Cardiovascular disease

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Cardiovascular disease
Classification and external resources
Cardiac amyloidosis very high mag movat.jpg
Micrograph of a heart with fibrosis (yellow) and amyloidosis (brown). Movat's stain.
ICD-10 I51.6
ICD-9 429.2
DiseasesDB 28808
MeSH D002318

Cardiovascular disease (also called heart disease) is a class of diseases that involve the heart, the blood vessels (arteries, capillaries, and veins) or both.[1]

Cardiovascular disease refers to any disease that affects the cardiovascular system, principally cardiac disease, vascular diseases of the brain and kidney, and peripheral arterial disease.[2] The causes of cardiovascular disease are diverse but atherosclerosis and/or hypertension are the most common. In addition, with aging come a number of physiological and morphological changes that alter cardiovascular function and lead to increased risk of cardiovascular disease, even in healthy asymptomatic individuals.[3]

Cardiovascular disease is the leading cause of deaths worldwide, though, since the 1970s, cardiovascular mortality rates have declined in many high-income countries.[4][5] At the same time, cardiovascular deaths and disease have increased at a fast rate in low- and middle-income countries.[6] Although cardiovascular disease usually affects older adults, the antecedents of cardiovascular disease, notably atherosclerosis, begin in early life, making primary prevention efforts necessary from childhood.[7] There is therefore increased emphasis on preventing atherosclerosis by modifying risk factors, such as healthy eating, exercise, and avoidance of smoking tobacco.

Types[edit]

Disability-adjusted life year for inflammatory heart diseases per 100,000 inhabitants in 2004.[8]
  no data
  less than 70
  70-140
  140-210
  210-280
  280-350
  350-420
  420-490
  490-560
  560-630
  630-700
  700-770
  more than 770

Risk factors[edit]

Evidence suggests a number of risk factors for heart diseases: age, gender, high blood pressure, hyperlipidemia, diabetes mellitus, tobacco smoking, excessive alcohol consumption, sugar consumption,[9][10] family history, obesity, lack of physical activity, psychosocial factors, and air pollution.[2] While the individual contribution of each risk factor varies between different communities or ethnic groups the consistency of the overall contribution of these risk factors to epidemiological studies is remarkably strong.[11] Some of these risk factors, such as age, gender or family history, are immutable; however, many important cardiovascular risk factors are modifiable by lifestyle change, social change, drug treatment and prevention of Serrano's Cardiac Triad: hypertension, hyperlipidemia, and diabetes.

Age[edit]

Calcified heart of an older woman with cardiomegaly.

Age is by far the most important risk factor in developing cardiovascular or heart diseases, with approximately a tripling of risk with each decade of life.[6] It is estimated that 82 percent of people who die of coronary heart disease are 65 and older.[12] At the same time, the risk of stroke doubles every decade after age 55.[13]

Multiple explanations have been proposed to explain why age increases the risk of cardiovascular/heart diseases. One of them is related to serum cholesterol level.[14] In most populations, the serum total cholesterol level increases as age increases. In men, this increase levels off around age 45 to 50 years. In women, the increase continues sharply until age 60 to 65 years.[14]

Aging is also associated with changes in the mechanical and structural properties of the vascular wall, which leads to the loss of arterial elasticity and reduced arterial compliance and may subsequently lead to coronary artery disease.[15]

===Sex plz Men are at greater risk of heart disease than pre-menopausal women.[6][16] Once past menopause, it has been argued that a woman's risk is similar to a man's[16] although more recent data from the WHO and UN disputes this.[6]

Among middle-aged people, coronary heart disease is 2 to 5 times more common in men than in women.[14] In a study done by the World Health Organization, sex contributes to approximately 40% of the variation in the sex ratios of coronary heart disease mortality.[17] Another study reports similar results that gender difference explains nearly half of the risk associated with cardiovascular diseases[14] One of the proposed explanations for the gender difference in cardiovascular disease is hormonal difference.[14] Among women, estrogen is the predominant sex hormone. Estrogen may have protective effects through glucose metabolism and hemostatic system, and it may have a direct effect on improving endothelial cell function.[14] The production of estrogen decreases after menopause, and may change the female lipid metabolism toward a more atherogenic form by decreasing the HDL cholesterol level and by increasing LDL and total cholesterol levels.[14] Women who have experienced early menopause, either naturally or because they have had a hysterectomy, are twice as likely to develop heart disease as women of the same age group who have not yet gone through menopause.[citation needed]

Among men and women, there are notable differences in body weight, height, body fat distribution, heart rate, stroke volume, and arterial compliance.[15] In the very elderly, age-related large artery pulsatility and stiffness is more pronounced in women.[15] This may be caused by the smaller body size and arterial dimensions independent of menopause.[15]

Air pollution[edit]

Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, PM2.5 is the major focus, in which gradients are used to determine CVD risk. For every 10 μg/m3 of PM2.5 long-term exposure, there was an estimated 8-18% CVD mortality risk.[18] Women had a higher relative risk (RR) (1.42) for PM2.5 induced coronary artery disease than men (0.90) did.[18] Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m3 of PM2.5 resulted in a 48% increase of CVD mortality risk.[19] In addition, after only 5 days of exposure, a rise in systolic (2.8 mmHg) and diastolic (2.7 mmHg) blood pressure occurred for every 10.5 μg/m3 of PM2.5.[19] Other research has implicated PM2.5 in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure.[19][20] PM2.5 is also linked to carotid artery thickening and increased risk of acute myocardial infarction.[19][20]

Pathophysiology[edit]

Population-based studies show that atherosclerosis, the major precursor of cardiovascular disease, begins in childhood. The Pathobiological Determinants of Atherosclerosis in Youth Study demonstrated that intimal lesions appear in all the aortas and more than half of the right coronary arteries of youths aged 7–9 years.[21]

This is extremely important considering that 1 in 3 people will die from complications attributable to atherosclerosis. In order to stem the tide, education and awareness that cardiovascular disease poses the greatest threat, and measures to prevent or reverse this disease must be taken.

Obesity and diabetes mellitus are often linked to cardiovascular disease,[22] as are a history of chronic kidney disease and hypercholesterolaemia.[23] In fact, cardiovascular disease is the most life-threatening of the diabetic complications and diabetics are two- to four-fold more likely to die of cardiovascular-related causes than nondiabetics.[24][25][26]

Screening[edit]

Screening ECGs (either at rest or with exercise) are not recommended in those without symptoms who are at low risk.[27] In those at higher risk the evidence for screening with ECGs is inconclusive.[27]

Some biomarkers may add to conventional cardiovascular risk factors in predicting the risk of future cardiovascular disease; however, the clinical value of some biomarkers is still questionable.[28][29] Currently, biomarkers that may reflect a higher risk of cardiovascular disease include the following:

Prevention[edit]

Currently practiced measures to prevent cardiovascular disease include:

  • A low-fat, high-fiber diet including whole grains and plenty of fresh fruit and vegetables (at least five portions a day)[34][35]
  • Tobacco cessation and avoidance of second-hand smoke[34]
  • Limit alcohol consumption to the recommended daily limits[34] consumption of 1-2 standard alcoholic drinks per day may reduce risk by 30%[36][37] However excessive alcohol intake increases the risk of cardiovascular disease.[38]
  • Lower blood pressures, if elevated
  • Decrease body fat (BMI) if overweight or obese[39]
  • Increase daily activity to 30 minutes of vigorous exercise per day at least five times per week (multiply by three if horizontal);[34]
  • Reduce sugar consumptions
  • Decrease psychosocial stress.[40] Stress however plays a relatively minor role in hypertension.[41] Specific relaxation therapies are not supported by the evidence.[42]

For adults without a known diagnosis of hypertension, diabetes, hyperlipidemia, or cardiovascular disease, routine counseling to advise them to improve their diet and increase their physical activity has not been found to significantly alter behavior, and thus is not recommended.[43]

Diet[edit]

Evidence suggests that the Mediterranean diet may improve cardiovascular outcomes.[44] This may be by about 30% in those at high risk.[45] There is also evidence that a Mediterranean diet may be more effective than a low-fat diet in bringing about long-term changes to cardiovascular risk factors (e.g., lower cholesterol level and blood pressure).[46] The DASH diet (high in nuts, fish, fruits and vegetables, and low in sweets, red meat and fat) has been shown to reduce blood pressure,[47] lower total and low density lipoprotein cholesterol [48] and improve metabolic syndrome;[49] but the long term benefits outside the context of a clinical trial have been questioned.[50] A high fiber diet appears to lower the risk.[51]

Total fat intake does not appear to be an important risk factor.[52] A diet high in trans fatty acids; however, does appear to increase rates of cardiovascular disease.[52][53] Worldwide, dietary guidelines recommend a reduction in saturated fat.[54] However, there are some questions around the effect of saturated fat on cardiovascular disease in the medical literature.[55][56] A 2014 review did not find evidence of harm from saturated fats.[53] A 2012 Cochrane review found suggestive evidence of a small benefit from replacing dietary saturated fat by unsaturated fat.[57] A 2013 meta analysis concludes that substitution with omega 6 linoleic acid (a type of unsaturated fat) may increase cardiovascular risk.[54] Replacement of saturated fats with carbohydrates does not change or may increase risk.[58][59] Benefits from replacement with polyunsaturated fat appears greatest[52][60] however supplementation with omega-3 fatty acids (a type of polysaturated fat) does not appear have an effect.[61]

The effect of a low-salt diet is unclear. A Cochrane review concluded that any benefit in either hypertensive or normal-tensive people is small if present.[62] In addition, the review suggested that a low-salt diet may be harmful in those with congestive heart failure.[62] However, the review was criticized in particular for not excluding a trial in heart failure where people had low-salt and -water levels due to diuretics.[63] When this study is left out, the rest of the trials show a trend to benefit.[63][64] Another review of dietary salt concluded that there is strong evidence that high dietary salt intake increases blood pressure and worsens hypertension, and that it increases the number of cardiovascular disease events; the latter happen both through the increased blood pressure and, quite likely, through other mechanisms.[65][66] Moderate evidence was found that high salt intake increases cardiovascular mortality; and some evidence was found for an increase in overall mortality, strokes, and left-ventricular hypertrophy.[65]

Supplements[edit]

While a healthy diet is beneficial, in general the effect of antioxidant supplementation (vitamin E, vitamin C, etc.) or vitamins has not been shown to protection against cardiovascular disease and in some cases may possibly result in harm.[67][68] Mineral supplements have also not been found to be useful.[69] Niacin, a type of vitamin B3, may be an exception with a modest decrease in the risk of cardiovascular events in those at high risk.[70][71] Magnesium supplementation lowers high blood pressure in a dose dependent manner.[72] Magnesium therapy is recommended for patients with ventricular arrhythmia associated with torsade de pointes who present with long QT syndrome as well as for the treatment of patients with digoxin intoxication-induced arrhythmias.[73] Evidence to support omega-3 fatty acid supplementation is lacking.[74]

Medication[edit]

Aspirin has been found to be of benefit overall in those at low risk of heart disease as the risk of serious bleeding is equal to the benefit with respect to cardiovascular problems.[75]

Statins are effective in preventing further cardiovascular disease in people with a history of cardiovascular disease.[76] As the event rate is higher in men than in women, the decrease in events is more easily seen in men than women.[76] In those without cardiovascular disease but risk factors statins appear to also be beneficial with a decrease in mortality and further heart disease.[77] The time course over which statins provide preventation against death appears to be long, of the order of one year, which is much longer than the duration of their effect on lipids.[78]

Management[edit]

Cardiovascular disease is treatable with initial treatment primarily focused on diet and lifestyle interventions.[79][80][81]

Epidemiology[edit]

Disability-adjusted life year for cardiovascular diseases per 100,000 inhabitants in 2004.[82]
  no data
  <900
  900-1650
  1650-2300
  2300-3000
  3000-3700
  3700-4400
  4400-5100
  5100-5800
  5800-6500
  6500-7200
  7200-7900
  >7900

Cardiovascular diseases are the leading cause of death. In 2008, 30% of all global death is attributed to cardiovascular diseases. Death caused by cardiovascular diseases are also higher in low- and middle-income countries as over 80% of all global death caused by cardiovascular diseases occurred in those countries. It is also estimated that by 2030, over 23 million people will die from cardiovascular diseases each year.

Research[edit]

The first studies on cardiovascular health were performed in year 1949 by Jerry Morris using occupational health data and were published in year 1958.[83] The causes, prevention, and/or treatment of all forms of cardiovascular disease remain active fields of biomedical research, with hundreds of scientific studies being published on a weekly basis.

A fairly recent emphasis is on the link between low-grade inflammation that hallmarks atherosclerosis and its possible interventions. C-reactive protein (CRP) is a common inflammatory marker that has been found to be present in increased levels in patients who are at risk for cardiovascular disease.[84] Also osteoprotegerin, which is involved with regulation of a key inflammatory transcription factor called NF-κB, has been found to be a risk factor of cardiovascular disease and mortality.[85][86]

Some areas currently being researched include the possible links between infection with Chlamydophila pneumoniae (a major cause of pneumonia) and coronary artery disease. The Chlamydia link has become less plausible with the absence of improvement after antibiotic use.[87]

Several research also investigated the benefits of melatonin on cardiovascular diseases prevention and cure. Melatonin is a pineal gland secretion and it is shown to be able to lower total cholesterol, very-low-ensity and low-density lipoprotein cholesterol levels in the blood plasma of rats. Reduction of blood pressure is also observed when pharmacological doses are applied. Thus, it is deemed to be a plausible treatment for hypertension. However, further research needs to be conducted to investigate the side-effects, optimal dosage, etc. before it can be licensed for use.[88]

References[edit]

  1. ^ Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey: Prentice Hall. ISBN 0-13-981176-1. 
  2. ^ a b Bridget B. Kelly; Institute of Medicine; Fuster, Valentin (2010). Promoting Cardiovascular Health in the Developing World: A Critical Challenge to Achieve Global Health. Washington, D.C: National Academies Press. ISBN 0-309-14774-3. 
  3. ^ Dantas AP, Jimenez-Altayo F, Vila E (August 2012). "Vascular aging: facts and factors". Frontiers in Vascular Physiology 3 (325): 1–2. doi:10.3389/fphys.2012.00325. PMID 22934073. 
  4. ^ Countries, Committee on Preventing the Global Epidemic of Cardiovascular Disease: Meeting the Challenges in Developing; Fuster, Board on Global Health ; Valentin; Academies, Bridget B. Kelly, editors ; Institute of Medicine of the National (2010). Promoting cardiovascular health in the developing world : a critical challenge to achieve global health. Washington, D.C.: National Academies Press. pp. Chapter 2. ISBN 978-0-309-14774-3. 
  5. ^ Mendis, S.; Puska, P.; Norrving, B.(editors) (2011), Global Atlas on cardiovascular disease prevention and control, ISBN 978-92-4-156437-3 
  6. ^ a b c d Finegold, JA; Asaria, P; Francis, DP (Dec 4, 2012). "Mortality from ischaemic heart disease by country, region, and age: Statistics from World Health Organisation and United Nations.". International journal of cardiology 168 (2): 934–945. doi:10.1016/j.ijcard.2012.10.046. PMID 23218570. 
  7. ^ McGill HC, McMahan CA, Gidding SS (March 2008). "Preventing heart disease in the 21st century: implications of the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study". Circulation 117 (9): 1216–27. doi:10.1161/CIRCULATIONAHA.107.717033. PMID 18316498. 
  8. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov 11, 2009. 
  9. ^ Howard, BV; Wylie-Rosett, J (Jul 23, 2002). "Sugar and cardiovascular disease: A statement for healthcare professionals from the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association.". Circulation 106 (4): 523–7. PMID 12135957. 
  10. ^ Finks, SW; Airee, A; Chow, SL; Macaulay, TE; Moranville, MP; Rogers, KC; Trujillo, TC (April 2012). "Key articles of dietary interventions that influence cardiovascular mortality.". Pharmacotherapy 32 (4): e54–87. doi:10.1002/j.1875-9114.2011.01087.x. PMID 22392596. 
  11. ^ Yusuf S, Hawken S, Ounpuu S, et al. (2004). "Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study". Lancet 364 (9438): 937–52. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185. 
  12. ^ "Understand Your Risk of Heart Attack". American Heart Association.http://www.heart.org/HEARTORG/Conditions/HeartAttack/UnderstandYourRiskofHeartAttack/Understand-Your-Risk-of-Heart-Attack_UCM_002040_Article.jsp#
  13. ^ Mackay, Mensah, Mendis, et al. The Atlas of Heart Disease and Stroke. World Health Organization. January 2004.
  14. ^ a b c d e f g Jousilahti Vartiainen, Tuomilehto Puska (1999). "Sex, Age,Cardiovascular Risk Factors, and coronary heart disease". Circulation 99: 1165–1172. 
  15. ^ a b c d Jani B, Rajkumar C (2006). "Ageing and vascular ageing". Postgrad Med J 82: 357–362. 
  16. ^ a b http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors
  17. ^ Jackson R, Chambles L, Higgins M, Kuulasmaa K, Wijnberg L, Williams D (WHO MONICA Project, and ARIC Study.) Sex difference in ischaemic heart disease mortality and risk factors in 46 communities: an ecologic analysis. Cardiovasc Risk Factors. 1999; 7:43-54.
  18. ^ a b Khallaf, Mohamed (2011). The Impact of Air Pollution on Health, Economy, Environment and Agricultural Sources. InTech. pp. 69–92. ISBN 978-953-307-528-0. 
  19. ^ a b c d Franchini M, Mannucci PM (2012). "Air pollution and cardiovascular disease". Thrombosis Research 129 (3): 230–4. doi:10.1016/j.thromres.2011.10.030. PMID 22113148. 
  20. ^ a b "Cardiovascular Effects of Ambient Particulate Air Pollution Exposure". Circulation 121 (25): 2755–65. 2010. doi:10.1161/CIRCULATIONAHA.109.893461. PMC 2924678. PMID 20585020. 
  21. ^ Vanhecke TE, Miller WM, Franklin BA, Weber JE, McCullough PA (Oct 2006). "Awareness, knowledge, and perception of heart disease among adolescents". Eur J Cardiovasc Prev Rehabil. 13 (5): 718–23. doi:10.1097/01.hjr.0000214611.91490.5e. PMID 17001210. 
  22. ^ Highlander P, Shaw GP (2010). "Current pharmacotherapeutic concepts for the treatment of cardiovascular disease in diabetics". Ther Adv Cardiovasc Dis. 4: 43–54. 
  23. ^ NPS Medicinewise (1 March 2011). "NPS Prescribing Practice Review 53: Managing lipids". Retrieved 1 August 2011. 
  24. ^ Kvan E., Pettersen K.I., Sandvik L., Reikvam A. (2007). "High mortality in diabetic patient with acute myocardial infarction: cardiovascular co-morbidities contribute most to the high risk". Int J Cardiol 121: 184–188. 
  25. ^ Norhammar A., Malmberg K., Diderhol E., Lagerqvist B., Lindahl B., Ryde et al. (2004). "Diabetes mellitus: the major risk factor in unstable coronary artery disease even after consideration of the extent of coronary artery disease and benefits of revascularization. J". Am Coll Cardiol 43: 585–591. 
  26. ^ DECODE , European Diabetes Epidemiology Group (1999). "Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria". Lancet 354: 617–621. doi:10.1016/S0140-6736(98)12131-1. PMID 10466661. 
  27. ^ a b Moyer, VA; U.S. Preventive Services Task, Force (Oct 2, 2012). "Screening for coronary heart disease with electrocardiography: U.S. Preventive Services Task Force recommendation statement.". Annals of Internal Medicine 157 (7): 512–8. doi:10.7326/0003-4819-157-7-201210020-00514. PMID 22847227. 
  28. ^ Wang TJ, Gona P, Larson MG, Tofler GH, Levy D, Newton-Cheh C, Jacques PF, Rifai N, Selhub J, Robins SJ, Benjamin EJ, D'Agostino RB, Vasan RS (2006). "Multiple biomarkers for the prediction of first major cardiovascular events and death". N. Engl. J. Med. 355 (25): 2631–billy bob joe9. doi:10.1056/NEJMoa055373. PMID 17182988. 
  29. ^ Spence JD (2006). "Technology Insight: ultrasound measurement of carotid plaque--patient management, genetic research, and therapy evaluation". Nat Clin Pract Neurol 2 (11): 611–9. doi:10.1038/ncpneuro0324. PMID 17057748. 
  30. ^ a b Bertazzo, S. et al. Nano-analytical electron microscopy reveals fundamental insights into human cardiovascular tissue calcification. Nature Materials 12, 576-583 (2013).
  31. ^ Inaba, Y; Chen, JA; Bergmann, SR (January 2012). "Carotid plaque, compared with carotid intima-media thickness, more accurately predicts coronary artery disease events: a meta-analysis.". Atherosclerosis 220 (1): 128–33. doi:10.1016/j.atherosclerosis.2011.06.044. PMID 21764060. 
  32. ^ J Clin Lipidol. 2007 Dec;1(6) 583-92. doi: 10.1016/j.jacl.2007.10.001. LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study - Implications for LDL Management.
  33. ^ Wang TJ, Larson MG, Levy D, et al. (Feb 2004). "Plasma natriuretic peptide levels and the risk of cardiovascular events and death". N Engl J Med. 350 (7): 655–63. doi:10.1056/NEJMoa031994. PMID 14960742. 
  34. ^ a b c d NHS Direct
  35. ^ Ignarro, LJ; Balestrieri, ML, Napoli, C (Jan 15, 2007). "Nutrition, physical activity, and cardiovascular disease: an update.". Cardiovascular research 73 (2): 326–40. doi:10.1016/j.cardiores.2006.06.030. PMID 16945357. 
  36. ^ World Heart Federation (5 October 2011). "World Heart Federation: Cardiovascular disease risk factors". Retrieved 5 October 2011. 
  37. ^ The National Heart, Lung, and Blood Institute (NHLBI) (5 October 2011). "How To Prevent and Control Coronary Heart Disease Risk Factors - NHLBI, NIH". Retrieved 5 October 2011. 
  38. ^ Klatsky AL (May 2009). "Alcohol and cardiovascular diseases". Expert Rev Cardiovasc Ther 7 (5): 499–506. doi:10.1586/erc.09.22. PMID 19419257. 
  39. ^ McTigue KM, Hess R, Ziouras J (September 2006). "Obesity in older adults: a systematic review of the evidence for diagnosis and treatment". Obesity (Silver Spring) 14 (9): 1485–97. doi:10.1038/oby.2006.171. PMID 17030958. 
  40. ^ Linden W, Stossel C, Maurice J (April 1996). "Psychosocial interventions for patients with coronary artery disease: a meta-analysis". Arch. Intern. Med. 156 (7): 745–52. doi:10.1001/archinte.1996.00440070065008. PMID 8615707. 
  41. ^ Marshall, IJ; Wolfe, CD; McKevitt, C (Jul 9, 2012). "Lay perspectives on hypertension and drug adherence: systematic review of qualitative research.". BMJ (Clinical research ed.) 345: e3953. doi:10.1136/bmj.e3953. PMC 3392078. PMID 22777025. 
  42. ^ Dickinson, HO; Mason, JM; Nicolson, DJ; Campbell, F; Beyer, FR; Cook, JV; Williams, B; Ford, GA (February 2006). "Lifestyle interventions to reduce raised blood pressure: a systematic review of randomized controlled trials.". Journal of hypertension 24 (2): 215–33. doi:10.1097/01.hjh.0000199800.72563.26. PMID 16508562. 
  43. ^ Moyer, VA; U.S. Preventive Services Task, Force (Sep 4, 2012). "Behavioral counseling interventions to promote a healthful diet and physical activity for cardiovascular disease prevention in adults: U.S. Preventive Services Task Force recommendation statement.". Annals of Internal Medicine 157 (5): 367–71. doi:10.7326/0003-4819-157-5-201209040-00486. PMID 22733153. 
  44. ^ Walker C, Reamy BV (April 2009). "Diets for cardiovascular disease prevention: what is the evidence?". Am Fam Physician 79 (7): 571–8. PMID 19378874. 
  45. ^ Estruch, Ramón et al (February 25, 2013). "Primary Prevention of Cardiovascular Disease with a Mediterranean Diet". New England Journal of Medicine. doi:10.1056/NEJMoa1200303. Retrieved February 25, 2013. 
  46. ^ Nordmann, AJ; Suter-Zimmermann, K; Bucher, HC; Shai, I; Tuttle, KR; Estruch, R; Briel, M (September 2011). "Meta-analysis comparing Mediterranean to low-fat diets for modification of cardiovascular risk factors.". The American Journal of Medicine 124 (9): 841–51.e2. doi:10.1016/j.amjmed.2011.04.024. PMID 21854893. 
  47. ^ Sacks FM, Svetkey LP, Vollmer WM, et al. (January 2001). "Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group". N. Engl. J. Med. 344 (1): 3–10. doi:10.1056/NEJM200101043440101. PMID 11136953. 
  48. ^ Obarzanek E, Sacks FM, Vollmer WM, et al. (July 2001). "Effects on blood lipids of a blood pressure-lowering diet: the Dietary Approaches to Stop Hypertension (DASH) Trial". Am. J. Clin. Nutr. 74 (1): 80–9. PMID 11451721. 
  49. ^ Azadbakht L, Mirmiran P, Esmaillzadeh A, Azizi T, Azizi F (December 2005). "Beneficial effects of a Dietary Approaches to Stop Hypertension eating plan on features of the metabolic syndrome". Diabetes Care 28 (12): 2823–31. PMID 16306540. 
  50. ^ Logan AG (March 2007). "DASH Diet: time for a critical appraisal?". Am. J. Hypertens. 20 (3): 223–4. doi:10.1016/j.amjhyper.2006.10.006. PMID 17324730. 
  51. ^ Threapleton, D. E.; Greenwood, D. C.; Evans, C. E. L.; Cleghorn, C. L.; Nykjaer, C.; Woodhead, C.; Cade, J. E.; Gale, C. P.; Burley, V. J. (19 December 2013). "Dietary fibre intake and risk of cardiovascular disease: systematic review and meta-analysis". BMJ 347 (dec19 2): f6879–f6879. doi:10.1136/bmj.f6879. 
  52. ^ a b c Willett, WC (July 2012). "Dietary fats and coronary heart disease.". Journal of internal medicine 272 (1): 13–24. doi:10.1111/j.1365-2796.2012.02553.x. PMID 22583051. 
  53. ^ a b Chowdhury, Rajiv; Warnakula, Samantha; Kunutsor, Setor; Crowe, Francesca; Ward, Heather A.; Johnson, Laura; Franco, Oscar H.; Butterworth, Adam S.; Forouhi, Nita G.; Thompson, Simon G.; Khaw, Kay-Tee; Mozaffarian, Dariush; Danesh, John; Di Angelantonio, Emanuele (18 March 2014). "Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk". Annals of Internal Medicine 160 (6): 398–406. doi:10.7326/M13-1788. 
  54. ^ a b Ramsden, CE; Zamora, D; Leelarthaepin, B; Majchrzak-Hong, SF; Faurot, KR; Suchindran, CM; Ringel, A; Davis, JM; Hibbeln, JR (Feb 4, 2013). "Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.". BMJ (Clinical research ed.) 346: e8707. PMID 23386268. 
  55. ^ Stamler J (March 2010). "Diet-heart: a problematic revisit". Am. J. Clin. Nutr. 91 (3): 497–9. doi:10.3945/ajcn.2010.29216. PMID 20130097. 
  56. ^ Siri-Tarino, PW; Sun Q, Hu FB, Krauss RM (March 2010). "Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.". The American Journal of Clinical Nutrition 91 (3): 535–46. doi:10.3945/ajcn.2009.27725. PMC 2824152. PMID 20071648. 
  57. ^ Hooper, L; Summerbell, CD; Thompson, R; Sills, D; Roberts, FG; Moore, HJ; Davey Smith, G (May 16, 2012). "Reduced or modified dietary fat for preventing cardiovascular disease.". Cochrane database of systematic reviews (Online) 5: CD002137. doi:10.1002/14651858.CD002137.pub3. PMID 22592684. 
  58. ^ Siri-Tarino Patty W, Sun Qi, Hu Frank B, Krauss Ronald M (2010). "Saturated fat, carbohydrate, and cardiovascular disease". American Journal of Clinical Nutrition 91 (3): 502–509. doi:10.3945/ajcn.2008.26285. PMC 2824150. PMID 20089734. 
  59. ^ Micha, R; Mozaffarian, D (October 2010). "Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence.". Lipids 45 (10): 893–905. doi:10.1007/s11745-010-3393-4. PMC 2950931. PMID 20354806. 
  60. ^ Astrup, A; Dyerberg, J; Elwood, P; Hermansen, K; Hu, FB; Jakobsen, MU; Kok, FJ; Krauss, RM; Lecerf, JM; LeGrand, P; Nestel, P; Risérus, U; Sanders, T; Sinclair, A; Stender, S; Tholstrup, T; Willett, WC (April 2011). "The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?". The American journal of clinical nutrition 93 (4): 684–8. doi:10.3945/ajcn.110.004622. PMC 3138219. PMID 21270379. 
  61. ^ Rizos, EC; Ntzani, EE; Bika, E; Kostapanos, MS; Elisaf, MS (Sep 12, 2012). "Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis.". JAMA: the Journal of the American Medical Association 308 (10): 1024–33. doi:10.1001/2012.jama.11374. PMID 22968891. 
  62. ^ a b Taylor, RS; Ashton, KE; Moxham, T; Hooper, L; Ebrahim, S (Jul 6, 2011). "Reduced dietary salt for the prevention of cardiovascular disease.". Cochrane database of systematic reviews (Online) (7): CD009217. doi:10.1002/14651858.CD009217. PMID 21735439. 
  63. ^ a b He, F J; MacGregor G A (2011). "Salt reduction lowers cardiovascular risk: meta-analysis of outcome trials". The Lancet 378: 380–382. doi:10.1016/S0140-6736(11)61174-4. PMID 21803192. 
  64. ^ Paterna, S; Gaspare P, Fasullo S, Sarullo FM, Di Pasquale P (2008). "Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend?". Clin Sci (Lond) 114: 221–230. doi:10.1042/CS20070193. PMID 17688420. 
  65. ^ a b Bochud, M; Marques-Vidal, P; Burnier, M; Paccaud, F (2012). "Dietary Salt Intake and Cardiovascular Disease: Summarizing the Evidence". Public Health Reviews 33: 530–552. 
  66. ^ Cook, N R; et al. (2007). "Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP)". BMJ 334 (7599): 334. doi:10.1136/bmj.39147.604896.55. PMC 1857760. PMID 17449506. 
  67. ^ Bhupathiraju, SN; Tucker, KL (Aug 17, 2011). "Coronary heart disease prevention: nutrients, foods, and dietary patterns.". Clinica chimica acta; international journal of clinical chemistry 412 (17-18): 1493–514. doi:10.1016/j.cca.2011.04.038. PMID 21575619. 
  68. ^ Myung, SK; Ju, W; Cho, B; Oh, SW; Park, SM; Koo, BK; Park, BJ; for the Korean Meta-Analysis (KORMA) Study, Group (Jan 18, 2013). "Efficacy of vitamin and antioxidant supplements in prevention of cardiovascular disease: systematic review and meta-analysis of randomised controlled trials.". BMJ (Clinical research ed.) 346: f10. PMC 3548618. PMID 23335472. 
  69. ^ Fortmann, SP; Burda, BU; Senger, CA; Lin, JS; Whitlock, EP (Nov 12, 2013). "Vitamin and Mineral Supplements in the Primary Prevention of Cardiovascular Disease and Cancer: An Updated Systematic Evidence Review for the U.S. Preventive Services Task Force.". Annals of internal medicine 159 (12): 824–34. doi:10.7326/0003-4819-159-12-201312170-00729. PMID 24217421. 
  70. ^ Bruckert, E; Labreuche, J; Amarenco, P (June 2010). "Meta-analysis of the effect of nicotinic acid alone or in combination on cardiovascular events and atherosclerosis". Atherosclerosis 210 (2): 353–61. doi:10.1016/j.atherosclerosis.2009.12.023. PMID 20079494. 
  71. ^ Lavigne, PM; Karas, RH (Jan 29, 2013). "The current state of niacin in cardiovascular disease prevention: a systematic review and meta-regression.". Journal of the American College of Cardiology 61 (4): 440–6. doi:10.1016/j.jacc.2012.10.030. PMID 23265337. 
  72. ^ Jee SH, Miller ER III, Guallar E et al. (2002). "The effect of magnesium supplementation on blood pressure: a meta-analysis of randomized clinical trials". Am J Hypertens 15 (8): 691–696. doi:10.1016/S0895-7061(02)02964-3. PMID 12160191. 
  73. ^ Zipes DP, Camm AJ, Borggrefe M et al. (2012). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation 114 (10): e385–e484. doi:10.1161/CIRCULATIONAHA.106.178233. PMID 16935995. 
  74. ^ Kwak, SM; Myung, SK; Lee, YJ; Seo, HG; for the Korean Meta-analysis Study, Group (Apr 9, 2012). "Efficacy of Omega-3 Fatty Acid Supplements (Eicosapentaenoic Acid and Docosahexaenoic Acid) in the Secondary Prevention of Cardiovascular Disease: A Meta-analysis of Randomized, Double-blind, Placebo-Controlled Trials.". Archives of Internal Medicine. doi:10.1001/archinternmed.2012.262. PMID 22493407. 
  75. ^ Berger, JS; Lala, A; Krantz, MJ; Baker, GS; Hiatt, WR (July 2011). "Aspirin for the prevention of cardiovascular events in patients without clinical cardiovascular disease: a meta-analysis of randomized trials.". American heart journal 162 (1): 115–24.e2. doi:10.1016/j.ahj.2011.04.006. PMID 21742097. 
  76. ^ a b Gutierrez, J; Ramirez, G; Rundek, T; Sacco, RL (Jun 25, 2012). "Statin Therapy in the Prevention of Recurrent Cardiovascular Events: A Sex-Based Meta-analysisStatin Therapy to Prevent Recurrent CV Events.". Archives of Internal Medicine 172 (12): 909–19. doi:10.1001/archinternmed.2012.2145. PMID 22732744. 
  77. ^ Taylor, F; Huffman, MD; Macedo, AF; Moore, TH; Burke, M; Davey Smith, G; Ward, K; Ebrahim, S (Jan 31, 2013). "Statins for the primary prevention of cardiovascular disease.". Cochrane database of systematic reviews (Online) 1: CD004816. doi:10.1002/14651858.CD004816.pub5. PMID 23440795. 
  78. ^ Francis, DP (May 19, 2011). "Duration and magnitude of the effect of a single statin tablet in primary prevention of cardiovascular events.". International journal of cardiology 149 (1): 102–7. doi:10.1016/j.ijcard.2010.11.013. PMID 21183232. 
  79. ^ Ornish, Dean, "et al." (Jul 1990). "'Can lifestyle changes reverse coronary heart disease?' The Lifestyle Heart Trial.". Lancet 336 (8708): 129–33. doi:10.1016/0140-6736(90)91656-U. PMID 1973470. 
  80. ^ Ornish, D., Scherwitz, L. W., Doody, R. S., Kesten, D., McLanahan, S. M., Brown, S. E. "et al." (1983). "Effects of stress management training and dietary changes in treating ischemic heart disease". JAMA 249 (54): 54. doi:10.1001/jama.249.1.54. PMID 6336794. 
  81. ^ Ornish, D., Scherwitz, L. W., Billings, J. H., Brown, S. E., Gould, K. L., Merritt, T. A. "et al." (1998). "Intensive lifestyle changes for reversal of coronary heart disease". JAMA 280 (23): 2001–7. doi:10.1001/jama.280.23.2001. PMID 9863851. 
  82. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov 11, 2009. 
  83. ^ Morris J. N., Crawford Margaret D. (1958). "Coronary Heart Disease and Physical Activity of Work". British Medical Journal 2 (5111): 1485–1496. PMC 2027542. PMID 13608027. 
  84. ^ Karakas M, Koenig W (December 2009). "CRP in cardiovascular disease". Herz 34 (8): 607–13. doi:10.1007/s00059-009-3305-7. PMID 20024640. 
  85. ^ 20448212
  86. ^ Venuraju SM, Yerramasu A, Corder R, Lahiri A (May 2010). "Osteoprotegerin as a predictor of coronary artery disease and cardiovascular mortality and morbidity". J. Am. Coll. Cardiol. 55 (19): 2049–61. doi:10.1016/j.jacc.2010.03.013. PMID 20447527. 
  87. ^ Andraws R, Berger JS, Brown DL (Jun 2005). "Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials". JAMA 293 (21): 2641–7. doi:10.1001/jama.293.21.2641. PMID 15928286. 
  88. ^ Dominguez-Rodriguez, Alberto (January 2012). "Melatonin and Cardiovascular Disease: Myth or Reality?". Rev Esp Cardiol 65: 215–218. 

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