7. "Behavioral counseling in primary care to promote physical activity: recommendation and rationale". Ann. Intern. Med. 137 (3): 205–7. 2002. PMID 12160370.
  8. 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
  9. 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.
  10. Key TJ, Fraser GE, Thorogood M, Appleby PN, Beral V, Reeves G, Burr ML, Chang-Claude J, Frentzel-Beyme R, Kuzma JW, Mann J, McPherson K (1998). "Mortality in vegetarians and non-vegetarians: a collaborative analysis of 8300 deaths among 76,000 men and women in five prospective studies". Public Health Nutr. 1 (1): 33–41. PMID 10555529.
  11. Willett WC, Sacks F, Trichopoulou A, Drescher G, Ferro-Luzzi A, Helsing E, Trichopoulos D. (1995). "Mediterranean diet pyramid: a cultural model for healthy eating". Am J Clin Nutr. 61 (6 Suppl): 1402S–1406S. PMID 7754995.
  12. Perez-Llamas, F., et.al., J Hum Nutr Diet, Dec 1996, 9:6:463-471
  13. Alberti-Fidanza A, Paolacci CA, Chiuchiu MP, Coli R, Fruttini D, Verducci G, Fidanza F. (1994). "Dietary studies on two rural Italian population groups of the Seven Countries Study. 1. Food and nutrient intake at the thirty-first year follow-up in 1991". Eur J Clin Nutr. 48 (2): 85–91. PMID 8194497.
  14. 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.
  15. 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.
  16. 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.
  17. "Aspirin for the primary prevention of cardiovascular events: recommendation and rationale". Ann Intern Med. 136 (2): 157–60. 2002. PMID 11790071.
  18. http://www.med-decisions.com/
  19. 19.0 19.1 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)
  20. http://circ.ahajournals.org/cgi/content/abstract/CIRCULATIONAHA.107.181546v1