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In people with heart failure, stress testing or coronary angiography may be performed to identify and treat underlying coronary artery disease.
In people with heart failure, stress testing or coronary angiography may be performed to identify and treat underlying coronary artery disease.If not treated correctly


== Prevention ==
== Prevention ==

Revision as of 18:24, 12 May 2014

Coronary artery disease
SpecialtyCardiology, pediatric cardiac surgery Edit this on Wikidata

Coronary artery disease (CAD) also known as atherosclerotic heart disease,[1] coronary heart disease,[2] or ischemic heart disease (IHD),[3] is the most common type of heart disease and cause of heart attacks.[4] The disease is caused by plaque building up along the inner walls of the arteries of the heart, which narrows the arteries and reduces blood flow to the heart.

While the symptoms and signs of coronary artery disease are noted in the advanced state of disease, most individuals with coronary artery disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arises. Symptoms of stable ischaemic heart disease include angina (characteristic chest pain on exertion) and decreased exercise tolerance. Unstable IHD presents itself as chest pain or other symptoms at rest, or rapidly worsening angina. The risk of artery narrowing increases with age, smoking, high blood cholesterol, diabetes, high blood pressure, and is more common in men and those who have close relatives with CAD. Other causes include coronary vasospasm,[5] a spasm of the blood vessels of the heart, it is usually called Prinzmetal's angina.[6]

Diagnosis of IHD is with an electrocardiogram, blood tests (cardiac markers), cardiac stress testing or a coronary angiogram. Depending on the symptoms and risk, treatment may be with medication, percutaneous coronary intervention (angioplasty) or coronary artery bypass surgery (CABG).

It was as of 2012 the most common cause of death in the world,[7] and a major cause of hospital admissions.[8] There is limited evidence for population screening, but prevention (with a healthy diet and sometimes medication for diabetes, cholesterol and high blood pressure) is used both to prevent IHD and to decrease the risk of complications.

Signs and symptoms

Angina (chest pain) that occurs regularly with activity, after heavy meals, or at other predictable times is termed stable angina and is associated with high grade narrowings of the heart arteries. The symptoms of angina are often treated with betablocker therapy such as metoprolol or atenolol. Nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms are also effective in relieving symptoms but are not known to reduce the chances of future heart attacks. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.

Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction. About 80% of chest pains have nothing to do with the heart.

Risk factors

Risk factors can be classified as: fixed (such as age, sex, family history) and modifiable (such as smoking, hypertension, diabetes mellitus, obesity, etc.)

There are various risk assessment systems for determining the risk of coronary artery disease, with various emphasis on different variables above. A notable example is Framingham Score, used in the Framingham Heart Study. It is mainly based on age, gender, diabetes, total cholesterol, HDL cholesterol, tobacco smoking and systolic blood pressure.[9]

Coronary artery disease has a number of well determined risk factors. The most common risk factors include smoking, family history, hypertension, obesity, diabetes, high alcohol consumption, lack of exercise, stress, and hyperlipidemia.[10] Smoking is associated with about 54% of cases and obesity 20%.[11] Lack of exercise has been linked to 7–12% of cases.[11][12]

Job stress appears to play a minor role accounting for about 3% of cases.[11] In one study, women who were free of stress from work life saw an increase in the diameter of their blood vessels, leading to decreased progression of atherosclerosis.[13] Contrastingly, women who had high levels of work-related stress experienced a decrease in the diameter of their blood vessels and significantly increased disease progression.[13] Also, having a type A behavior pattern, a group of personality characteristics including time urgency, competitiveness, hostility, and impatience [14] is linked to an increased risk of coronary disease.[15]

Confirmed

  1. Hypercholesterolemia (specifically, serum LDL concentrations)[16]
  2. Smoking[16]
  3. Hypertension (high systolic pressure seems to be most significant in this regard)[16]
  4. Hyperglycemia (due to diabetes mellitus or otherwise)[citation needed]
  5. Type A Behavioural Patterns, TABP. Added in 1981 as an independent risk factor after a majority of research into the field discovered that TABP's were twice as likely to exhibit CAD as any other personality type.[citation needed]
  6. Hemostatic factors:[17] High levels of fibrinogen and coagulation factor VII are associated with an increased risk of CAD. Factor VII levels are higher in individuals with a high intake of dietary fat[citation needed]. Decreased fibrinolytic activity has been reported in patients with coronary atherosclerosis.
  7. Genetics
  8. High levels of Lipoprotein(a),[18][19][20] a compound formed when LDL cholesterol combines with a substance known as Apoliprotein (a).

Indirect

Pathophysiology

Illustration depicting atherosclerosis in coronary artery.
Illustration depicting coronary artery disease

Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. Myocardial cells may die from lack of oxygen and this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage, heart muscle death and later myocardial scarring without heart muscle regrowth. Chronic high-grade stenosis of the coronary arteries can induce transient ischemia which leads to the induction of a ventricular arrhythmia, which may terminate into ventricular fibrillation leading to death.

Typically, coronary artery disease occurs when part of the smooth, elastic lining inside a coronary artery (the arteries that supply blood to the heart muscle) develops atherosclerosis. With atherosclerosis, the artery's lining becomes hardened, stiffened, and swollen with all sorts of "gunge" - including calcium deposits, fatty deposits, and abnormal inflammatory cells - to form a plaque. Deposits of calcium phosphates (hydroxyapatites) in the muscular layer of the blood vessels appear to play not only a significant role in stiffening arteries but also for the induction of an early phase of coronary arteriosclerosis. This can be seen in a so-called metastatic mechanism of calcification as it occurs in chronic kidney disease and haemodialysis (Rainer Liedtke 2008). Although these patients suffer from a kidney dysfunction, almost fifty percent of them die due to coronary artery disease. Plaques can be thought of as large "pimples" that protrude into the channel of an artery, causing a partial obstruction to blood flow. Patients with coronary artery disease might have just one or two plaques, or might have dozens distributed throughout their coronary arteries. However, there is a term in medicine called cardiac syndrome X, which describes chest pain (Angina pectoris) and chest discomfort in people who do not show signs of blockages in the larger coronary arteries of their hearts when an angiogram (coronary angiogram) is being performed.[23]

No one knows exactly what causes cardiac syndrome X. One explanation is microvascular dysfunction.[24] It is not completely clear why women are more likely than men to have it however, hormones and other risk factors unique to women may play a role.[25]

Diagnosis

Coronary angiogram of a man
Coronary angiogram of a woman

For symptomatic patients, stress echocardiography can be used to make a diagnosis for obstructive coronary artery disease.[26] The use of echocardiography is not recommended on individuals who are exhibiting no symptoms and are otherwise at low risk for developing coronary disease.[26]

CAD has always been a tough disease to diagnose without the use of invasive or stressful activities. The development of the Multifunction Cardiogram (MCG) has changed the way CAD is diagnosed. The MCG consists of a 2 lead resting EKG signal is transformed into a mathematical model and compared against tens of thousands of clinical trials to diagnose a patient with an objective severity score, as well as secondary and tertiary results about the patients condition. The results from MCG tests have been validated in 8 clinical trials [citation needed] which resulted in a database of over 50,000 patients where the system has demonstrated accuracy comparable to coronary angiography (90% overall sensitivity, 85% specificity). This level of accuracy comes from the application of advanced techniques in signal processing and systems analysis combined with a large scale clinical database which allows MCG to provide quantitative, evidence-based results to assist physicians in reaching a diagnosis. The MCG has also been awarded a Category III CPT code by the American Medical Association in the July 2009 CPT update [citation needed].

The diagnosis of "Cardiac Syndrome X" - the rare coronary artery disease that is more common in women, as mentioned, an "exclusion" diagnosis. Therefore, usually the same tests are used as in any patient with the suspicion of coronary artery disease:

The diagnosis of coronary disease underlying particular symptoms depends largely on the nature of the symptoms. The first investigation is an electrocardiogram (ECG/EKG), both for "stable" angina and acute coronary syndrome. An X-ray of the chest and blood tests may be performed.

Stable angina

Main article: Angina pectoris

In "stable" angina, chest pain with typical features occurring at predictable levels of exertion, various forms of cardiac stress tests may be used to induce both symptoms and detect changes by way of electrocardiography (using an ECG), echocardiography (using ultrasound of the heart) or scintigraphy (using uptake of radionuclide by the heart muscle). If part of the heart seems to receive an insufficient blood supply, coronary angiography may be used to identify stenosis of the coronary arteries and suitability for angioplasty or bypass surgery.

Acute coronary syndrome

Main article: Acute coronary syndrome

Diagnosis of acute coronary syndrome generally takes place in the emergency department, where ECGs may be performed sequentially to identify "evolving changes" (indicating ongoing damage to the heart muscle). Diagnosis is clear-cut if ECGs show elevation of the "ST segment", which in the context of severe typical chest pain is strongly indicative of an acute myocardial infarction (MI); this is termed a STEMI (ST-elevation MI), and is treated as an emergency with either urgent coronary angiography and percutaneous coronary intervention (angioplasty with or without stent insertion) or with thrombolysis ("clot buster" medication), whichever is available. In the absence of ST-segment elevation, heart damage is detected by cardiac markers (blood tests that identify heart muscle damage). If there is evidence of damage (infarction), the chest pain is attributed to a "non-ST elevation MI" (NSTEMI). If there is no evidence of damage, the term "unstable angina" is used. This process usually necessitates admission to hospital, and close observation on a coronary care unit for possible complications (such as cardiac arrhythmias – irregularities in the heart rate).

Depending on the risk assessment, stress testing or angiography may be used to identify and treat coronary artery disease in patients who have had an NSTEMI or unstable angina.

Heart failure

Main article: Heart failure

In people with heart failure, stress testing or coronary angiography may be performed to identify and treat underlying coronary artery disease.If not treated correctly

Prevention

Prevention involves: exercise, decreasing obesity, treating hypertension, a healthy diet, decreasing cholesterol levels, and stopping smoking. Medications and exercise are roughly equally effective.[27]

In diabetes mellitus, there is little evidence that very tight blood sugar control improves cardiac risk although improved sugar control appears to decrease other problems like kidney failure and blindness. The World Health Organization (WHO) recommends "low to moderate alcohol intake" to reduce risk of coronary artery disease although this remains without scientific cause and effect proof.[28]

Diet

Main article: Diet and heart disease

It has been suggested that coronary artery disease is partially reversible using an intense dietary regimen coupled with regular cardiovascular exercise.[29] A high fiber diet appears to lower the risk.[30]

  • Vegetarian diet: Vegetarians have been shown to have a 24% reduced risk of dying of heart disease.[31]
  • Cretan Mediterranean diet: The Seven Countries Study found that Cretan men had exceptionally low death rates from heart disease, despite moderate to high intake of fat. The Cretan diet is similar to other traditional Mediterranean diets: consisting mostly of olive oil, bread, abundant fruit and vegetables, a moderate amount of wine and fat-rich animal products such as lamb, and goat cheese.[32][33]

The consumption of trans fat (commonly found in hydrogenated products such as margarine) has been shown to cause the development of endothelial dysfunction, a precursor to atherosclerosis.[34] The consumption of trans fatty acids has been shown to increase the risk of coronary artery disease[35]

Avoiding fats that are readily oxidized (e.g., trans-fats), and limiting carbohydrates and processed sugars may reduce low density lipoproteins, triacylglycerol and apolipoprotein-B thus decreasing the risk.

Evidence does not support a beneficial role for omega-3 fatty acid supplementation in preventing cardiovascular disease (including myocardial infarction and sudden cardiac death).[36][37] Menaquinone (Vitamin K2), but not phylloquinone (Vitamin K1), intake may reduce the risk of CAD mortality.[38]

Secondary prevention

Secondary prevention is preventing further sequelae of already established disease. Regarding coronary artery disease, this can mean risk factor management that is carried out during cardiac rehabilitation, a 4-phase process beginning in hospital after MI, angioplasty or heart surgery and continuing for a minimum of three months. Exercise is a main component of cardiac rehabilitation along with diet, smoking cessation, and blood pressure and cholesterol management. Beta blockers may also be used for this purpose.[39]

Treatment

There are three main treatment options for coronary artery disease:[40]

  1. Medical treatment - drugs (e.g. cholesterol lowering medications, beta-blockers, nitroglycerin, calcium antagonists, etc.);
  2. Coronary interventions as angioplasty and coronary stent;
  3. Coronary artery bypass grafting (CABG)

Lifestyle

Lifestyle changes have been shown to be effective in reducing (and in the case of diet, reversing) coronary disease:

  • Weight control
  • Smoking cessation
  • Avoiding the consumption of trans fats (in hydrogenated oils)
  • Exercise Aerobic exercise, like walking, jogging, or swimming, can help decrease blood pressure and the amount of blood cholesterol(LDL) over time. It also increases HDL cholesterol which is considered as a " good cholesterol " [44][45]
  • Decrease psychosocial stress.[46]

In people with coronary artery disease, aerobic exercise can reduce the risk of mortality.[47] Separate to the question of the benefits of exercise; it is unclear whether doctors should spend time counseling patients to exercise. The U.S. Preventive Services Task Force, found 'insufficient evidence' to recommend that doctors counsel patients on exercise, but "it did not review the evidence for the effectiveness of physical activity to reduce chronic disease, morbidity and mortality", it only examined the effectiveness of the counseling itself.[48] The American Heart Association, based on a non-systematic review, recommends that doctors counsel patients on exercise.[49]

Medications

Aspirin

In those with no other heart problems aspirin decreases the risk of a myocardial infarction in men but not women and increases the risk of bleeding, most of which is from the stomach. It does not affect the overall risk of death in either men or women.[51] It is thus only recommended in adults who are at increased risk for coronary artery disease[52] where increased risk is defined as 'men older than 90 years of age, postmenopausal women, and younger persons with risk factors for coronary artery disease (for example, hypertension, diabetes, or smoking) are at increased risk for heart disease and may wish to consider aspirin therapy'. More specifically, high-risk persons are 'those with a 5-year risk ≥ 3%'.[citation needed]

Anti-platelet therapy

Clopidogrel plus aspirin reduces cardiovascular events more than aspirin alone in those with an STEMI. In others at high risk but not having an acute event the evidence is weak.[53]

Surgery

Revascularization for acute coronary syndrome has a mortality benefit.[54] Revascularization for stable ischaemic heart disease does not appear to have benefits over medical therapy alone.[55] In those with disease in more than one artery coronary artery bypass grafts appear better than percutaneous coronary interventions.[56][57]

Epidemiology

Disability-adjusted life year for ischaemic heart disease per 100,000 inhabitants in 2004.[58]
  no data
  <350
  350–700
  700–1050
  1050–1400
  1400–1750
  1750–2100
  2100–2450
  2450–2800
  2800–3150
  3150–3500
  3500–4000
  >4000

CAD as of 2010 was the leading cause of death globally resulting in over 7 million deaths.[59] This is up from 5.2 million deaths in 1990.[59] It may affect individuals at any age but becomes dramatically more common at progressively older ages, with approximately a tripling with each decade of life.[7] Males are affected more often than females.[7]

Coronary heart disease (CHD) is the leading cause of death for both men and women and accounts for approximately 600,000 deaths in the United States every year.[60] According to present trends in the United States, half of healthy 40-year-old males will develop CAD in the future, and one in three healthy 40-year-old women.[61] It is the most common reason for death of men and women over 20 years of age in the United States.[62] The Maasai of Africa have almost no heart disease.

Research

Further information: atheroma and atherosclerosis

Recent research efforts focus on new angiogenic treatment modalities (angiogenesis) and various (adult) stem cell therapies.

A region on Chromosome 17 was confined to families with multiple cases of myocardial infarction.[63]

A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.[64] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.[citation needed] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.[65]

Since the 1990s the search for new treatment options for coronary artery disease patients, particularly for so called "no-option" coronary patients, focused on usage of angiogenesis[66] and (adult) stem cell therapies. Numerous clinical trials were performed, either applying protein (angiogenic growth factor) therapies, such as FGF-1 or VEGF, or cell therapies using different kinds of adult stem cell populations. Research is still going on - with first promising results particularly for FGF-1[67][68] and utilization of endothelial progenitor cells.

Myeloperoxidase has been proposed as a biomarker.[69]

References

  1. ^ "Coronary heart disease - causes, symptoms, prevention". Southern Cross Healthcare Group. Retrieved 15 September 2013.
  2. ^ "Coronary heart disease". ADAM. Retrieved 15 September 2013.
  3. ^ Bhatia, Sujata K. (2010). Biomaterials for clinical applications (Online-Ausg. ed.). New York: Springer. p. 23. ISBN 9781441969200.
  4. ^ "Heart attack/coronary artery disease". Mount Sinai Hospital, New York.
  5. ^ Williams MJ, Restieaux NJ, Low CJ (February 1998). "Myocardial infarction in young people with normal coronary arteries". Heart. 79 (2): 191–4. doi:10.1136/hrt.79.2.191. PMC 1728590. PMID 9538315.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Rezkalla SH, Kloner RA (October 2007). "Cocaine-induced acute myocardial infarction". Clin Med Res. 5 (3): 172–6. doi:10.3121/cmr.2007.759. PMC 2111405. PMID 18056026.
  7. ^ a b c Finegold, JA (4 December 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): 934–45. doi:10.1016/j.ijcard.2012.10.046. PMID 23218570. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  8. ^ World Health Organization Department of Health Statistics and Informatics in the Information, Evidence and Research Cluster (2004). The global burden of disease 2004 update. Geneva: WHO. ISBN 92-4-156371-0.
  9. ^ framinghamheartstudy.org > Coronary Heart Disease (10-year risk)(based on Wilson, D'Agostino, Levy et al. 'Prediction of Coronary Heart Disease using Risk Factor Categories', Circulation 1998)
  10. ^ "Causes". Coronary artery disease. Mayo Foundation for Medical Education and Research. 29 June 2012. DS00064.
  11. ^ a b c Kivimäki M, Nyberg ST, Batty GD; et al. (October 2012). "Job strain as a risk factor for coronary heart disease: a collaborative meta-analysis of individual participant data". Lancet. 380 (9852): 1491–7. doi:10.1016/S0140-6736(12)60994-5. PMC 3486012. PMID 22981903. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  12. ^ Lee IM, Shiroma EJ, Lobelo F, Puska P, Blair SN, Katzmarzyk PT (July 2012). "Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy". Lancet. 380 (9838): 219–29. doi:10.1016/S0140-6736(12)61031-9. PMC 3645500. PMID 22818936.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ a b Wang HX, Leineweber C, Kirkeeide R; et al. (March 2007). "Psychosocial stress and atherosclerosis: family and work stress accelerate progression of coronary disease in women. The Stockholm Female Coronary Angiography Study". J. Intern. Med. 261 (3): 245–54. doi:10.1111/j.1365-2796.2006.01759.x. PMID 17305647. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  14. ^ Andreassi, John L. (2000). Psychophysiology : human behavior and physiological response. Mahwah NJ: L. Erlbaum. p. 287.
  15. ^ McCann S.J.H. (November 2001). "The precocity-longevity hypothesis: earlier peaks in career achievement predict shorter lives". Pers Soc Psychol Bull. 27 (11): 1429–39. doi:10.1177/01461672012711004.
    Rhodewalt; Smith (1991). "Current issues in Type A behaviour, coronary proneness, and coronary heart disease". In Snyder, C.R.; Forsyth, D.R. (eds.). Handbook of social and clinical psychology: the health perspective. New York: Pergamon. pp. 197–220. ISBN 0080361285.
  16. ^ a b c d Underwood and Cross, James, (2009). General ans Systematic Pathology. London: Churchhill livingstone. p. 279.{{cite book}}: CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
  17. ^ Smith FB, Lee AJ, Fowkes FG, Price JF, Rumley A, Lowe GD (November 1997). "Hemostatic factors as predictors of ischemic heart disease and stroke in the Edinburgh Artery Study". Arterioscler Thromb Vasc Biol. 17 (11): 3321–5. doi:10.1161/01.ATV.17.11.3321. PMID 9409328.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ Danesh J, Collins R, Peto R (2000). "Lipoprotein(a) and coronary heart disease. Meta-analysis of prospective studies". Circulation. 102 (10): 1082–5. doi:10.1161/01.CIR.102.10.1082. PMID 10973834.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  19. ^ Smolders B, Lemmens R, Thijs V (2007). "Lipoprotein (a) and stroke: a meta-analysis of observational studies". Stroke. 38 (6): 1959–66. doi:10.1161/STROKEAHA.106.480657. PMID 17478739.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  20. ^ Schreiner PJ, Morrisett JD, Sharrett AR, Patsch W, Tyroler HA, Wu K, Heiss G (1993). "Lipoprotein(a) as a risk factor for preclinical atherosclerosis" (PDF). Arterioscler. Thromb. 13 (6): 826–33. doi:10.1161/01.ATV.13.6.826. PMID 8499402.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ "Women and heart disease | Health News | Find Articles at BNET". [dead link]
  22. ^ Padmanaban P, Toora BD. Hemoglobin: Emerging marker in stable coronary artery disease. Chron Young Sci [serial online] 2011 [cited 2011 Jul 24];2:109-10. Available from: http://www.cysonline.org/text.asp?2011/2/2/109/82971
  23. ^ Lanza GA (February 2007). "Cardiac syndrome X: a critical overview and future perspectives". Heart. 93 (2): 159–66. doi:10.1136/hrt.2005.067330. PMC 1861371. PMID 16399854.
  24. ^ Jones, E (August 2012). "Cardiac syndrome X and microvascular coronary dysfunction". Trends in Cardiovascular Medicine. 22 (6): 161–8. doi:10.1016/j.tcm.2012.07.014. PMC 3490207. PMID 23026403. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  25. ^ Kaski JC (February 2004). "Pathophysiology and management of patients with chest pain and normal coronary arteriograms (cardiac syndrome X)". Circulation. 109 (5): 568–72. doi:10.1161/01.CIR.0000116601.58103.62. PMID 14769677.
  26. ^ a b American Society of Echocardiography. "Five Things Physicians and Patients Should Question". Choosing Wisely: an initiative of the ABIM Foundation. American Society of Echocardiography. Retrieved 27 February 2013Template:Inconsistent citations{{cite journal}}: CS1 maint: postscript (link), citing
    • Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1016/j.jacc.2010.11.002, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1016/j.jacc.2010.11.002 instead.
    • Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1016/S0735-1097(02)02848-6, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1016/S0735-1097(02)02848-6 instead.
    • Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1016/j.jacc.2010.09.001, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1016/j.jacc.2010.09.001 instead.
  27. ^ Naci, H.; Ioannidis, J. P. A. (1 October 2013). "Comparative effectiveness of exercise and drug interventions on mortality outcomes: metaepidemiological study". BMJ. 347 (oct01 1): f5577–f5577. doi:10.1136/bmj.f5577.
  28. ^ "5. Population nutrient intake goals for preventing diet-related chronic diseases". WHO.
  29. ^ Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA, McLanahan SM, Kirkeeide RL, Brand RJ, Gould KL. (1990). "Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial". Lancet. 336 (8708): 129–33. doi:10.1016/0140-6736(90)91656-U. PMID 1973470.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  30. ^ Threapleton, D. E. (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. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  31. ^ Key TJ, Fraser GE, Thorogood M, Appleby PN, Beral V, Reeves G, Burr ML, Chang-Claude J, Frentzel-Beyme R, Kuzma JW, Mann J, McPherson K (1998). "Mortality in vegetarians and non-vegetarians: a collaborative analysis of 8300 deaths among 76,000 men and women in five prospective studies". Public Health Nutr. 1 (1): 33–41. doi:10.1079/PHN19980006. PMID 10555529.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  32. ^ Willett WC, Sacks F, Trichopoulou A, Drescher G, Ferro-Luzzi A, Helsing E, Trichopoulos D. (1995). "Mediterranean diet pyramid: a cultural model for healthy eating". Am J Clin Nutr. 61 (6 Suppl): 1402S–1406S. PMID 7754995.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  33. ^ Perez-Llamas, F., et al., J Hum Nutr Diet, December 1996, 9:6:463-471
  34. ^ Lopez-Garcia E, Schulze MB, Meigs JB, Manson JE, Rifai N, Stampfer MJ, Willett WC, Hu FB. (2005). "Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction". J Nutr. 135 (3): 562–6. PMID 15735094.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  35. ^ Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC (April 2006). "Trans fatty acids and cardiovascular disease". N. Engl. J. Med. 354 (15): 1601–13. doi:10.1056/NEJMra054035. PMID 16611951.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  36. ^ Evangelos C. Rizos, MD, PhD; Evangelia E. Ntzani, MD, PhD; Eftychia Bika, MD; Michael S. Kostapanos, MD; Moses S. Elisaf, MD, PhD, FASA, FRSH (September 2012). "Association Between Omega-3 Fatty Acid Supplementation and Risk of Major Cardiovascular Disease Events A Systematic Review and Meta-analysis". JAMA. 308 (10): 1024–1033. doi:10.1001/2012.jama.11374. PMID 22968891.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. ^ Kwak, SM (9 April 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. 172 (9): 686–94. doi:10.1001/archinternmed.2012.262. PMID 22493407. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  38. ^ Erkkilä AT, Booth SL (2008). "Vitamin K intake and atherosclerosis". Curr. Opin. Lipidol. 19 (1): 39–42. doi:10.1097/MOL.0b013e3282f1c57f. PMID 18196985.
  39. ^ Awtry, Eric H.; Joseph Loscalzo (2004). "Coronary Heart Disease". Cecil Essentials of Medicine (6 ed.). Philadelphia, PA: Saunders. pp. 87–108. ISBN 978-0-7216-0147-2.
  40. ^ Jameson JN, Kasper DL, Harrison TR, Braunwald E, Fauci AS, Hauser SL, Longo DL. (2005). Harrison's principles of internal medicine (16th ed.). New York: McGraw-Hill Medical Publishing Division. ISBN 0-07-140235-7. OCLC 54501403.{{cite book}}: CS1 maint: multiple names: authors list (link)
  41. ^ Esselstyn CB (2001). "Resolving the Coronary Artery Disease Epidemic Through Plant-Based Nutrition". Prev Cardiol. 4 (4): 171–7. doi:10.1111/j.1520-037X.2001.00538.x. PMID 11832674. at Prevent and Reverse Heart Disease site
  42. ^ a b "Treatments and drugs". Coronary artery disease. Mayo Foundation for Medical Education and Research. 29 June 2012. DS00064.
  43. ^ http://www.heartattackproof.com/Esselstyn_Caldwell_Article.pdf
  44. ^ http://heartdisease.about.com/cs/cholesterol/a/raiseHDL.htm
  45. ^ "Coronary Heart Disease (CHD)". Penguin Dictionary of Biology. 2004.
  46. ^ 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)
  47. ^ Swardfager W, Herrmann N, Cornish S, Mazereeuw G, Marzolini S, Sham L, Lanctôt KL (2012). "Exercise intervention and inflammatory markers in coronary artery disease: a meta-analysis". Am Heart J. 163 (4): 666–676. doi:10.1016/j.ahj.2011.12.017. PMID 22520533.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  48. ^ U.S. Preventive Services Task Force (2002). "Behavioral counseling in primary care to promote physical activity: recommendation and rationale". Ann. Intern. Med. 137 (3): 205–7. doi:10.7326/0003-4819-137-3-200208060-00014. PMID 12160370.
  49. ^ Thompson PD, Buchner D, Pina IL; American Heart Association Council On Nutrition (2003). "Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease: a statement from the Council on Clinical Cardiology (Subcommittee on Exercise, Rehabilitation, and Prevention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity)". Circulation. 107 (24): 3109–16. doi:10.1161/01.CIR.0000075572.40158.77. PMID 12821592.{{cite journal}}: CS1 maint: multiple names: authors list (link)
    Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease. Major Recommendations
  50. ^ Gutierrez, J (25 June 2012). "Statin therapy in the prevention of recurrent cardiovascular events: a sex-based meta-analysis". Archives of Internal Medicine. 172 (12): 909–19. doi:10.1001/archinternmed.2012.2145. PMID 22732744. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  51. ^ Wolff, T (17 March 2009). "Aspirin for the primary prevention of cardiovascular events: an update of the evidence for the U.S. Preventive Services Task Force". Annals of internal medicine. 150 (6): 405–10. doi:10.7326/0003-4819-150-6-200903170-00009. PMID 19293073. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  52. ^ U.S. Preventive Services Task Force*, (15 January 2002). "Aspirin for the primary prevention of cardiovascular events: recommendation and rationale". Ann Intern Med. 136 (2): 157–60. doi:10.7326/0003-4819-136-2-200201150-00015. PMID 11790071.{{cite journal}}: CS1 maint: extra punctuation (link)
  53. ^ Keller T, Squizzato A, Middeldorp S (2007). Squizzato, Alessandro (ed.). "Clopidogrel plus aspirin versus aspirin alone for preventing cardiovascular disease". Cochrane database of systematic reviews (Online) (3): CD005158. doi:10.1002/14651858.CD005158.pub2. PMID 17636787.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  54. ^ Braunwald E, Antman EM, Beasley JW; et al. (October 2002). "ACC/AHA guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction—2002: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina)". Circulation. 106 (14): 1893–900. doi:10.1161/01.CIR.0000037106.76139.53. PMID 12356647. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  55. ^ Stergiopoulos, Kathleen (2 December 2013). "Percutaneous Coronary Intervention Outcomes in Patients With Stable Obstructive Coronary Artery Disease and Myocardial Ischemia". JAMA Internal Medicine. doi:10.1001/jamainternmed.2013.12855. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  56. ^ Sipahi, Ilke (2 December 2013). "Coronary Artery Bypass Grafting vs Percutaneous Coronary Intervention and Long-term Mortality and Morbidity in Multivessel Disease". JAMA Internal Medicine. doi:10.1001/jamainternmed.2013.12844. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  57. ^ Sipahi, I (1 February 2014). "Coronary artery bypass grafting vs percutaneous coronary intervention and long-term mortality and morbidity in multivessel disease: meta-analysis of randomized clinical trials of the arterial grafting and stenting era". JAMA internal medicine. 174 (2): 223–30. doi:10.1001/jamainternmed.2013.12844. PMID 24296767. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  58. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved 11 November 2009.
  59. ^ a b Lozano, R (15 December 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2095–128. doi:10.1016/S0140-6736(12)61728-0. PMID 23245604. {{cite journal}}: |first10= missing |last10= (help); |first11= missing |last11= (help); |first12= missing |last12= (help); |first13= missing |last13= (help); |first14= missing |last14= (help); |first15= missing |last15= (help); |first16= missing |last16= (help); |first17= missing |last17= (help); |first18= missing |last18= (help); |first19= missing |last19= (help); |first20= missing |last20= (help); |first21= missing |last21= (help); |first22= missing |last22= (help); |first23= missing |last23= (help); |first24= missing |last24= (help); |first25= missing |last25= (help); |first26= missing |last26= (help); |first27= missing |last27= (help); |first28= missing |last28= (help); |first29= missing |last29= (help); |first2= missing |last2= (help); |first30= missing |last30= (help); |first3= missing |last3= (help); |first4= missing |last4= (help); |first5= missing |last5= (help); |first6= missing |last6= (help); |first7= missing |last7= (help); |first8= missing |last8= (help); |first9= missing |last9= (help)
  60. ^ "Kochanek KD, Xu JQ, Murphy SL, Miniño AM, Kung HC" (PDF). Retrieved 25 March 2013.
  61. ^ Rosamond W, Flegal K, Friday G (February 2007). "Heart disease and stroke statistics--2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee". Circulation. 115 (5): e69–171. doi:10.1161/CIRCULATIONAHA.106.179918. PMID 17194875.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  62. ^ American Heart Association:Heart Disease and Stroke Statistics-2007 Update. AHA, Dallas, Texas, 2007
  63. ^ Farrall M, Green FR, Peden JF, Olsson PG, Clarke R, Hellenius ML, Rust S, Lagercrantz J, Franzosi MG, Schulte H, Carey A, Olsson G, Assmann G, Tognoni G, Collins R, Hamsten A, Watkins H, on behalf of the PROCARDIS Consortium (2006). "Genome-Wide Mapping of Susceptibility to Coronary Artery Disease Identifies a Novel Replicated Locus on Chromosome 17". PLoS Genetics. 2 (5): e72. doi:10.1371/journal.pgen.0020072. PMC 1463045. PMID 16710446.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  64. ^ Saikku P, Leinonen M, Tenkanen L, Linnanmaki E, Ekman MR, Manninen V, Manttari M, Frick MH, Huttunen JK. (1992). "Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study". Ann Intern Med. 116 (4): 273–8. doi:10.7326/0003-4819-116-4-273. PMID 1733381.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  65. ^ Andraws R, Berger JS, Brown DL. (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)
  66. ^ Simons M, Bonow RO, Chronos NA (September 2000). "Clinical trials in coronary angiogenesis: issues, problems, consensus: An expert panel summary". Circulation. 102 (11): E73–86. doi:10.1161/01.CIR.102.11.e73. PMID 10982554.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  67. ^ Stegmann TJ (December 1998). "FGF-1: a human growth factor in the induction of neoangiogenesis". Expert Opin Investig Drugs. 7 (12): 2011–5. doi:10.1517/13543784.7.12.2011. PMID 15991943.
  68. ^ Wagoner, L.E., Merrill, W., Jacobs, J., Conway, G., Boehmer, J., Thomas, K., Stegmann, T.J.: "Angiogenesis Protein Therapy With Human Fibroblast Growth Factor (FGF-1) Results of a Phase I Open Label, Dose Escalation Study in Subjects With CAD Not Eligible For PCI Or CABG" Circulation 116: 443, 2007
  69. ^ Loria V, Dato I, Graziani F, Biasucci LM (2008). "Myeloperoxidase: a new biomarker of inflammation in ischemic heart disease and acute coronary syndromes". Mediators Inflamm. 2008: 135625. doi:10.1155/2008/135625. PMC 2276594. PMID 18382609.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)

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