Wikipedia

User:DocElisa/Cardiovascular disease

< User:DocElisa
DocElisa/Cardiovascular disease

Cardiovascular disease (also called heart disease) is a class of diseases that involve the heart or blood vessels (arteries, capillaries and veins).[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. Additionally, with aging come a number of physiological and morphological changes that alter cardiovascular function and lead to subsequently 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] At the same time, cardiovascular deaths and disease have increased at a fast rate in low- and middle-income countries.[5] 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.[6] There is therefore increased emphasis on preventing atherosclerosis by modifying risk factors, such as healthy eating, exercise, and avoidance of smoking.

Types edit

 
Disability-adjusted life year for inflammatory heart diseases per 100,000 inhabitants in 2004.[7]
  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

Epidemiology suggests a number of risk factors for heart disease: age, gender, high blood pressure, high serum cholesterol levels, tobacco smoking, excessive alcohol consumption, family history, obesity, lack of physical activity, psychosocial factors, diabetes mellitus, 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.[8] 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, drug treatment or social change.

Age edit

 
Calcified heart of older woman with Cardiomegaly taken at the Instituto Nacional de Cardiología, Mexico.

Age is an important risk factor in developing cardiovascular diseases. It is estimated that 87 percent of people who die of coronary heart disease are 60 and older.[9] At the same time, the risk of stroke doubles every decade after age 55.[10]

Multiple explanations have been proposed to explain why age increases the risk of cardiovascular diseases. One of them is related to serum cholesterol level.[11] 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.[11]

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.[12]

Sex edit

Men are at greater risk of heart disease than pre-menopausal women.[13] However, once past menopause, a woman’s risk is similar to a man’s.[13]

Among middle-aged people, coronary heart disease is 2 to 5 times more common in men than in women.[11] 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.[14] Another study reports similar results that gender difference explains nearly half of the risk associated with cardiovascular diseases[11] One of the proposed explanations for the gender difference in cardiovascular disease is hormonal difference.[11] 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.[11] 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.[11] 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}}: Empty citation (help)

Among men and women, there are differences in body weight, height, body fat distribution, heart rate, stroke volume, and arterial compliance.[12] In the very elderly, age related large artery pulsatility and stiffness is more pronounced in women.[12] This may be caused by the smaller body size and arterial dimensions independent of menopause.[12]

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.[15] Women had a higher relative risk (RR) (1.42) for PM2.5 induced coronary artery disease than men (0.90) did.[15] 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.[16] Additionally, 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.[16] Other research has implicated PM2.5 in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure.[16][17] PM2.5 is also linked to carotid artery thickening and increased risk of acute myocardial infarction.[16][17]

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.[18]

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,[19] as are a history of chronic kidney disease and hypercholesterolaemia.[20] 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.[21][22][23]

Screening edit

Screening ECGs (either at rest or with exercise) are not recommended in those without symptoms who are at low risk.[24] In those at higher risk the evidence for screening with ECGs is inconclusive.[24]

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.[25][26] Currently, biomarkers which may reflect a higher risk of cardiovascular disease include:

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)[29][30]
  • Tobacco cessation and avoidance of second-hand smoke;[29]
  • Limit alcohol consumption to the recommended daily limits;[29] consumption of 1-2 standard alcoholic drinks per day may reduce risk by 30%[31][32] However excessive alcohol intake increases the risk of cardiovascular disease.[33]
  • Lower blood pressures, if elevated, through the use of antihypertensive medications[citation needed];
  • Decrease body fat (BMI) if overweight or obese;[34]
  • Increase daily activity to 30 minutes of vigorous exercise per day at least five times per week;[29]
  • Decrease psychosocial stress.[35] Stress however plays a relatively minor role in hypertension.[36] Specific relaxation therapies are not supported by the evidence.[37]

Routine counselling of adults to advise them to improve their diet and increase their physical activity has not been found to significantly alter behaviour, and thus is not recommended.[38]

Diet edit

Evidence suggests that the Mediterranean diet may improve cardiovascular outcomes.[39] On February 25, 2013, medical researchers at the University of Barcelona, based on a five year study of 7,447 people, reported in the New England Journal of Medicine that the Mediterranean diet reduced the risk of heart disease in people at high risk by "about 30 percent".[40][41]

In clinical trials the DASH diet (high in fruits and vegetables, low in sweets, red meat and fat) has been shown to reduce blood pressure,[42] lower total and low density lipoprotein cholesterol [43] and improve metabolic syndrome;[44] but the long term benefits outside the context of a clinical trial have been questioned.[45]

The link between saturated fat intake and cardiovascular disease is controversial (see Saturated fat and cardiovascular disease controversy)[46][47] and scientific studies, both observational and clinical, show conflicting results.[48] Dietary substitution of polyunsaturated fats for saturated fats may reduce risk, substitution with carbohydrates does not change or may increase risk.[48][49] Increased dietary intake of Trans fatty acids significantly increases the risk of cardiovascular disease.[50]

The effect of a low salt diet is unclear with any benefit in either hypertensive or normal tensive people being small if present.[51] A low salt diet may be harmful in those with congestive heart failure.[51]

Supplements edit

Evidence to support omega-3 fatty acid supplementation is lacking.[52] As is evidence to support antioxidants and vitamins.[53]

Medication edit

Aspirin has not 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.[54] Statins are effective in preventing further cardiovascular disease in those with a history of cardiovascular disease.[55] A decreased risk of death however seems to only occur in men.[55]

Management edit

Cardiovascular disease is treatable with initial treatment primarily focused on diet and lifestyle interventions.[56][57][58] Medication may also be useful for prevention. [citation needed]

Mortality edit

 
Disability-adjusted life year for cardiovascular diseases per 100,000 inhabitants in 2004.[59]

According to the World Health Organization, 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 annually.

Research edit

The first studies on cardiovascular health were performed in 1949 by Jerry Morris using occupational health data and were published in 1958.[60] 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 trend has emerged, particularly in the early 2000s, in which numerous studies have revealed a link between fast food and an increase in heart disease. These studies include those conducted by the Ryan Mackey Memorial Research Institute, Harvard University and the Sydney Center for Cardiovascular Health. Many major fast food chains, particularly McDonald's, have protested the methods used in these studies and have responded with healthier menu options.

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 at risk for cardiovascular disease.[61] Also osteoprotegerin which 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.[62][63]

Some areas currently being researched include 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.[64]

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 density 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 and etc. before it can be licensed for use.[65]

References edit

  1. ^ Maton, Anthea (1993). Human Biology and Health. Englewood Cliffs, New Jersey: Prentice Hall. ISBN 0-13-981176-1. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  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 978-0-309-14774-3.{{cite book}}: CS1 maint: multiple names: authors list (link)
  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. PMC 3429093. PMID 22934073.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  4. ^ Countries, Committee on Preventing the Global Epidemic of Cardiovascular Disease: Meeting the Challenges in Developing (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. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  5. ^ Mendis, S.; Puska, P.; Norrving, B.(editors) (2011), Global Atlas on cardiovascular disease prevention and control, ISBN 978-92-4-156437-3 {{citation}}: |first3= has generic name (help)
  6. ^ 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. S2CID 13115938.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  7. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov. 11, 2009. {{cite web}}: Check date values in: |accessdate= (help)
  8. ^ 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. S2CID 30811593. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  9. ^ "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#
  10. ^ Mackay, Mensah, Mendis, et al. The Atlas of Heart Disease and Stroke. World Health Organization. January 2004.
  11. ^ a b c d e f g Jousilahti Vartiainen, Tuomilehto Puska (1999). "Sex, Age,Cardiovascular Risk Factors, and coronary heart disease". Circulation. 99 (9): 1165–1172. doi:10.1161/01.CIR.99.9.1165. PMID 10069784. S2CID 6125188.
  12. ^ a b c d Jani B, Rajkumar C (2006). "Ageing and vascular ageing". Postgrad Med J. 82 (968): 357–362. doi:10.1136/pgmj.2005.036053. S2CID 6698288.
  13. ^ a b http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors
  14. ^ 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.
  15. ^ 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. {{cite book}}: More than one of |author= and |last= specified (help)
  16. ^ 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.
  17. ^ a b Sun, Qinghua; Hong, Xinru; Wold, Loren E. (2010). "Cardiovascular Effects of Ambient Particulate Air Pollution Exposure". Circulation. 121 (25): 2755–65. doi:10.1161/CIRCULATIONAHA.109.893461. PMC 2924678. PMID 20585020.
  18. ^ 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. S2CID 36312234.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  19. ^ Highlander P, Shaw GP (2010). "Current pharmacotherapeutic concepts for the treatment of cardiovascular disease in diabetics". Ther Adv Cardiovasc Dis. 4: 43–54. doi:10.1177/1753944709354305. S2CID 23913203.
  20. ^ NPS Medicinewise (1 March 2011). "NPS Prescribing Practice Review 53: Managing lipids". Retrieved 1 August 2011.
  21. ^ 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 (2): 184–188. doi:10.1016/j.ijcard.2006.11.003.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  22. ^ 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 (4): 585–591. doi:10.1016/j.jacc.2003.08.050. PMID 14975468. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  23. ^ DECODE , European Diabetes Epidemiology Group (1999). "Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria". Lancet. 354 (9179): 617–621. doi:10.1016/S0140-6736(98)12131-1. PMID 10466661. S2CID 54227479.
  24. ^ a b Moyer, Virginia A.; U.S. Preventive Services Task Force (2012 Oct 2). "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. S2CID 23062338. {{cite journal}}: Check date values in: |date= (help)
  25. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. ^ 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. S2CID 26077254.
  27. ^ Inaba, Yoichi; Chen, Jennifer A.; Bergmann, Steven R. (2012 Jan). "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. {{cite journal}}: Check date values in: |date= (help)
  28. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  29. ^ a b c d NHS Direct
  30. ^ Ignarro, L.; Balestrieri, M.; Napoli, C. (2007 Jan 15). "Nutrition, physical activity, and cardiovascular disease: an update". Cardiovascular Research. 73 (2): 326–40. doi:10.1016/j.cardiores.2006.06.030. PMID 16945357. S2CID 12846661. {{cite journal}}: Check date values in: |date= (help)
  31. ^ World Heart Federation (5 October 2011). "World Heart Federation: Cardiovascular disease risk factors". Retrieved 5 October 2011.
  32. ^ 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.{{cite web}}: CS1 maint: multiple names: authors list (link)
  33. ^ Klatsky AL (May 2009). "Alcohol and cardiovascular diseases". Expert Rev Cardiovasc Ther. 7 (5): 499–506. doi:10.1586/erc.09.22. PMID 19419257. S2CID 23782870.{{cite journal}}: CS1 maint: date and year (link)
  34. ^ 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. S2CID 45241607.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  35. ^ 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.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  36. ^ Marshall, I. J.; Wolfe, C. D.; McKevitt, C. (2012 Jul 9). "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. {{cite journal}}: Check date values in: |date= (help)
  37. ^ Dickinson, Heather O.; Mason, James M.; Nicolson, Donald J.; Campbell, Fiona; Beyer, Fiona R.; Cook, Julia V.; Williams, Bryan; Ford, Gary A. (2006 Feb). "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. S2CID 9125890. {{cite journal}}: Check date values in: |date= (help)
  38. ^ Moyer, Virginia A.; U.S. Preventive Services Task Force (2012 Sep 4). "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. S2CID 24224874. {{cite journal}}: Check date values in: |date= (help)
  39. ^ Walker C, Reamy BV (April 2009). "Diets for cardiovascular disease prevention: what is the evidence?". Am Fam Physician. 79 (7): 571–8. PMID 19378874.{{cite journal}}: CS1 maint: date and year (link)
  40. ^ "Primary Prevention of Cardiovascular Disease with a Mediterranean Diet". New England Journal of Medicine. 368 (14): 1279–1290. February 25, 2013. doi:10.1056/NEJMoa1200303. PMID 23432189. Retrieved February 25, 2013. {{cite journal}}: Cite uses deprecated parameter |authors= (help)
  41. ^ Kolata, Gina (February 25, 2013). "Mediterranean Diet Can Cut Heart Disease, Study Finds". New York Times. Retrieved February 25, 2013.
  42. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  43. ^ 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. doi:10.1093/ajcn/74.1.80. PMID 11451721. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  44. ^ 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. doi:10.2337/diacare.28.12.2823. PMID 16306540.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  45. ^ 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. S2CID 11983316.{{cite journal}}: CS1 maint: date and year (link)
  46. ^ 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.{{cite journal}}: CS1 maint: date and year (link)
  47. ^ Siri-Tarino, Patty W.; Sun, Qi; Hu, Frank B.; Krauss, Ronald M. (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. {{cite journal}}: Unknown parameter |mont h= ignored (help)
  48. ^ a b 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ^ Micha, Renata; Mozaffarian, Dariush (2010 Oct). "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. {{cite journal}}: Check date values in: |date= (help)
  50. ^ Mozaffarian, D.; Aro, A.; Willett, W. C. (2009 May). "Health effects of trans-fatty acids: experimental and observational evidence". European Journal of Clinical Nutrition. 63 Suppl 2: S5-21. doi:10.1038/sj.ejcn.1602973. PMID 19424218. S2CID 8969850. {{cite journal}}: Check date values in: |date= (help)
  51. ^ a b Taylor, Rod S.; Ashton, Kate E.; Moxham, Tiffany; Hooper, Lee; Ebrahim, Shah (2011 Jul 6). Taylor, Rod S (ed.). "Reduced dietary salt for the prevention of cardiovascular disease". Cochrane Database of Systematic Reviews (Online) (7): CD009217. doi:10.1002/14651858.CD009217. PMC 4160847. PMID 21735439. {{cite journal}}: Check date values in: |date= (help)
  52. ^ Kwak, SM (2012 Apr 9). "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. 172 (9): 686–694. doi:10.1001/archinternmed.2012.262. PMID 22493407. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  53. ^ Myung, SK (2013 Jan 18). "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. doi:10.1136/bmj.f10. PMC 3548618. PMID 23335472. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  54. ^ Berger, Jeffrey S.; Lala, Anuradha; Krantz, Mori J.; Baker, Gizelle S.; Hiatt, William R. (2011 Jul). "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. {{cite journal}}: Check date values in: |date= (help)
  55. ^ a b Gutierrez, J.; Ramirez, G.; Rundek, T.; Sacco, R. L. (2012 Jun 25). "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. {{cite journal}}: Check date values in: |date= (help)
  56. ^ 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. S2CID 4513736. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: date and year (link)
  57. ^ 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): 54–59. doi:10.1001/jama.249.1.54. PMID 6336794. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  58. ^ 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. S2CID 21508600. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  59. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov. 11, 2009. {{cite web}}: Check date values in: |accessdate= (help)
  60. ^ Morris J. N., Crawford Margaret D. (1958). "Coronary Heart Disease and Physical Activity of Work". British Medical Journal. 2 (5111): 1485–1496. doi:10.1136/bmj.2.5111.1485. PMC 2027542. PMID 13608027.
  61. ^ Karakas M, Koenig W (December 2009). "CRP in cardiovascular disease". Herz. 34 (8): 607–13. doi:10.1007/s00059-009-3305-7. PMID 20024640. S2CID 5587888.{{cite journal}}: CS1 maint: date and year (link)
  62. ^ 20448212
  63. ^ 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.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  64. ^ 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.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  65. ^ Dominguez-Rodriguez, Alberto (January 2012). "Melatonin and Cardiovascular Disease: Myth or Reality?". Rev Esp Cardiol. 65: 215-218. doi:10.1016/j.recesp.2011.10.009.{{cite journal}}: CS1 maint: date and year (link)
Retrieved from "https://en.wikipedia.org/w/index.php?title=User:DocElisa/Cardiovascular_disease&oldid=1118717930"