Cardiovascular disease

Diabetes Why managing blood sugar is so important.

Diseases of the heart and blood vessels. The risk of suffering from a cardiovascular disease is increased by a number of factors including high blood pressure, obesity, smoking, psychological stress, and lack of exercise. See also atherosclerosis and coronary heart disease.

Any one of a number of abnormal conditions that involve dysfunction of the heart and blood vessels, including but not limited to systemic hypertension, atherosclerosis and coronary heart disease, and rheumatic heart disease.

Cardiovascular disease is a general diagnostic category consisting of several separate diseases of the heart and circulatory system. Cardiovascular diseases have been the major health problem and the leading cause of death in the United States for several decades. Despite impressive and sustained declines in the mortality rates from these diseases, the magnitude of the problem is still staggering. In 1997 alone, nearly 1 million people died of cardiovascular disease, which was about 40 percent of all deaths. The two most important components are coronary heart disease and cerebrovascular disease, with 460,390 dying of coronary heart disease and 158,060 dying of cerebrovascular disease in 1998. In 2000, it was estimated that cardiovascular diseases carried a direct heath expenditure cost of $186 billion and additional indirect costs of $190 billion, making these diseases a continuing major contributor to the escalating cost of health care in the United States.

These diseases have not always been the major health problem of the United States. In 1900 the five leading causes of death were: (1) pneumonia and influenza; (2) tuberculosis; (3) diarrhea, enteritis, and ulceration of the intestines; (4) diseases of the heart; and (5) intracranial lesions of vascular origin. These categories all had rates greater than 100 per 100,000 population. By 1940, only two disease categories still had rates greater than 100 per 100,000: diseases of the heart and cancer and other malignant tumors. The infectious diseases had been substantially reduced, but the "epidemic" of cardiovascular disease, especially coronary heart disease had begun. By 1963, the mortality rate from coronary heart disease reached its pear, and there has been a progressive and steady decline since then. Despite the continued magnitude of the coronary heart disease problem, the focus recently has been on this dramatic reversal. Not only is the percentage of decline large (56% from 1963 to 1998), but this has greatly impacted the total number of deaths in the United States, leading to an increase in life expectancy. To illustrate the impact of this change, it is estimated that if the rate of coronary heart disease mortality had not changed from its peak in 1963, in the year 1998 an additional 684,000 Americans would have died from this cause.

Risk Factors in Cardiovascular Disease

From several studies around the world, several risk factors for cardiovascular disease have been identified. These risk factors can be grouped into two broad categories: unmodifiable factors (such as male gender, and family history of premature heart diseases) and potentially modifiable factors (such as cigarette smoking, high blood pressure, high blood-cholesterol level, physical inactivity, diabetes, and obesity). These factors can be used to identify those in the population who are at especially high risk of developing cardiovascular disease.

Cigarette Smoking. Cigarette smoking has been established as a risk factor not only for lung cancer, emphysema, and bronchitis but also for coronary, cerebral, and peripheral vascular disease. This association has been seen in many countries, among widely diverse ethnic groups, in both sexes, and across various adult age groups. In addition, the risk increases with heavier cigarette use and the longer one has smoked. Equally important has been the observation that this increased risk falls rapidly over time when people quit smoking. For coronary heart disease, approximately 40 percent of the increased risk is removed within five years of quitting, although it takes several more years of nonsmoking to achieve the level associated with someone who has never smoked.

High Blood Pressure. High blood pressure is a powerful risk factor for cerebrovascular disease as well as for coronary heart disease. An estimated 50 million people have high blood pressure, defined as a level equal to or greater than 140 mmHg systolic pressure or 90 mmHg diastolic pressure, or as being on a regimen of antihypertensive medication. An important result of epidemiologic studies has been the observation that the relationship between blood pressure and cardiovascular risk is not only a positive one (higher blood pressure results in higher disease rates) but also a smooth one (there was no sharp breakpoint in the curve such that below a certain blood pressure level the risk remained constant or became nonexistent). Thus, the lower the blood pressure, within reasonable physiologic limits, the lower the level of risk. These observations prompted several important intervention trials, which have now clearly established the value of aggressively treating elevated blood pressure.

Blood Cholesterol Levels. A clear and positive relationship between blood cholesterol levels and subsequent coronary heart disease has repeatedly been demonstrated. Recent information has refined the nature of this association but not weakened it. Cholesterol in the plasma is transported by lipoproteins. The cholesterol level associated with the low-density lipoprotein (LDL) fraction is positively correlated with coronary heart disease, whereas the cholesterol associated with the high-density lipoprotein (HDL) is negatively correlated (the higher the level, the lower the risk). These observations have been verified in several different populations and have been shown to be independent of each other, as well as of other known risk factors. The evidence regarding HDL, although more recent than that for LDL, supports a powerful and independent role for HDL in lowering coronary heart disease risk and probably explains a significant portion of the difference in risk between men and women, with women having higher average levels of HDL than men.

Physical Inactivity. An association between a less active lifestyle and increased risk of coronary heart disease has been shown in multiple longitudinal and cross-sectional studies in such diverse groups as London transit workers, United States longshoremen, and United States college graduates. Traditionally, this risk factor was considered less important and less powerful than the three already mentioned. However, recent reviews of the total body of scientific evidence have led to the classification of this risk factor as one of the four major modifiable risk factors for coronary heart disease. Consequently, there are more consistent recommendations for an active lifestyle and recognition of its importance not only to health but also to disease prevention.

Obesity. Initial epidemiologic data identified obesity as an important risk factor for coronary heart disease. Subsequent analyses, however, suggested that obesity was not a primary risk factor, but rather acted indirectly through elevation of blood pressure and cholesterol levels. More recent analyses of the data from the Framingham Heart Study, with longer follow-up of people in the cohort, have once again suggested that obesity is indeed a primary risk factor that acts independently of those other factors. Clinically, the resolution of this issue of primary versus secondary causation is somewhat irrelevant. Weight reduction should lower the risk of coronary heart disease, whether it acts through a lowered blood pressure and/or cholesterol level or as a lowered risk factor itself.

Diabetes. Diabetes is a powerful and independent risk factor for cardiovascular disease, which remains the major cause of death in diabetic persons. An important remaining issue is whether and elevated blood-glucose level is responsible for the observed higher rate of cardiovascular disease and, if it is, whether lowering or, preferably, normalizing the glucose level will lower the risk. Regardless of the answers, for the present the important observation is that diabetic individuals are at higher risk of cardiovascular disease, and thus careful attention should be paid not just to the blood-glucose level and its control but also to the other risk factors that may coexist in a given patient and additionally elevate the risk.

Other risk factors for cardiovascular disease, such as homocysteine and LPa, have been identified in single or multiple studies, but further information is needed to establish them as independent, important prognostic factors.

(SEE ALSO: Atherosclerosis; Blood Lipids; Blood Pressure; Coronary Artery Disease; Diabetes Mellitus; Fats; Foods and Diets; HDL Cholesterol; LDL Cholesterol; Lifestyle; Lipoproteins; Physical Activity; Smoking Behavior; Smoking Cessation; Tobacco Control)

Bibliography

Goldman, L., and Cook, E. F. (1984). "The Decline in Ischemic Heart Disease Mortality Rates: An Analysis of the Comparative Effects of Medical Interventions and Changes in Lifestyle." Annals of Internal Medicine 101:825.

National Center for Health Statistics. Health, United States, 2000. Washington, DC: U.S. Department of Health and Human Services.

National Heart, Lung, and Blood Institute (1994). "Second Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults." Circulation 89:1333–1445.

National Institutes of Health (1997). The Sixth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda, MD: Author.

World Health Organization. World Health Report, 2000. Geneva: Author.

— WILLIAM T. FRIEDEWALD

Cardiovascular disease is a set of diseases affecting the heart and blood vessels. As with most chronic diseases whose incidence increases with age, it involves both inherited and environmental contributors and is therefore classified as a complex genetic disease. Most researchers believe that all major risk factors for cardiovascular disease have been identified. It is estimated that cigarette smoking, hypertension, abnormal serum cholesterol (low-density lipoprotein cholesterol or high-density lipoprotein cholesterol), obesity, lack of physical exercise, and diabetes account for 50 percent of the variability of risk in high-risk populations. The remaining risk is likely composed of a large number of yet-to-be identified minor risk factors or genetic influences that account for the development of disease in most individuals. Investigators who have attempted to estimate the overall contribution of genetics to the development of cardiovascular disease have proposed numbers ranging from 20 to 60 percent, based upon the analysis of large epidemiologic studies.

Finding Genes for Cardiovascular Disease

Genetics studies of cardiovascular disease involve searches for genes in two general classes: causative genes and disease-susceptibility (or disease-modifying) genes. These are sought through gene-linkage analysis or candidate-gene studies, respectively. Identifying causative genes for this disease is likely several years away at best. Before that time, however, a new understanding will have been reached regarding the relationship between inherited risks and outcomes in cardiovascular disease. With the development of new technology, we also have the promise of a detailed catalogue of disease-modifying genes that may open the door to therapeutic advances.

Gene-linkage analyses involve the study of families that express the cardiovascular trait of interest. In such studies, it is important also to establish the relative risk. Relative risk is defined as the probability of developing a condition (such as cardiovascular disease) if a risk factor (such as a gene) is present, divided by the probability of developing the condition if the risk factor is absent. A relative risk greater than 4.0 (that is, a four-fold greater risk due to presence of a gene or genes) will be associated with a reasonable likelihood of success in finding associated genes, given a study of 200 sibling pairs demonstrating the condition.

One of the best-studied types of cardiovascular disease is early-onset (or premature) coronary artery disease, which has a particularly strong genetic or inherited component. The coronary arteries are those around the heart that supply it with blood. Early-onset is defined as disease presentation (as reversible heart pain, heart attack, or cardiovascular surgery) before the age of 50. Approximately 8 to 10 percent of the U.S. population with cardiovascular disease presents before age 50, according to most surveys. Based upon a number of relatively small epidemiologic studies and several genetics studies in twins, a conservative estimate of the relative risk ratio contributed by genetics to the development of early-onset cardiovascular disease is between 4.0 and 8.0. Despite the fact that it has an inherited component, the actual genes responsible for familial predisposition to early-onset coronary artery disease have been incompletely investigated and remain obscure.

While population-level relative risk for developing cardiovascular disease can be known with a great deal of accuracy, therefore, this knowledge cannot be used to counsel or direct therapy for an individual in any given family. In fact, it has become clear to most practicing cardiologists that even when we know which cardiovascular risk factors are present, we have a very limited ability to predict the development of disease in most individuals.

Ongoing Studies

The ongoing studies of the genetics of cardiovascular disease consist of two general types: those that accumulate individual cases with the goal of performing association candidate-gene studies, and those that collect data from families (sibling pairs or extended families) with the idea of performing gene-linkage studies. Candidate-gene studies examine variations in genes that code for proteins that are likely to be involved in a disease or its prevention, such as genes controlling cholesterol metabolism or blood pressure. Linkage studies look for chromosome regions that are co-inherited with risk for disease, and then look carefully at the region to determine what genes are present.

Patients for both types of studies may be located in similar ways. Disease registry databases contain information on patients with particular conditions, which may have been collected by hospitals, charitable organizations, or research organizations. Clinical trials databases are generated during the testing of a new drug or other treatment. Population-based longitudinal studies collect data on a large number of randomly selected people (not just those with disease) and follow them over many years, to determine what factors lead to development of disease. Each study has its own contribution to make, and only through the combined efforts of multiple studies and approaches will we discover and understand the genetic contributions to the development of cardiovascular disease.

Goals of Genetic Studies

Many of the promises of genetics investigations have probably been grossly overstated. The immediate potential of the ongoing and planned investigations into the genetics of cardiovascular disease is more promising for gene-directed therapy (the use of genetic information to guide the judicious use of medical interventions) than for somatic gene therapy (the use of a gene or gene product which, when introduced into a human organ, changes the function of the organ).

The realistic promises of current genetics studies include the elucidation of disease mechanisms; the identification of new targets for the development of therapeutic pharmacologic agents; and the use of genetic markers to identify individuals for whom a particular agent is either effective or unusually hazardous. This approach, called pharmacogenomics, improves the safety and efficacy of treatments, and enhances the ability to preferentially select subjects for clinical trials based upon genetic predispostion and for gene-directed therapy. In the latter case, for example, a genetic contributor to the development of early-onset cardiovascular disease might be used as an additional risk factor whose identification could focus the allocation of preventive resources, whether educational, behavioral, or pharmacologic, to populations at particularly high risk for the disease.

Bibliography

Lander, E. S., and N. J. Schork. "Genetic Dissection of Complex Traits." Science 265 (1994): 2035-2048.

—Bill Kraus

A disease of the heart and blood vessels. Risk factors include hypertension. obesity, smoking, psychological stress, and lack of exercise.

Cardiovascular Disease is the name of a group of ailments that affect the heart and blood vessels, including but not limited to hypertension, heart attack, stroke, congenital and rheumatic heart disease, and arrhythmia. The leading cause of death in America in the early twenty-first century, heart disease strikes both men and women across racial and ethnic lines, with people age 35 to 64 years old the most susceptible. Approximately one million Americans die of heart disease annually. For the millions of Americans with some form of heart disease, premature and permanent disability is a constant threat.

The diagnosis and treatment of heart disease developed slowly. In the eighteenth century one of the first steps toward diagnosis was Viennese scientist Leopold Auenbrugger's method of percussion. Striking the patient's chest to listen and feel the reverberation allowed Auenbrugger to estimate the size of the heart and the presence of fluid in the chest. Auenbrugger's method was improved by the invention of the stethoscope by French physician René Laënnec. These methods worked well for diseases that produced physical symptoms but not for ailments with no physical signs. Two other important eighteenth-century physicians were Englishmen William Heberden and John Hunter, who concentrated on the manifestation of the disease instead of the causes. The first to use the term "angina pectoris" in a 1772 lecture, Heberden separated myocardial infarction (heart attack) from other types of chest pain.

In 1902 Willem Einthoven, a Dutch physiologist, published the first electrocardiogram, which he recorded on a string galvanometer he had adapted for this purpose. This device was the forerunner of the electrocardiograph (EKG), a device that reads and records the heart's electrical activity. The EKG built on the work of English physicians James Mackenzie, developer of the polygraph, and Thomas Lewis. In Europe, physicians tended to deemphasize the role of technology in diagnoses but American physician James Herrick saw the potential usefulness of the EKG in diagnosing conditions that could not be detected using the unaided senses. In 1912 Herrick was the first to describe coronary artery disease, or hardening of the arteries, as a form of heart disease.

In the spring of 1929, Werner Forssmann, a German physician, took another important step in cardiac research. Forssmann, fascinated by research conducted by nineteenth-century French doctors, inserted a urethral catheter into a main vein in his arm and guided the catheter into his own heart. Three years later two American doctors, Dickinson Richards, Jr. and André Cournand, moved Forssmann's research forward. Richards and Cournand began with the belief that the heart, lungs, and circulatory system were actually a single system. By 1942 the doctors successfully reached the right ventricle, and two years later they successfully inserted a catheter into a patient's pulmonary artery. Using a catheter, the doctors could measure hemodynamic pressure and oxygen in each side of the heart. Richards and Cournand received federal funds to continue their research.

With advances in technology, methods for treating patients suffering from heart disease increased. By 1938 the American Robert Gross had performed the first heart surgery, and by 1952 another American, F. John Lewis, performed the first open-heart surgery. In 1967 the South African surgeon Christiaan Barnard completed the first whole-heart transplant. One of the most striking medical advances is the artificial heart. The Jarvik-7, developed by the American doctor Robert K. Jarvik, was made to operate like a real heart. Made of aluminum, plastic, and Dacron polyester and needing a power source, the Jarvik-7 is bulky and meant to serve only as a temporary solution for those on a transplant list. Jarvik's heart, first used in the 1980s, was not the first artificial heart. In 1957 the Dutch physician Willem Kolff and his team tested an artificial heart in animals, and by 1969 another team led by Denton Cooley of the Texas Heart Institute kept a human artificial-heart patient alive for more than sixty hours. In 1982 the first Jarvik heart was transferred to Barney Clark by a team led by University of Utah's William DeVries. Clark lived for 112 days after the transplant.

Treatments less drastic than transplant surgery were also developed. For instance, in the late 1960s and early 1970s surgeons rerouted blood flow to the heart with coronary artery bypass surgery. Another less invasive procedure called percutaneous transluminal coronary angioplasty was developed in the late 1970s to open occluded cardiac arteries without opening the chest. Angioplasty uses a small device that is threaded through blood vessels to reach a blockage in the cardiac arteries. For patients suffering from abnormal or slow heart rhythm, doctors use a pacemaker, developed in the 1980s. Pacemakers, using lithium batteries lasting seven to ten years, are inserted in the body with wires attached to the heart. When the heart rhythm becomes dangerous the pacemaker delivers a shock to restore a normal heartbeat. The key to survival for heart attack victims is getting to the hospital quickly. Fortunately public awareness and widespread knowledge about CPR, cardiopulmonary resuscitation, greatly increases victims' chances.

Doctors and researchers have also identified certain risk factors that increase a person's chance of developing heart disease. In 1948 the Framingham Heart Study was initiated to track 5,209 people, examining each person every two years. The study's findings demonstrated that men, older people, and people with a family history of heart disease were more likely to develop heart problems. Further, the study indicated that those who smoke, have a poor diet, and lead sedentary lifestyles, are more likely to develop heart disease. The American Heart Association (AHA) was formed in 1924 to help doctors educate the public about heart disease. After launching a public awareness campaign in 1948, the AHA grew rapidly and remains one of the loudest voices for public health in America.

Bibliography

Howell, Joel D. "Concepts of Heart-Related Diseases." In The Cambridge World History of Human Diseases. Kiple, Kenneth F., ed. New York: Cambridge University Press, 1993.

—Lisa A. Ennis

This article is in need of attention from an expert on the subject. WikiProject Medicine/Cardiology task force may be able to help recruit one. (November 2009)

Cardiovascular dhe and Heart disease
Classification and external resources
ICD-10	I51.6
DiseasesDB	28808
MeSH	D002318

Cardiovascular disease or cardiovascular diseases is the class of diseases that involve the heart or blood vessels (arteries and veins). ^[1] While the term technically refers to any disease that affects the cardiovascular system (as used in MeSH), it is usually used to refer to those related to atherosclerosis (arterial disease). These conditions have similar causes, mechanisms, and treatments. In practice, cardiovascular disease is treated by cardiologists, thoracic surgeons, vascular surgeons, neurologists, and interventional radiologists, depending on the organ system that is being treated. There is considerable overlap in the specialties, and it is common for certain procedures to be performed by different types of specialists in different hospitals.

Most countries face high and increasing rates of cardiovascular disease. Each year, heart disease kills more Americans than cancer.^[2]

It is the number one cause of death and disability in the United States and most European countries (data available through 2005). A large histological study (PDAY) showed vascular injury accumulates from adolescence, making primary prevention efforts necessary from childhood.^[3][4]

By the time that heart problems are detected, the underlying cause (atherosclerosis) is usually quite advanced, having progressed for decades. There is therefore increased emphasis on preventing atherosclerosis by modifying risk factors, such as healthy eating, exercise and avoidance of smoking.

Contents 1 Classification 2 Causes 3 Pathophysiology 4 Diagnosis 4.1 Associated diagnostic markers 5 Screening 6 Management 7 Epidemiology 8 Research 9 See also 10 References 11 External links

Classification

• Aneurysm
• Angina
• Atherosclerosis
• Cerebrovascular Accident (Stroke)
• Cerebrovascular disease
• Congestive Heart Failure
• Coronary Artery Disease
• Myocardial infarction (Heart Attack)
• Peripheral vascular disease

Causes

In his book "The Heart Healthy Program", the cardiologist Dr Richard M. Fleming has identified several key dietary factors that can lower the risk of heart disease, including:

• Lowering of LDL cholesterol by reducing saturated fat intake.
• Lowering of Triglyceride levels by reducing consumption of sugary and processed foods.
• Reduction of Homocysteine levels by supplementation with Vitamins B6 and B12, and folic acid.
• Increased antioxidant activity by higher consumption of fruits and vegetables.
• Lowering of fibrinogen and growth factors by cutting back on foods such as red meat, dairy products, poultry and eggs.

Pathophysiology

Population based studies in the youth show that the precursors of heart disease start in adolescence. The process of atherosclerosis evolves over decades, and begins as early as 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. However, most adolescents are more concerned about other risks such as HIV, accidents, and cancer than cardiovascular disease.^[5] This is extremely important considering that 1 in 3 people will die from complications attributable to atherosclerosis. In order to stem the tide of cardiovascular disease, primary prevention is needed. Primary prevention starts with education and awareness that cardiovascular disease poses the greatest threat and measures to prevent or reverse this disease must be taken

Diagnosis

Platelet and Fibrin complexes can be seen with the technique of dark field microscopy. They are much bigger than red blood cells and easily block capillaries. These complexes are clearly visible in dark field but not in stained bright field samples because the different staining methods disburse them. However, they are not visible in unstained blood smears. This method of early detection allows to identify people at risk and take appropriate measures.^[6]

Associated diagnostic markers

• Low-density lipoprotein
• Lipoprotein(a)
• Apolipoprotein A1
• Apolipoprotein B
• Ratio of Apolipoprotein A1/Apolipoprotein B

This section requires expansion.

Screening

Some biomarkers are thought to offer a more detailed risk of cardiovascular disease. However, the clinical value of these biomarkers is questionable.^[7] Currently, biomarkers which may reflect a higher risk of cardiovascular disease include:

• Higher fibrinogen and PAI-1 blood concentrations
• Elevated homocysteine, or even upper half of normal
• Elevated blood levels of asymmetric dimethylarginine
• High inflammation as measured by C-reactive protein
• Elevated blood levels of brain natriuretic peptide (also known as B-type) (BNP) ^[8]

Management

Unlike many other chronic medical conditions, Cardiovascular disease is treatable and reversible, even after a long history of disease. Treatment is primarily focused on diet and stress reduction.^{[4] [9] [10] [11] [12]}

Epidemiology

Disability-adjusted life year for cardiovascular diseases per 100,000 inhabitants in 2004.^[13]

     no data      less than 900      900-1650      1650-2300      2300-3000      3000-3700      3700-4400      4400-5100      5100-5800      5800-6500      6500-7200      7200-7900      Over 9000

Research

The first studies on cardiovascular health were performed in 1949 by Jerry Morris (physician) using occupational health data and were published in 1958.^[14] 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 an inflammatory marker that may be present in increased levels in the blood in patients at risk for cardiovascular disease. Its exact role in predicting disease is the subject of debate.

Some areas currently being researched include possible links between infection with Chlamydophila pneumoniae and coronary artery disease. The Chlamydia link has become less plausible with the absence of improvement after antibiotic use.^[15]

See also

• Alcohol and cardiovascular disease

References

1. ^ Maton, Anthea (1993). Human Biology and Health. Englewood Cliffs, New Jersey: Prentice Hall. ISBN 0-13-981176-1. 
2. ^ United States (1999). "Chronic Disease Overview". United States Government. http://www.cdc.gov/nccdphp/overview_text.htm. Retrieved 2007-02-07. 
3. ^ Rainwater DL, McMahan CA, Malcom GT, et al. (Mar 1999). "Lipid and apolipoprotein predictors of atherosclerosis in youth: apolipoprotein concentrations do not materially improve prediction of arterial lesions in PDAY subjects. The PDAY Research Group". Arterioscler Thromb Vasc Biol. 19 (3): 753–61. PMID 10073983. http://atvb.ahajournals.org/cgi/pmidlookup?view=long&pmid=10073983. 
4. ^ ^{a b} McGill HC, McMahan CA, Zieske AW, et al. (Aug 2000). "Associations of coronary heart disease risk factors with the intermediate lesion of atherosclerosis in youth. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group". Arterioscler Thromb Vasc Biol. 20 (8): 1998–2004. PMID 10938023. http://atvb.ahajournals.org/cgi/pmidlookup?view=long&pmid=10938023. 
5. ^ 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. 
6. ^ [1]
7. ^ 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. 
8. ^ Wang TJ, Larson MG, Levy D, et al. (Feb 2004). "Plasma natriuretic peptide alksdjalkdj levels and the risk of cardiovascular events and death". N Engl J Med. 350 (7): 655–63. doi:10.1056/NEJMoa031994. PMID 14960742. <!kjk-- Pls confirm this ref-->
9. ^ Ornish Dean (Jan 1996). Dean Dr. Dean Ornish's Programme for Reversing Heart Disease Ivy Books. New York: Ivy Books. ISBN 0-8041-1038-7. 
10. ^ 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. 
11. ^ Ornish, D., Scherwitz, L. W., Doody, R. S., Kesten, D., McLanahan, S. M., Brown, S. E. "et al." (1983). "Effects of stress management training and dietary changes in treating ischemic heart disease". JAMA 249 (54): 54. doi:10.1001/jama.249.1.54. 
12. ^ 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 (280): 2001. doi:10.1001/jama.280.23.2001. PMID 9863851. 
13. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. http://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html. Retrieved Nov. 11, 2009. 
14. ^ Coronary Heart Disease and Physical Activity of Work by J. N. Morris and Margaret D. Crawford, British Medical Journal 1958 ; 2(5111): 1485–1496 [2]
15. ^ 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. 

External links

Informational

• Total Cholesterol Distribution vs. CHD deaths
• Heart Disease and Stroke Statistics - 2006 Update from the American Heart Association
• Cardiovascular Disease Foundation
• The British Heart Foundation
• World Health Organization cardiovascular disease site
• European Association for Cardiovascular Disease Prevention and Rehabilitation (EACPR)

Risk Assessment

• www.HeartScore.org Cardiovascular disease risk assessment and management tool for health professionals - developed by the European Society of Cardiology

Public information

• HeartFailureMatters.org Informations website for patients, families and care givers with animations, interviews and glossary - Created by the Heart Failure Association of the European Society of Cardiology.
• Health-EU Portal Cardiovascular Diseases in the EU

v • d • e Pathology: Medical conditions (Diseases/Disorders/Illness, Syndromes/Sequences, Symptoms/Signs, Injuries, etc.) and ICD codes (A/B, 001-139) Infectious disease/Infection: Bacterial disease (G+, G-) · Virus disease · Parasitic disease (Protozoan infection, Helminthiasis, Ectoparasitic infestation) · Mycosis · Zoonosis (C/D, 140-239 & 280-289) Cancer (C00-D48, 140-239) Tumor Myeloid hematologic (D50-D77, 280-289) Anemia · Coagulopathy Lymphoid immune (D80-D89, 279) Immunodeficiency · Immunoproliferative disorder · Hypersensitivity (E, 240-278) Endocrine disease · Nutrition disorder · Inborn error of metabolism (F, 290-319) Mental disorder (G, 320-359) Nervous system disease (CNS, PNS) · Neuromuscular disease (H, 360-389) Eye disease · Ear disease (I, 390-459) Cardiovascular disease (Heart disease, Vascular disease) (J, 460-519) Respiratory disease (Obstructive lung disease, Restrictive lung disease, Pneumonia) (K, 520-579) Stomatognathic disease (Tooth disease) · Digestive disease (Esophageal, Stomach, Enteropathy, Liver, Pancreatic) (L, 680-709) Skin disease · skin appendages (Nail disease, Hair disease, Sweat gland disease) (M, 710-739) Musculoskeletal disorders · Osteochondropathy (Osteopathy, Chondropathy) (N, 580-629) Urologic disease (Nephropathy, Urinary bladder disease) · Male genital disease · Breast disease · Female genital disease (O, 630-679) Complications of pregnancy · Obstetric labor complication · Puerperal disorder (P, 760-779) Fetal disease (Q, 740-759) Congenital disorder (R, 780-799) Syndromes · Medical signs (Eponymous) (S/T, 800-999) Bone fracture · Joint dislocation · Sprain · Strain · subluxation · Head injury · Chest trauma · Poisoning

v • d • e Cardiovascular disease: heart disease · Circulatory system pathology (I00-I52, 390-429) Ischaemic CD/CHD CAD · Coronary thrombosis · Coronary vasospasm · Coronary artery aneurysm · Coronary artery dissection · Myocardial Bridge Active ischemia Angina pectoris (Prinzmetal's angina, Stable angina) · Acute coronary (Unstable angina, Myocardial infarction / heart attack) Sequelae hours (Myocardial stunning, Hibernating myocardium) · days (Myocardial rupture) · weeks (Aneurysm of heart/Ventricular aneurysm, Dressler's syndrome) Layers Pericardium Pericarditis (Acute, Chronic/Constrictive) · Pericardial effusion (Hemopericardium, Cardiac tamponade) Myocardium Myocarditis (Chagas disease) Cardiomyopathy: Dilated (Alcoholic) · Hypertrophic · Restrictive (Loeffler endocarditis, Cardiac amyloidosis, Endocardial fibroelastosis) Arrhythmogenic right ventricular dysplasia Endocardium/ valves Endocarditis Infective endocarditis (Subacute bacterial endocarditis) · noninfective endocarditis (Nonbacterial thrombotic endocarditis, Libman-Sacks endocarditis) Valves mitral (regurgitation, prolapse, stenosis) · aortic (stenosis, insufficiency) · tricuspid (stenosis, insufficiency) · pulmonary (stenosis, insufficiency) Conduction/ arrhythmia Bradycardia Sinus bradycardia · Sick sinus syndrome Heart block: Sinoatrial · AV (1°, 2°, 3°) · Intraventricular (Bundle branch/Right/Left, Left anterior fascicular/Left posterior fascicular, Bifascicular/Trifascicular) · Adams-Stokes syndrome Tachycardia (paroxysmal and sinus) Supraventricular Atrial (Multifocal) · Junctional (AV nodal reentrant, Junctional ectopic) Ventricular Torsades de pointes · Catecholaminergic polymorphic · Accelerated idioventricular rhythm Premature contraction Atrial · Ventricular Pre-excitation syndrome Wolff-Parkinson-White · Lown-Ganong-Levine Flutter/fibrillation Atrial flutter · Ventricular flutter · Atrial fibrillation (Familial) · Ventricular fibrillation Pacemaker Wandering pacemaker · Ectopic pacemaker/Ectopic beat · Parasystole · Multifocal atrial tachycardia · Pacemaker syndrome Long QT syndrome Romano-Ward syndrome · Andersen-Tawil syndrome · Jervell and Lange-Nielsen syndrome Cardiac arrest Sudden cardiac death · Asystole · Pulseless electrical activity · Sinoatrial arrest Other/ungrouped hexaxial reference system (Right axis deviation, Left axis deviation) · QT (Short QT syndrome) · T (T wave alternans) · ST (Osborn wave, ST elevation, ST depression) Cardiomegaly Ventricular hypertrophy (Left, Right/Cor pulmonale) · Atrial enlargement (Left, Right) Other Cardiac fibrosis · Heart failure (Cardiac asthma) · Rheumatic fever heart navs: anat/physio/dev, noncongen/congen/neoplasia, symptoms+signs/eponymous, proc

v • d • e Cardiovascular disease: vascular disease · Circulatory system pathology (I70-I99, 440-456) Arteries, arterioles and capillaries Inflammation Arteritis (Aortitis) · Buerger's disease Arterial occlusive disease/ peripheral vascular disease Arteriosclerosis Atherosclerosis (Foam cell, Fatty streak, Atheroma, Intermittent claudication) · Monckeberg's arteriosclerosis · Arteriolosclerosis (Hyaline, Hyperplastic, oxycholesterol, cholesterol, LDL, trans fat) Stenosis Renal artery stenosis · Carotid artery stenosis Other Fibromuscular dysplasia · Degos disease · Aortoiliac occlusive disease · Raynaud's phenomenon/Raynaud's disease · Erythromelalgia Aneurysm/dissection/ pseudoaneurysm torso: Aortic aneurysm (Thoracic aortic aneurysm, Abdominal aortic aneurysm) · Aortic dissection · Coronary artery aneurysm head/neck: Cerebral aneurysm · Intracranial berry aneurysm · Carotid artery dissection · Vertebral artery dissection · Familial aortic dissection Vascular malformation Arteriovenous fistula · Telangiectasia (Hereditary hemorrhagic telangiectasia) Vascular nevus Spider angioma · Halo nevus · Cherry hemangioma Veins Inflammation Phlebitis Venous thrombosis/ Thrombophlebitis primarily lower limb (Deep vein thrombosis) abdomen (May-Thurner syndrome, Portal vein thrombosis, Budd-Chiari syndrome, Renal vein thrombosis) upper limb/torso (Paget-Schroetter disease, Mondor's disease) head (Cerebral venous sinus thrombosis) Post-thrombotic syndrome Varicose veins Varicocele · Gastric varices · Portacaval anastomosis (Hemorrhoid, Esophageal varices, Caput medusae) Other Superior vena cava syndrome · Inferior vena cava syndrome · Venous ulcer · Chronic venous insufficiency · Chronic cerebrospinal venous insufficiency Arteries or veins Vasculitis · Thrombosis · Embolism (Pulmonary embolism, Cholesterol embolism, Paradoxical embolism) · Angiopathy (Macroangiopathy, Microangiopathy) Blood pressure Hypertension Hypertensive heart disease · Hypertensive nephropathy · Essential hypertension  · Secondary hypertension (Renovascular hypertension) · Pulmonary hypertension · Malignant hypertension · Benign hypertension · Systolic hypertension · White coat hypertension Hypotension Orthostatic hypotension vascular navs: anat/physio/dev, noncongen/systemic vasculitis/congen/neoplasia, symptoms+signs/eponymous, proc

v • d • e Certain conditions originating in the perinatal period / fetal disease (P, 760-779) Maternal factors and complications placenta (Placenta praevia, Placental insufficiency) · Chorion/Amnion/Umbilical cord Chorioamnionitis  · Umbilical cord prolapse · Nuchal cord  · Twin-to-twin transfusion syndrome Length of gestation and fetal growth Small for gestational age · Large for gestational age · Preterm birth · Postmature birth Birth trauma Cephalhematoma · Brachial plexus lesion (Erb's palsy, Klumpke paralysis) By system Respiratory Intrauterine hypoxia · Infant respiratory distress syndrome · Transient tachypnea of the newborn · Meconium aspiration syndrome · pleural disease (Pneumothorax, Pneumomediastinum) · Wilson-Mikity syndrome · Bronchopulmonary dysplasia Cardiovascular Pneumopericardium · Persistent fetal circulation Haemorrhagic and haematological/ hematologic disease Vitamin K deficiency (Haemorrhagic disease of the newborn) · Hemolytic disease of the newborn (ABO HDN • Anti-Kell HDN • Rhesus c HDN • Rhesus D HDN • Rhesus E HDN) · Rh disease · Hydrops fetalis · Hyperbilirubinemia (Kernicterus, Neonatal jaundice) Velamentous cord insertion Digestive system Ileus · Necrotizing enterocolitis · Meconium peritonitis Integument and temperature regulation Erythema toxicum Nervous system Periventricular leukomalacia Musculoskeletal system Gray baby syndrome · muscle tone (Congenital hypertonia, Congenital hypotonia) Other disorders Perinatal infection (Congenital rubella syndrome, Neonatal herpes simplex) · Omphalitis Stillbirth/Perinatal mortality obstetric navs: pregnancy, conditions of mother/conditions of fetus, eponymous signs, proc

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