Misplaced Pages

Revision as of 15:00, 29 January 2015

It has been suggested that Cardiovascular pathology be merged into this article. (Discuss) Proposed since January 2015.

Cardiovascular disease
Specialty	Cardiology

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

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. The causes of cardiovascular disease are diverse but atherosclerosis and 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.

Cardiovascular diseases are the leading cause of deaths on the globally. According to a World Bank analysis, cardiovascular mortality has been declining in many high-income countries since 1970s. At the same time, cardiovascular deaths and disease have increased at a fast rate in low- and middle-income countries. 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. Consequently, there is increased emphasis on preventing atherosclerosis by modifying risk factors, for example by healthy eating, exercise, and avoidance of smoking tobacco and excessive alcohol intake.

Types

• Coronary artery disease (also known as coronary heart disease and ischemic heart disease)
• Cardiomyopathy – diseases of cardiac muscle
• Hypertensive heart disease – diseases of the heart secondary to high blood pressure or hypertension
• Heart failure
• Pulmonary heart disease – a failure at the right side of the heart with respiratory system involvement
• Cardiac dysrhythmias – abnormalities of heart rhythm
• Inflammatory heart disease
  • Endocarditis – inflammation of the inner layer of the heart, the endocardium. The structures most commonly involved are the heart valves.
  • Inflammatory cardiomegaly
  • Myocarditis – inflammation of the myocardium, the muscular part of the heart.
• Valvular heart disease
• Cerebrovascular disease – disease of blood vessels that supply blood to the brain (includes stroke)
• Peripheral arterial disease – disease of blood vessels that supply blood to the arms and legs
• Congenital heart disease – heart structure malformations existing at birth
• Rheumatic heart disease – heart muscles and valves damage due to rheumatic fever caused by Streptococcus pyogenes a group A streptococcal infection.

Risk factors

There are several risk factors for heart diseases: age, gender, tobacco use, physical inactivity, excessive alcohol consumption, unhealthy diet, obesity, family history of cardiovascular disease, raised blood pressure (hypertension), raised blood sugar (diabetes mellitus), raised blood cholesterol (hyperlipidemia), psychosocial factors, poverty and low educational status, and air pollution. While the individual contribution of each risk factor varies between different communities or ethnic groups the overall contribution of these risk factors is very consistent. 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 hypertension, hyperlipidemia, and diabetes.

Age

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. It is estimated that 82 percent of people who die of coronary heart disease are 65 and older. At the same time, the risk of stroke doubles every decade after age 55.

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. 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.

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.

Sex

Men are at greater risk of heart disease than pre-menopausal women. Once past menopause, it has been argued that a woman's risk is similar to a man's although more recent data from the WHO and UN disputes this. If a female has diabetes, she is more likely to develop heart disease than a male with diabetes.

Coronary heart diseases are 2 to 5 times more common among middle-aged men than women. In a study done by the World Health Organization, sex contributes to approximately 40% of the variation in sex ratios of coronary heart disease mortality. Another study reports similar results finding that gender differences explains nearly half the risk associated with cardiovascular diseases One of the proposed explanations for gender differences in cardiovascular diseases is hormonal difference. Among women, estrogen is the predominant sex hormone. Estrogen may have protective effects through glucose metabolism and hemostatic system, and may have direct effect in improving endothelial cell function. The production of estrogen decreases after menopause, and this may change the female lipid metabolism toward a more atherogenic form by decreasing the HDL cholesterol level while increasing LDL and total cholesterol levels.

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

Tobacco

Cigarettes are the major form of smoked tobacco. Risks to health from tobacco use result not only from direct consumption of tobacco, but also from exposure to second-hand smoke. Approximately 10% of cardiovascular disease is attributed to smoking, however people who quit smoking by age 30 have almost as low a risk of death as never smokers.

Physical inactivity

Insufficient physical activity (defined as less than 5 x 30 minutes of moderate activity per week, or less than 3 x 20 minutes of vigorous activity per week) is currently the fourth leading risk factor for mortality worldwide. In 2008, 31.3% of adults aged 15 or older (28.2% men and 34.4% women) were insufficiently physically active. The risk of ischemic heart disease and diabetes mellitus is reduced by almost a third in adults who participate in 150 minutes of moderate physical activity each week (or equivalent). In addition, physical activity assists weight loss and improves blood glucose control, blood pressure, lipid profile and insulin sensitivity. These effects may, at least in part, explain its cardiovascular benefits.

Excessive alcohol consumption

The relationship between alcohol consumption and cardiovascular disease is complex, and may depend on the amount of alcohol consumed. There is a direct relationship between high levels of alcohol consumption and risk of cardiovascular disease. Drinking at low levels without episodes of heavy drinking may be associated with a reduced risk of cardiovascular disease. Overall alcohol consumption at the population level is associated with multiple health risks that exceed any potential benefits.

Unhealthy diet

High dietary intakes of saturated fat, trans-fats and salt, and low intake of fruits, vegetables and fish are linked to cardiovascular risk, although whether all these associations are causal is disputed. The World Health Organization attributes approximately 1.7 million deaths worldwide to low fruit and vegetable consumption. The amount of dietary salt consumed is also an important determinant of blood pressure levels and overall cardiovascular risk. Frequent consumption of high-energy foods, such as processed foods that are high in fats and sugars, promotes obesity and may increase cardiovascular risk. High trans-fat intake has adverse effects on blood lipids and circulating inflammatory markers, and elimination of trans-fat from diets has been widely advocated. There is evidence that higher consumption of sugar is associated with higher blood pressure and unfavorable blood lipids, and sugar intake also increases the risk of diabetes mellitus. High consumption of processed meats is associated with an increased risk of cardiovascular disease, possibly in part due to increased dietary salt intake.

Socioeconomic disadvantage

Cardiovascular disease affects low- and middle-income countries even more than high-income countries. There is relatively little information regarding social patterns of cardiovascular disease within low- and middle-income countries, but within high-income countries low income and low educational status are consistently associated with greater risk of cardiovascular disease. Policies that have resulted in increased socio-economic inequalities have been associated with greater subsequent socio-economic differences in cardiovascular disease implying a cause and effect relationship. Psychosocial factors, environmental exposures, health behaviours, and health-care access and quality contribute to socio-economic differentials in cardiovascular disease. The Commission on Social Determinants of Health recommended that more equal distributions of power, wealth, education, housing, environmental factors, nutrition, and health care were needed to address inequalities in cardiovascular disease and non-communicable diseases.

Air pollution

Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, PM_2.5 is the major focus, in which gradients are used to determine CVD risk. For every 10 μg/m of PM_2.5 long-term exposure, there was an estimated 8–18% CVD mortality risk. Women had a higher relative risk (RR) (1.42) for PM_2.5 induced coronary artery disease than men (0.90) did. Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m of PM_2.5 resulted in a 48% increase of CVD mortality risk. 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/m of PM_2.5. Other research has implicated PM_2.5 in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure. PM_2.5 is also linked to carotid artery thickening and increased risk of acute myocardial infarction.

Pathophysiology

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.

This is extremely important considering that 1 in 3 people 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, as are a history of chronic kidney disease and hypercholesterolaemia. 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.

Screening

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

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. Currently, biomarkers that may reflect a higher risk of cardiovascular disease include the following:

• Coronary artery calcification
• Carotid intima-media thickness
• Carotid total plaque area
• Higher fibrinogen and PAI-1 blood concentrations
• Elevated homocysteine
• Elevated blood levels of asymmetric dimethylarginine
• Inflammation as measured by C-reactive protein
• Elevated Low-density lipoprotein-p
• Elevated blood levels of brain natriuretic peptide (also known as B-type) (BNP)

Prevention

Currently practiced measures to prevent cardiovascular disease include:

• A low-fat, high-fiber diet including whole grains and fruit and vegetables. Five portions a day reduces risk by about 25%.
• Tobacco cessation and avoidance of second-hand smoke
• Limit alcohol consumption to the recommended daily limits consumption of 1–2 standard alcoholic drinks per day may reduce risk by 30% However excessive alcohol intake increases the risk of cardiovascular disease.
• Lower blood pressures, if elevated
• Decrease body fat if overweight or obese
• Increase daily activity to 30 minutes of vigorous exercise per day at least five times per week (multiply by three if horizontal);
• Reduce sugar consumptions
• Decrease psychosocial stress. This measure may be complicated by imprecise definitions of what constitute psychosocial interventions. Mental stress–induced myocardial ischemia is associated with an increased risk of heart problems in those with previous heart disease. Severe emotional and physical stress leads to a form of heart dysfunction known as Takotsubo syndrome in some people. Stress however plays a relatively minor role in hypertension. Specific relaxation therapies are of unclear benefit.

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. It is unclear whether or not dental care in those with periodontitis affects the risk of cardiovascular disease. Exercise in those who are at high risk of heart disease has not been well studied as of 2014.

Diet

A diet high in fruits and vegetables decreases the risk of cardiovascular disease and death. Evidence suggests that the Mediterranean diet may improve cardiovascular outcomes. 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). 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, lower total and low density lipoprotein cholesterol and improve metabolic syndrome; but the long term benefits outside the context of a clinical trial have been questioned. A high fiber diet appears to lower the risk.

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

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. In addition, the review suggested that a low-salt diet may be harmful in those with congestive heart failure. 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. When this study is left out, the rest of the trials show a trend to benefit. 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. 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.

Supplements

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. Mineral supplements have also not been found to be useful. 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. Magnesium supplementation lowers high blood pressure in a dose dependent manner. Magnesium therapy is recommended for patients with ventricular arrhythmia associated with torsades de pointes who present with long QT syndrome as well as for the treatment of patients with digoxin intoxication-induced arrhythmias. Evidence to support omega-3 fatty acid supplementation is lacking.

Medication

Aspirin has been found to be of only modest benefit in those at low risk of heart disease as the risk of serious bleeding is almost equal to the benefit with respect to cardiovascular problems. In those at really low risk it is not recommended.

Statins are effective in preventing further cardiovascular disease in people with a history of cardiovascular disease. As the event rate is higher in men than in women, the decrease in events is more easily seen in men than women. In those without cardiovascular disease but risk factors statins appear to also be beneficial with a decrease in mortality and further heart disease. 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. The medications niacin, fibrates and CETP Inhibitors, while they may increase HDL cholesterol do not affect the risk of cardiovascular disease in those who are already on statins.

Management

Cardiovascular disease is treatable with initial treatment primarily focused on diet and lifestyle interventions.

Epidemiology

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

The first studies on cardiovascular health were performed in year 1949 by Jerry Morris using occupational health data and were published in year 1958. 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. 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.

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.

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, etc. before it can be licensed for use.

References

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. ^ 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.{{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: multiple names: authors list (link) CS1 maint: unflagged free DOI (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. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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. doi:10.1161/01.cir.0000019552.77778.04. 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. Micha, R; Michas, G; Mozaffarian, D (Dec 2012). "Unprocessed red and processed meats and risk of coronary artery disease and type 2 diabetes—an updated review of the evidence". Current atherosclerosis reports. 14 (6): 515–24. doi:10.1007/s11883-012-0282-8. PMC 3483430. PMID 23001745.
12. Shanthi Mendis; Pekka Puska; Bo Norrving (2011). Global Atlas on Cardiovascular Disease Prevention and Control. World Health Organization in collaboration with the World Heart Federation and the World Stroke Organization. ISBN 978-92-4-156437-3.
13. 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
14. "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#
15. Mackay, Mensah, Mendis, et al. The Atlas of Heart Disease and Stroke. World Health Organization. January 2004.
16. ^ Jousilahti Vartiainen, Tuomilehto Puska (1999). "Sex, Age,Cardiovascular Risk Factors, and coronary heart disease". Circulation. 99: 1165–1172. doi:10.1161/01.cir.99.9.1165.
17. ^ Jani B, Rajkumar C (2006). "Ageing and vascular ageing". Postgrad Med J. 82: 357–362. doi:10.1136/pgmj.2005.036053.
18. ^ http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors
19. "Diabetes raises women's risk of heart disease more than for men". NPR.org. May 22, 2014. Retrieved May 23, 2014.
20. 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.
21. ^ "MendisPuska2011"
22. Richard Doll, Richard Peto, Jillian Boreham & Isabelle Sutherland (June 2004). "Mortality in relation to smoking: 50 years' observations on male British doctors". BMJ (Clinical research ed.). 328 (7455): 1519. doi:10.1136/bmj.38142.554479.AE. PMID 15213107.{{cite journal}}: CS1 maint: multiple names: authors list (link)
23. World Health Organization; UNAIDS (1 January 2007). Prevention of Cardiovascular Disease. World Health Organization. pp. 3–. ISBN 978-92-4-154726-0.
24. Mukamal, Kenneth J.; Chen, Chiung M.; Rao, Sowmya R.; Breslow, Rosalind A. (2010). "Alcohol Consumption and Cardiovascular Mortality Among U.S. Adults, 1987 to 2002". Journal of the American College of Cardiology. 55 (13): 1328–1335. doi:10.1016/j.jacc.2009.10.056. ISSN 0735-1097.
25. World Health Organization (2011). Global Status Report on Alcohol and Health. World Health Organization. ISBN 978-92-4-156415-1.
26. Booker, C.S.; Mann, J.I. (2008). "Trans fatty acids and cardiovascular health: Translation of the evidence base". Nutrition, Metabolism and Cardiovascular Diseases. 18 (6): 448–456. doi:10.1016/j.numecd.2008.02.005. ISSN 0939-4753.
27. Remig, Valentina; Franklin, Barry; Margolis, Simeon; Kostas, Georgia; Nece, Theresa; Street, James C. (2010). "Trans Fats in America: A Review of Their Use, Consumption, Health Implications, and Regulation". Journal of the American Dietetic Association. 110 (4): 585–592. doi:10.1016/j.jada.2009.12.024. ISSN 0002-8223.
28. Te Morenga, L. A.; Howatson, A. J.; Jones, R. M.; Mann, J. (2014). "Dietary sugars and cardiometabolic risk: systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids". American Journal of Clinical Nutrition. 100 (1): 65–79. doi:10.3945/ajcn.113.081521. ISSN 0002-9165.
29. "Wylie-Rosett2002"
30. Micha, Renata; Michas, Georgios; Mozaffarian, Dariush (2012). "Unprocessed Red and Processed Meats and Risk of Coronary Artery Disease and Type 2 Diabetes – An Updated Review of the Evidence". Current Atherosclerosis Reports. 14 (6): 515–524. doi:10.1007/s11883-012-0282-8. ISSN 1523-3804.
31. ^ Mariachiara Di Cesare, Young-Ho Khang, Perviz Asaria, Tony Blakely, Melanie J. Cowan, Farshad Farzadfar, Ramiro Guerrero, Nayu Ikeda, Catherine Kyobutungi, Kelias P. Msyamboza, Sophal Oum, John W. Lynch, Michael G. Marmot & Majid Ezzati (2013). "Inequalities in non-communicable diseases and effective responses". Lancet. 381 (9866): 585–597. doi:10.1016/S0140-6736(12)61851-0. PMID 23410608. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
32. J. P. Mackenbach, A. E. Cavelaars, A. E. Kunst & F. Groenhof (2000). "Socioeconomic inequalities in cardiovascular disease mortality; an international study". European heart journal. 21 (14): 1141–1151. doi:10.1053/euhj.1999.1990. PMID 10924297. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
33. Alexander M. Clark, Marie DesMeules, Wei Luo, Amanda S. Duncan & Andy Wielgosz (2009). "Socioeconomic status and cardiovascular disease: risks and implications for care". Nature reviews. Cardiology. 6 (11): 712–722. doi:10.1038/nrcardio.2009.163. PMID 19770848. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
34. World Health Organization (2008). Closing the Gap in a Generation: Health Equity Through Action on the Social Determinants of Health : Commission on Social Determinants of Health Final Report. World Health Organization. pp. 26–. ISBN 978-92-4-156370-3.
35. ^ 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.
36. ^ 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.
37. ^ "Cardiovascular Effects of Ambient Particulate Air Pollution Exposure". Circulation. 121 (25): 2755–65. 2010. doi:10.1161/CIRCULATIONAHA.109.893461. PMC 2924678. PMID 20585020.
38. ^ Bertazzo, S. et al. Nano-analytical electron microscopy reveals fundamental insights into human cardiovascular tissue calcification. Nature Materials 12, 576–583 (2013).
39. 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
40. 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.
41. NPS Medicinewise (1 March 2011). "NPS Prescribing Practice Review 53: Managing lipids". Retrieved 1 August 2011.
42. 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. doi:10.1016/j.ijcard.2006.11.003.{{cite journal}}: CS1 maint: multiple names: authors list (link)
43. 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. doi:10.1016/j.jacc.2003.08.050. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
44. 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.
45. ^ Moyer, VA (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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
46. Maron, B. J.; Friedman, R. A.; Kligfield, P.; Levine, B. D.; Viskin, S.; Chaitman, B. R.; Okin, P. M.; Saul, J. P.; Salberg, L.; Van Hare, G. F.; Soliman, E. Z.; Chen, J.; Matherne, G. P.; Bolling, S. F.; Mitten, M. J.; Caplan, A.; Balady, G. J.; Thompson, P. D. (15 September 2014). "Assessment of the 12-Lead ECG as a Screening Test for Detection of Cardiovascular Disease in Healthy General Populations of Young People (12–25 Years of Age): A Scientific Statement From the American Heart Association and the American College of Cardiology". Circulation. doi:10.1161/CIR.0000000000000025.
47. 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)
48. 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.
49. 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.
50. 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.
51. 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: multiple names: authors list (link)
52. ^ NHS Direct
53. Ignarro, LJ (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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
54. ^ Wang, X; Ouyang, Y; Liu, J; Zhu, M; Zhao, G; Bao, W; Hu, FB (Jul 29, 2014). "Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies". BMJ (Clinical research ed.). 349: g4490. doi:10.1136/bmj.g4490. PMID 25073782.
55. World Heart Federation (5 October 2011). "World Heart Federation: Cardiovascular disease risk factors". Retrieved 5 October 2011.
56. 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)
57. Klatsky AL (May 2009). "Alcohol and cardiovascular diseases". Expert Rev Cardiovasc Ther. 7 (5): 499–506. doi:10.1586/erc.09.22. PMID 19419257.
58. 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
59. 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: multiple names: authors list (link)
60. Thompson, D. R.; Ski, C. F. (2013). "Psychosocial interventions in cardiovascular disease - what are they?". European Journal of Preventive Cardiology. 20 (6): 916–917. doi:10.1177/2047487313494031. ISSN 2047-4873.
61. Wei, J; Rooks, C; Ramadan, R; Shah, AJ; Bremner, JD; Quyyumi, AA; Kutner, M; Vaccarino, V (15 July 2014). "Meta-analysis of mental stress-induced myocardial ischemia and subsequent cardiac events in patients with coronary artery disease". The American journal of cardiology. 114 (2): 187–92. PMID 24856319.
62. Pelliccia, F; Greco, C; Vitale, C; Rosano, G; Gaudio, C; Kaski, JC (August 2014). "Takotsubo syndrome (stress cardiomyopathy): an intriguing clinical condition in search of its identity". The American journal of medicine. 127 (8): 699–704. PMID 24754972.
63. 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.
64. 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.
65. Abbott, RA; Whear, R; Rodgers, LR; Bethel, A; Thompson Coon, J; Kuyken, W; Stein, K; Dickens, C (May 2014). "Effectiveness of mindfulness-based stress reduction and mindfulness based cognitive therapy in vascular disease: A systematic review and meta-analysis of randomised controlled trials". Journal of psychosomatic research. 76 (5): 341–51. PMID 24745774.
66. Moyer, VA (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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
67. Li, C; Lv, Z; Shi, Z; Zhu, Y; Wu, Y; Li, L; Iheozor-Ejiofor, Z (Aug 15, 2014). "Periodontal therapy for the management of cardiovascular disease in patients with chronic periodontitis". The Cochrane database of systematic reviews. 8: CD009197. doi:10.1002/14651858.CD009197.pub2. PMID 25123257.
68. Seron, P; Lanas, F; Pardo Hernandez, H; Bonfill Cosp, X (Aug 13, 2014). "Exercise for people with high cardiovascular risk". The Cochrane database of systematic reviews. 8: CD009387. doi:10.1002/14651858.CD009387.pub2. PMID 25120097.
69. Walker C, Reamy BV (April 2009). "Diets for cardiovascular disease prevention: what is the evidence?". Am Fam Physician. 79 (7): 571–8. PMID 19378874.
70. 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.
71. 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: multiple names: authors list (link)
72. 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
73. 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: multiple names: authors list (link)
74. 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.
75. 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. PMC 3898422. PMID 24355537.
76. "Fats and fatty acids in human nutrition Report of an expert consultation". World Health Organization. WHO/FAO. Retrieved 20 December 2014.
77. ^ 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.
78. ^ Chowdhury, Rajiv (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. PMID 24723079. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
79. ^ 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. doi:10.1136/bmj.e8707. PMID 23386268.
80. 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.
81. 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.
82. 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.
83. 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)
84. 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.
85. Astrup, A (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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
86. 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.
87. ^ 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.
88. ^ He, F J; MacGregor G A (2011). "Salt reduction lowers cardiovascular risk: meta-analysis of outcome trials" (PDF). The Lancet. 378 (9789): 380–382. doi:10.1016/S0140-6736(11)61174-4. PMID 21803192.
89. 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 (3): 221–230. doi:10.1042/CS20070193. PMID 17688420.
90. ^ 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.
91. 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. {{cite journal}}: Explicit use of et al. in: |author2= (help)
92. 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.
93. Myung, SK (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. doi:10.1136/bmj.f10. PMC 3548618. PMID 23335472. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
94. 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.
95. 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.
96. 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.
97. 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
98. 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
99. 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.
100. 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.
101. "Final Recommendation Statement Aspirin for the Prevention of Cardiovascular Disease: Preventive Medication". http://www.uspreventiveservicestaskforce.org/. March 2009. Retrieved 15 January 2015. {{cite web}}: External link in |website= (help)
102. ^ 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.
103. Taylor, F (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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
104. 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.
105. Keene, D; Price, C; Shun-Shin, MJ; Francis, DP (Jul 18, 2014). "Effect on cardiovascular risk of high density lipoprotein targeted drug treatments niacin, fibrates, and CETP inhibitors: meta-analysis of randomised controlled trials including 117,411 patients". BMJ (Clinical research ed.). 349: g4379. doi:10.1136/bmj.g4379. PMID 25038074.
106. 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. {{cite journal}}: Explicit use of et al. in: |author= (help)
107. 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): 54–9. 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)
108. 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
109. "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov 11, 2009.
110. 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.
111. Karakas M, Koenig W (December 2009). "CRP in cardiovascular disease". Herz. 34 (8): 607–13. doi:10.1007/s00059-009-3305-7. PMID 20024640.
112. 20448212
113. 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: multiple names: authors list (link)
114. 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: multiple names: authors list (link)
115. Dominguez-Rodriguez, Alberto (January 2012). "Melatonin and Cardiovascular Disease: Myth or Reality?". Rev Esp Cardiol. 65: 215–218.

External links

• Template:Dmoz
• European Guidelines on cardiovascular disease prevention in clinical practice (version 2012)

Template:Medical conditions

• Articles to be merged from January 2015
• Heart diseases