Tobacco smoking is the practice where tobacco is burned and the vapors either tasted or inhaled. The practice began as early as 5000–3000 BCE. Many civilizations burned incense during religious rituals, which was later adopted for pleasure or as a social tool. Tobacco was introduced to Eurasia in the late 16th century where it followed common trade routes. The substance was met with frequent criticism but became popular, nonetheless.

German scientists formally identified the link between smoking and lung cancer in the late 1920s. Their studies lead to the first anti-smoking campaign in modern history. The campaign failed to reach across enemy lines during the Second World War and quickly became unpopular, thereafter. In 1950, health authorities again began to suggest a relationship between smoking and cancer. Scientific evidence continued to mount in the 1980s, which prompted political action against the practice. Rates of consumption since 1965 in the developed world have either peaked or declined. However, they continue to climb in the developing world.

Smoking is the most common method of consuming tobacco, and tobacco is the most common substance smoked. The agricultural product is often mixed with additives and then pyrolyzed. The resulting vapors are then inhaled and the active substances absorbed through the alveoli in the lungs. The active substances trigger chemical reactions in nerve endings, which heighten heart rate, memory, alertness, and reaction time. Dopamine and endorphins are released, which are often associated with pleasure. As of 2000, smoking is practiced by approximately 1.22 billion people. Men are more likely to smoke than are women, though the gender gap declines with the younger age.

Many smokers begin during adolescence or early adulthood. Usually, during the early stages, smoking provides pleasurable sensations and serves as a source of positive reinforcement. After an individual has smoked for many years, the avoidance of withdrawal symptoms and negative reinforcement become the key motivations to continue.

History

Early years*

Smoking's history dates back to as early as 5000–3000 BC when the agricultural product began to be cultivated in South America; consumption later evolved into burning the plant substance either by accident or with intent of exploring other means of consumption. The practice worked its way into shamanistic rituals. Many ancient civilizations--such as the Babylonians, the Indians, and the Chinese--burnt incense during religious rituals. The practice was later adopted by the Catholic and the Orthodox churches. Smoking in the Americas probably had its origins in the incense-burning ceremonies of shamans but was later adopted for pleasure or as a social tool. The smoking of tobacco and various hallucinogenic drugs was used to achieve trances and to come into contact with the spirit world.

Eastern North American tribes would carry large amounts of tobacco in pouches as a readily accepted trade item and would often smoke it in pipes, either in sacred ceremonies or to seal bargains. Adults as well as children enjoyed the practice. It was believed that tobacco was a gift from the Creator and that the exhaled tobacco smoke was capable of carrying one's thoughts and prayers to heaven.

Apart from smoking, tobacco had a number of uses as medicine. As a pain killer it was used for earache and toothache and occasionally as a poultice. Smoking was said by the desert Indians to be a cure for colds, especially if the tobacco was mixed with the leaves of the small Desert Sage, ''Salvia Dorrii'', or the root of Indian Balsam or Cough Root, ''Leptotaenia multifida'', the addition of which was thought to be particularly good for asthma and tuberculosis.

Popularization

In 1612, six years after the settlement of Jamestown, John Rolfe was credited as the first settler to successfully raise tobacco as a cash crop. The demand quickly grew as tobacco, referred to as "brown gold", reviving the Virginia joint stock company from its failed gold expeditions. In order to meet demands from the Old World, tobacco was grown in succession, quickly depleting the soil. This became a motivator to settle west into the unknown continent, and likewise an expansion of tobacco production. Indentured servitude became the primary labor force up until Bacon's Rebellion, from which the focus turned to slavery. This trend abated following the American revolution as slavery became regarded as unprofitable. However, the practice was revived in 1794 with the invention of the cotton gin.

Frenchman Jean Nicot (from whose name the word nicotine is derived) introduced tobacco to France in 1560, and tobacco then spread to England. The first report of a smoking Englishman is of a sailor in Bristol in 1556, seen "emitting smoke from his nostrils". Tobacco was introduced around 1600 by French merchants in what today is modern-day Gambia and Senegal. At the same time caravans from Morocco brought tobacco to the areas around Timbuktu and the Portuguese brought the commodity (and the plant) to southern Africa, establishing the popularity of tobacco throughout all of Africa by the 1650s.

Soon after its introduction to the Old World, tobacco came under frequent criticism from state and religious leaders. Murad IV, sultan of the Ottoman Empire 1623-40 was among the first to attempt a smoking ban by claiming it was a threat to public moral and health. The Chinese emperor Chongzhen issued an edict banning smoking two years before his death and the overthrow of the Ming dynasty. Later, the Manchu of the Qing dynasty, who were originally a tribe of nomadic horse warriors, would proclaim smoking "a more heinous crime than that even of neglecting archery". In Edo period Japan, some of the earliest tobacco plantations were scorned by the shogunate as being a threat to the military economy by letting valuable farmland go to waste for the use of a recreational drug instead of being used to plant food crops.

Religious leaders have often been prominent among those who considered smoking immoral or outright blasphemous. In 1634 the Patriarch of Moscow forbade the sale of tobacco and sentenced men and women who flouted the ban to have their nostrils slit and their backs whipped until skin came off their backs. The Western church leader Urban VII likewise condemned smoking on holy places in a papal bull of 1624. Despite many concerted efforts, restrictions and bans were almost universally ignored. When James I of England, a staunch anti-smoker and the author of a ''A Counterblaste to Tobacco'', tried to curb the new trend by enforcing a 4000% tax increase on tobacco in 1604, it proved a failure, as London had some 7,000 tobacco sellers by the early 17th century. Later, scrupulous rulers would realise the futility of smoking bans and instead turned tobacco trade and cultivation into lucrative government monopolies.

By the mid-17th century every major civilization had been introduced to tobacco smoking and in many cases had already assimilated it into the native culture, despite the attempts of many rulers to eliminate the practice with harsh penalties or fines. Tobacco, both product and plant, followed the major trade routes to major ports and markets, and then on into the hinterlands. The English language term ''smoking'' was coined in the late 18th century; before then the practice was called ''drinking smoke''.

Growth remained stable until the American Civil War in 1860s, when the primary labor force shifted from slavery to share cropping. This, along with a change in demand, lead to the industrialization of tobacco production with the cigarette. James Bonsack, a craftsman, in 1881 produce a machine to speed the production in cigarettes.

Social stigma

In Germany, anti-smoking groups, often associated with anti-liquor groups, first published advocacy against the consumption of tobacco in the journal ''Der Tabakgegner'' (The Tobacco Opponent) in 1912 and 1932. In 1929, Fritz Lickint of Dresden, Germany, published a paper containing formal statistical evidence of a lung cancer–tobacco link. During the Great depression Adolf Hitler condemned his earlier smoking habit as a waste of money, and later with stronger assertions. This movement was further strengthened with Nazi reproductive policy as women who smoked were viewed as unsuitable to be wives and mothers in a German family.

The anti-tobacco movement in Nazi Germany did not reach across enemy lines during the Second World War, as anti-smoking groups quickly lost popular support. By the end of the Second World War, American cigarette manufacturers quickly reentered the German black market. Illegal smuggling of tobacco became prevalent, and leaders of the Nazi anti-smoking campaign were silenced. As part of the Marshall Plan, the United States shipped free tobacco to Germany; with 24,000 tons in 1948 and 69,000 tons in 1949. Per capita yearly cigarette consumption in post-war Germany steadily rose from 460 in 1950 to 1,523 in 1963. By the end of the 20th century, anti-smoking campaigns in Germany were unable to exceed the effectiveness of the Nazi-era climax in the years 1939–41 and German tobacco health research was described by Robert N. Proctor as "muted".

Richard Doll in 1950 published research in the British Medical Journal showing a close link between smoking and lung cancer. Four years later, in 1954 the British Doctors Study, a study of some 40 thousand doctors over 20 years, confirmed the suggestion, based on which the government issued advice that smoking and lung cancer rates were related. In 1964 the United States Surgeon General's Report on Smoking and Health likewise began suggesting the relationship between smoking and cancer.

As scientific evidence mounted in the 1980s, tobacco companies claimed contributory negligence as the adverse health effects were previously unknown or lacked substantial credibility. Health authorities sided with these claims up until 1998, from which they reversed their position. The Tobacco Master Settlement Agreement, originally between the four largest US tobacco companies and the Attorneys General of 46 states, restricted certain types of tobacco advertisement and required payments for health compensation; which later amounted to the largest civil settlement in United States history.

From 1965 to 2006, rates of smoking in the United States declined from 42% to 20.8%. The majority of those who quit were professional, affluent men. Although the per-capita number of smokers decreased, the average number of cigarettes consumed per person per day increased from 22 in 1954 to 30 in 1978. This paradoxical event suggests that those who quit smoked less, while those who continued to smoke moved to smoke more light cigarettes. The trend has been paralleled by many industrialized nations as rates have either leveled-off or declined. In the developing world, however, tobacco consumption continues to rise at 3.4% in 2002. In Africa, smoking is in most areas considered to be modern, and many of the strong adverse opinions that prevail in the West receive much less attention. Today Russia leads as the top consumer of tobacco followed by Indonesia, Laos, Ukraine, Belarus, Greece, Jordan, and China.

Consumption

Methods

Tobacco is an agricultural product processed from the fresh leaves of plants in the genus ''Nicotiana''. The genus contains a number of species, however, ''Nicotiana tabacum'' is the commonly grown. ''Nicotiana rustica'' follows as second containing higher concentrations of nicotine. These leaves are harvested and cured to allow for the slow oxidation and degradation of carotenoids in tobacco leaf. This produces certain compounds in the tobacco leaves which can be attributed to sweet hay, tea, rose oil, or fruity aromatic flavors. Before packaging, the tobacco is often combined with other additives in order to: enhance the addictive potency, shift the products pH, or improve the effects of smoke by making it more palatable. In the United States these additives are regulated to 599 substances. The product is then processed, packaged, and shipped to consumer markets. Means of consumption has greatly expanded in scope as new methods of delivering the active substances with fewer by-products have encompassed or are beginning to encompass:

;Beedi : Beedis are thin South Asian cigarettes filled with tobacco flake and wrapped in a tendu leaf tied with a string at one end. They produce higher levels of carbon monoxide, nicotine, and tar than cigarettes typical in the United States. ;Cigars : Cigars are tightly rolled bundles of dried and fermented tobacco which are ignited so that smoke may be drawn into the smoker's mouth. They are generally not inhaled because the high alkalinity of the smoke, which can quickly become irritating to the trachea and lungs. The prevalence of cigar smoking varies depending on location, historical period, and population surveyed, and prevalence estimates vary somewhat depending on the survey method. The United States is the top consuming country by far, followed by Germany and the United Kingdom; the US and Western Europe account for about 75% of cigar sales worldwide. As of 2005 it is estimated that 4.3% of men and 0.3% of women smoke cigars. ;Cigarettes : ''Cigarettes'', French for "small cigar", are a product consumed through smoking and manufactured out of cured and finely cut tobacco leaves and reconstituted tobacco, often combined with other additives, which are then rolled or stuffed into a paper-wrapped cylinder. Cigarettes are ignited and inhaled, usually through a cellulose acetate filter, into the mouth and lungs. ;Electronic cigarette : Electronic cigarettes are an alternative to tobacco smoking, although no tobacco is consumed. It is a battery-powered device that provides inhaled doses of nicotine by delivering a vaporized propylene glycol/nicotine solution. Many legislation and public health investigations are currently pending in many countries due to its relatively recent emergence.Most electronic cigarettes are designed to resemble actual tobacco smoking implements, such as cigarettes, cigars, or pipes, but many take the form of ballpoint pens or screwdrivers since those designs are more practical to house the mechanisms involved. Most are also reusable, with replaceable and refillable parts, but some models are disposable. ;Hookah : ''Hookah'' are a single or multi-stemmed (often glass-based) water pipe for smoking. Originally from India. The hookah was a symbol of pride and honour for the landlords, kings and other such high class people.Now ,the hookah has gained immense popularity, especially in the Middle East. A hookah operates by water filtration and indirect heat. It can be used for smoking herbal fruits, tobacco, or cannabis. ;Kretek : ''Kretek'' are cigarettes made with a complex blend of tobacco, cloves and a flavoring "sauce". It was first introduced in the 1880s in Kudus, Java, to deliver the medicinal eugenol of cloves to the lungs. The quality and variety of tobacco play an important role in kretek production, from which kretek can contain more than 30 types of tobacco. Minced dried clove buds weighing about 1/3 of the tobacco blend are added to add flavoring. In 2004 the United States prohibited cigarettes from having a "characterizing flavor" of certain ingredients other than tobacco and menthol, thereby removing kretek from being classified as cigarettes. ;Passive smoking : Passive smoking is the usually involuntary consumption of smoked tobacco. Second-hand smoke (SHS) is the consumption where the burning end is present, environmental tobacco smoke (ETS) or third-hand smoke is the consumption of the smoke that remains after the burning end has been extinguished. Because of its perceived negative implications, this form of consumption has played a central role in the regulation of tobacco products. ;Pipe smoking : Pipe smoking typically consists of a small chamber (the bowl) for the combustion of the tobacco to be smoked and a thin stem (shank) that ends in a mouthpiece (the bit). Shredded pieces of tobacco are placed into the chamber and ignited. Tobaccos for smoking in pipes are often carefully treated and blended to achieve flavour nuances not available in other tobacco products. ;Roll-Your-Own : Roll-Your-Own or hand-rolled cigarettes, often called 'rollies', are very popular particularly in European countries. These are prepared from loose tobacco, cigarette papers, and filters all bought separately. They are usually much cheaper than ready-made cigarettes. ;Vaporizer : A vaporizer is a device used to sublimate the active ingredients of plant material. Rather than burning the herb, which produces potentially irritating, toxic, or carcinogenic by-products; a vaporizer heats the material in a partial vacuum so that the active compounds contained in the plant boil off into a vapor. Medical administration of a smoke substance often prefer this method as to directly pyrolyzing the plant material.

Physiology

The active substances in tobacco, especially cigarettes, is administered by burning the leaves and inhaling the vaporized gas that results. This quickly and effectively delivers substances into the bloodstream by absorption through the alveoli in the lungs. The lungs contain some 300 million alveoli, which amounts to a surface area of over 70 m² (about the size of a tennis court). This method is inefficient as not all of the smoke will be inhaled, and some amount of the active substances will be lost in the process of combustion, pyrolysis. Pipe and Cigar smoke are not inhaled because of its high alkalinity, which are irritating to the trachea and lungs. However, because of its higher alkalinity (pH 8.5) compared to cigarette smoke (pH 5.3), un-ionized nicotine is more readily absorbed through the mucous membranes in the mouth. Nicotine absorption from cigar and pipe, however, is much less than that from cigarette smoke.

The inhaled substances trigger chemical reactions in nerve endings. The cholinergic receptors are often triggered by the naturally occurring neurotransmitter acetylcholine. Acetylcholine and Nicotine express chemical similarities, which allows Nicotine to trigger the receptor as well. These nicotinic acetylcholine receptors takes are located in the central nervous system and at the nerve-muscle junction of skeletal muscles; whose activity increases heart rate, alertness, and faster reaction times. Nicotine acetylcholine stimulation is not directly addictive. However, since dopamine-releasing neurons are abundant on nicotine receptors, dopamine is released. This release of dopamine, which is associated with pleasure, is reinforcing and may also increase working memory. Nicotine and cocaine activate similar patterns of neurons, which supports the idea that common substrates among these drugs.

When tobacco is smoked, most of the nicotine is pyrolyzed. However, a dose sufficient to cause mild somatic dependency and mild to strong psychological dependency remains. There is also a formation of harmane (a MAO inhibitor) from the acetaldehyde in tobacco smoke. This seems to play an important role in nicotine addiction—probably by facilitating a dopamine release in the nucleus accumbens as a response to nicotine stimuli. Using rat studies, withdrawal after repeated exposure to nicotine results in less responsive nucleus accumbens cells, which produce dopamine responsible for reinforcement.

Demographics

As of 2000, smoking is practiced by 1.22 billion people. Assuming no change in prevalence it is predicted that 1.45 billion people will smoke in 2010 and 1.5 to 1.9 billion in 2025. Assuming that prevalence will decrease at 1% a year and that there will be a modest increase of income of 2%, it is predicted the number of smokers will stand at 1.3 billion in 2010 and 2025.

Smoking is generally five times higher among men than women, however the gender gap declines with younger age. In developed countries smoking rates for men have peaked and have begun to decline, however for women they continue to climb.

As of 2002, about twenty percent of young teens (13–15) smoke worldwide. From which 80,000 to 100,000 children begin smoking every day—roughly half of which live in Asia. Half of those who begin smoking in adolescent years are projected to go on to smoke for 15 to 20 years.

The World Health Organization (WHO) states that "Much of the disease burden and premature mortality attributable to tobacco use disproportionately affect the poor". Of the 1.22 billion smokers, 1 billion of them live in developing or transitional economies. Rates of smoking have leveled off or declined in the developed world. In the developing world, however, tobacco consumption is rising by 3.4% per year as of 2002.

The WHO in 2004 projected 58.8 million deaths to occur globally, from which 5.4 million are tobacco-attributed, and 4.9 million as of 2007. As of 2002, 70% of the deaths are in developing countries.

Psychology

Takeup

Most smokers begin during adolescence or early adulthood. Smoking has elements of risk-taking and rebellion, which often appeal to young people. The presence of peers that smoke and media featuring high-status models smoking may also encourage smoking. Because teenagers are influenced more by their peers than by adults, attempts by parents, schools, and health professionals at preventing people from trying cigarettes are unsuccessful.

Children of smoking parents are more likely to smoke than children with non-smoking parents. One study found that parental smoking cessation was associated with less adolescent smoking, except when the other parent currently smoked. A current study tested the relation of adolescent smoking to rules regulating where adults are allowed to smoke in the home. Results showed that restrictive home smoking policies were associated with lower likelihood of trying smoking for both middle and high school students.

Many anti-smoking organizations claim that teenagers begin their smoking habits due to peer pressure, and cultural influence portrayed by friends. However, one study found that direct pressure to smoke cigarettes did not play a significant part in adolescent smoking. In that study, adolescents also reported low levels of both normative and direct pressure to smoke cigarettes. A similar study showed that individuals play a more active role in starting to smoke than has previously been acknowledged and that social processes other than peer pressure need to be taken into account. Another study's results revealed that peer pressure was significantly associated with smoking behavior across all age and gender cohorts, but that intrapersonal factors were significantly more important to the smoking behavior of 12–13 year-old girls than same-age boys. Within the 14–15 year-old age group, one peer pressure variable emerged as a significantly more important predictor of girls' than boys' smoking. It is debated whether peer pressure or self-selection is a greater cause of adolescent smoking.

Psychologists such as Hans Eysenck have developed a personality profile for the typical smoker. Extraversion is the trait that is most associated with smoking, and smokers tend to be sociable, impulsive, risk taking, and excitement seeking individuals. Although personality and social factors may make people likely to smoke, the actual habit is a function of operant conditioning. During the early stages, smoking provides pleasurable sensations (because of its action on the dopamine system) and thus serves as a source of positive reinforcement.

Persistence

The reasons given by smokers for this activity are broadly categorized as ''addictive smoking'', ''pleasure from smoking'', ''tension reduction/relaxation'', ''social smoking'', ''stimulation'', ''habit/automatism'', and ''handling''. There are gender differences in how much each of these reasons contribute, with females more likely than males to cite ''tension reduction/relaxation'', ''stimulation'' and ''social smoking''.

Some smokers argue that the depressant effect of smoking allows them to calm their nerves, often allowing for increased concentration. However, according to the Imperial College London, "Nicotine seems to provide both a stimulant and a depressant effect, and it is likely that the effect it has at any time is determined by the mood of the user, the environment and the circumstances of use. Studies have suggested that low doses have a depressant effect, while higher doses have stimulant effect."

Patterns

A number of studies have established that cigarette sales and smoking follow distinct time-related patterns. For example, cigarette sales in the United States of America have been shown to follow a strongly seasonal pattern, with the high months being the months of summer, and the low months being the winter months.

Similarly, smoking has been shown to follow distinct circadian patterns during the waking day—with the high point usually occurring shortly after waking in the morning, and shortly before going to sleep at night.

Impact

Economic

In countries where there is a public health system, society covers the cost of medical care for smokers who become ill through in the form of increased taxes. Two arguments exist on this front, the "pro-smoking" argument suggesting that heavy smokers generally don't live long enough to develop the costly and chronic illnesses which affect the elderly, reducing society's healthcare burden. The "anti-smoking" argument suggests that the healthcare burden is increased because smokers get chronic illnesses younger and at a higher rate than the general population.

Data on both positions is limited. The Centers for Disease Control and Prevention published research in 2002 claiming that the cost of each pack of cigarettes sold in the United States was more than $7 in medical care and lost productivity. The cost may be higher, with another study putting it as high as $41 per pack, most of which however is on the individual and his/her family. This is how one author of that study puts it when he explains the very low cost for others: "The reason the number is low is that for private pensions, Social Security, and Medicare — the biggest factors in calculating costs to society — smoking actually saves money. Smokers die at a younger age and don't draw on the funds they've paid into those systems."

By contrast, some non-scientific studies, including one conducted by Philip Morris in the Czech Republic and another by the Cato Institute, support the opposite position. Philip Morris has explicitly apologised for the former study, saying: "The funding and public release of this study which, among other things, detailed purported cost savings to the Czech Republic due to premature deaths of smokers, exhibited terrible judgment as well as a complete and unacceptable disregard of basic human values. For one of our tobacco companies to commission this study was not just a terrible mistake, it was wrong. All of us at Philip Morris, no matter where we work, are extremely sorry for this. No one benefits from the very real, serious and significant diseases caused by smoking."

Between 1970 an 1995, per-capita cigarette consumption in poorer developing countries increased by 67 percent, while it dropped by 10 percent in the richer developed world. Eighty percent of smokers now live in less developed countries. By 2030, the World Health Organization (WHO) forecasts that 10 million people a year will die of smoking-related illness, making it the single biggest cause of death worldwide, with the largest increase to be among women. WHO forecasts the 21st century's death rate from smoking to be ten times the 20th century's rate. ("Washingtonian" magazine, December 2007).

Health

Tobacco use leads most commonly to diseases affecting the heart and lungs, with smoking being a major risk factor for heart attacks, strokes, chronic obstructive pulmonary disease (COPD), emphysema, and cancer (particularly lung cancer, cancers of the larynx and mouth, and pancreatic cancer). Cigarette smoking increases the risk of Crohn's disease as well as the severity of the course of the disease. It is also the number one cause of bladder cancer.

The World Health Organization estimate that tobacco caused 5.4 million deaths in 2004 and 100 million deaths over the course of the 20th century. Similarly, the United States Centers for Disease Control and Prevention describes tobacco use as "the single most important preventable risk to human health in developed countries and an important cause of premature death worldwide."

Lung cancer occurs at non-smokers in 3.4 cases per 100 000 population. At people smoking 0.5 packs of cigarettes a day this figure rises to 51.4 per 100 000, 1-2 packs - up to 143.9 per 100 000 and if the intensity of smoking is over 2 packs a day - up to 217.3 per 100,000 population.

Rates of smoking have leveled off or declined in the developed world. Smoking rates in the United States have dropped by half from 1965 to 2006 falling from 42% to 20.8% in adults. In the developing world, tobacco consumption is rising by 3.4% per year.

Passive smoking presents a very real health risk. Six hundred thousand deaths were attributable to second-hand smoke in 2004.

Social

Famous smokers of the past used cigarettes or pipes as part of their image, such as Jean Paul Sartre's Gauloises-brand cigarettes; Albert Einstein's, Kiana Lee Rosch's, Douglas MacArthur's, Bertrand Russell's, and Bing Crosby's pipes; or the news broadcaster Edward R. Murrow's cigarette. Writers in particular seem to be known for smoking, for example, Cornell Professor Richard Klein's book ''Cigarettes are Sublime'' for the analysis, by this professor of French literature, of the role smoking plays in 19th and 20th century letters. The popular author Kurt Vonnegut addressed his addiction to cigarettes within his novels. British Prime Minister Harold Wilson was well known for smoking a pipe in public as was Winston Churchill for his cigars. Sherlock Holmes, the fictional detective created by Sir Arthur Conan Doyle smoked a pipe, cigarettes, and cigars, besides injecting himself with cocaine, "to keep his overactive brain occupied during the dull London days, when nothing happened". The DC Vertigo comic book character, John Constantine, created by Alan Moore, is synonymous with smoking, so much so that the first storyline by Preacher creator, Garth Ennis, centered around John Constantine contracting lung cancer. Professional wrestler James Fullington, while in character as "The Sandman", is a chronic smoker in order to appear "tough".

The problem of smoking at home is particularly difficult for women in many cultures especially Arab cultures where it may not be acceptable for a woman to ask her husband not to smoke at home or in the presence of her children. Studies has shown that pollution levels in door places are higher than levels found on busy roadways, in closed motor garages, and during fire storms. Furthermore, smoke can spread from one room to another, even if doors to the smoking area are closed.

The ceremonial smoking of tobacco, and praying with a sacred pipe, is a prominent part of the religious ceremonies of a number of Native American Nations. ''Sema'', the Anishinaabe word for tobacco, is grown for ceremonial use and considered the ultimate sacred plant since its smoke was believed to carry prayers to the heavens. In most major religions, however, tobacco smoking is not specifically prohibited, although it may be discouraged as an immoral habit. Before the health risks of smoking were identified through controlled study, smoking was considered an immoral habit by certain Christian preachers and social reformers. The founder of the Latter Day Saint movement, Joseph Smith, Jr, recorded that on February 27, 1833, he received a revelation which discouraged tobacco use. This "Word of Wisdom" was later accepted as a commandment, and faithful Latter-day Saints abstain completely from tobacco. Jehovah's Witnesses base their stand against smoking on the Bible's command to "clean ourselves of every defilement of flesh" (2 Corinthians 7:1). The Jewish Rabbi Yisrael Meir Kagan (1838–1933) was one of the first Jewish authorities to speak out on smoking. In the Bahá'í Faith, smoking tobacco is discouraged though not forbidden.

Public policy

On February 27, 2005 the WHO Framework Convention on Tobacco Control, took effect. The FCTC is the world's first public health treaty. Countries that sign on as parties agree to a set of common goals, minimum standards for tobacco control policy, and to cooperate in dealing with cross-border challenges such as cigarette smuggling. Currently the WHO declares that 4 billion people will be covered by the treaty, which includes 168 signatories. Among other steps, signatories are to put together legislation that will eliminate secondhand smoke in indoor workplaces, public transport, indoor public places and, as appropriate, other public places.

Taxation

Many governments have introduced excise taxes on cigarettes in order to reduce the consumption of cigarettes.

In 2002, the Centers for Disease Control and Prevention said that each pack of cigarettes sold in the United States costs the nation more than $7 in medical care and lost productivity, around $3400 per year per smoker. Another study by a team of health economists finds the combined price paid by their families and society is about $41 per pack of cigarettes.

Substantial scientific evidence shows that higher cigarette prices result in lower overall cigarette consumption. Most studies indicate that a 10% increase in price will reduce overall cigarette consumption by 3% to 5%. Youth, minorities, and low-income smokers are two to three times more likely to quit or smoke less than other smokers in response to price increases. Smoking is often cited as an example of an inelastic good, however, i.e. a large rise in price will only result in a small decrease in consumption.

Many nations have implemented some form of tobacco taxation. As of 1997, Denmark had the highest cigarette tax burden of $4.02 per pack. Taiwan only had a tax burden of $0.62 per pack. The federal government of the United States charges $1.01 per pack.

Cigarette taxes vary widely from state to state in the United States. For example, Missouri has a cigarette tax of only 17 cents per pack, the nation's lowest, while New York has the highest cigarette tax in the U.S.: $4.35 per pack. In Alabama, Illinois, Missouri, New York City, Tennessee, and Virginia, counties and cities may impose an additional limited tax on the price of cigarettes. Sales taxes are also levied on tobacco products in most jurisdictions.

In the United Kingdom, a packet of 20 cigarettes typically costs between £5.22 and £8.00 depending on the brand purchased and where the purchase was made. The UK has a strong black market for cigarettes which has formed as a result of the high taxation, and it is estimated 27% of cigarette and 68% of handrolling tobacco consumption was non-UK duty paid (NUKDP).

In Australia total taxes account for 62.5% of the final price of a packet of cigarettes (2011 figures). These taxes include federal excise or customs duty, and the more recently introduced Goods and Services Tax (GST).

Restrictions

In June 1967, the Federal Communications Commission ruled that programs broadcast on a television station that discussed smoking and health were insufficient to offset the effects of paid advertisements that were broadcast for five to ten minutes each day. In April 1970, Congress passed the Public Health Cigarette Smoking Act banning the advertising of cigarettes on television and radio starting on January 2, 1971.

The Tobacco Advertising Prohibition Act 1992 expressly prohibited almost all forms of Tobacco advertising in Australia, including the sponsorship of sporting or other cultural events by cigarette brands.

All tobacco advertising and sponsorship on television has been banned within the European Union since 1991 under the Television Without Frontiers Directive (1989) This ban was extended by the Tobacco Advertising Directive, which took effect in July 2005 to cover other forms of media such as the internet, print media, and radio. The directive does not include advertising in cinemas and on billboards or using merchandising – or tobacco sponsorship of cultural and sporting events which are purely local, with participants coming from only one Member State as these fall outside the jurisdiction of the European Commission. However, most member states have transposed the directive with national laws that are wider in scope than the directive and cover local advertising. A 2008 European Commission report concluded that the directive had been successfully transposed into national law in all EU member states, and that these laws were well implemented.

Some countries also impose legal requirements on the packaging of tobacco products. For example in the countries of the European Union, Turkey, Australia and South Africa, cigarette packs must be prominently labeled with the health risks associated with smoking. Canada, Australia, Thailand, Iceland and Brazil have also imposed labels upon cigarette packs warning smokers of the effects, and they include graphic images of the potential health effects of smoking. Cards are also inserted into cigarette packs in Canada. There are sixteen of them, and only one comes in a pack. They explain different methods of quitting smoking. Also, in the United Kingdom, there have been a number of graphic NHS advertisements, one showing a cigarette filled with fatty deposits, as if the cigarette is symbolising the artery of a smoker.

Many countries have a smoking age, In many countries, including the United States, most European Union member states, New Zealand, Canada, South Africa, Israel, India, Brazil, Chile, Costa Rica and Australia, it is illegal to sell tobacco products to minors and in the Netherlands, Austria, Belgium, Denmark and South Africa it is illegal to sell tobacco products to people under the age of 16. On September 1, 2007 the minimum age to buy tobacco products in Germany rose from 16 to 18, as well as in Great Britain where on October 1, 2007 it rose from 16 to 18. Underlying such laws is the belief that people should make an informed decision regarding the risks of tobacco use. These laws have a lax enforcement in some nations and states. In China, Turkey, and many other countries usually a child will have little problem buying tobacco products, because they are often told to go to the store to buy tobacco for their parents.

Several countries such as Ireland, Latvia, Estonia, the Netherlands, France, Finland, Norway, Canada, Australia, Sweden, Portugal, Singapore, Italy, Indonesia, India, Lithuania, Chile, Spain, Iceland, United Kingdom, Slovenia and Malta have legislated against smoking in public places, often including bars and restaurants. Restaurateurs have been permitted in some jurisdictions to build designated smoking areas (or to prohibit smoking). In the United States, many states prohibit smoking in restaurants, and some also prohibit smoking in bars. In provinces of Canada, smoking is illegal in indoor workplaces and public places, including bars and restaurants. As of March 31, 2008 Canada has introduced a smoking ban in all public places, as well as within 10 meters of an entrance to any public place. In Australia, smoking bans vary from state to state. Currently, Queensland has total bans within all public interiors (including workplaces, bars, pubs and eateries) as well as patrolled beaches and some outdoor public areas. There are, however, exceptions for designated smoking areas. In Victoria, smoking is banned in train stations, bus stops and tram stops as these are public locations where second hand smoke can affect non-smokers waiting for public transport, and since July 1, 2007 is now extended to all indoor public places. In New Zealand and Brazil, smoking is banned in enclosed public places mainly bars, restaurants and pubs. Hong Kong banned smoking on January 1, 2007 in the workplace, public spaces such as restaurants, karaoke rooms, buildings, and public parks. Bars serving alcohol who do not admit minors were exempt until 2009. In Romania smoking is illegal in trains, metro stations, public institutions (except where designated, usually outside) and public transportation.

Product safety

An indirect public health problem posed by cigarettes is that of accidental fires, usually linked with consumption of alcohol. Numerous cigarette designs have been proposed, some by tobacco companies themselves, which would extinguish a cigarette left unattended for more than a minute or two, thereby reducing the risk of fire. Among American tobacco companies, some have resisted this idea, while others have embraced it. RJ Reynolds was a leader in making prototypes of these cigarettes in 1983 and will make all of their U.S. market cigarettes to be fire-safe by 2010. Phillip Morris is not in active support of it. Lorillard, the nation's third largest tobacco company, seems to be ambivalent.

Gateway drug theory

The relationship between tobacco and other drug use has been well-established, however the nature of this association remains unclear. The two main theories are the phenotypic causation (gateway) model and the correlated liabilities model. The causation model argues that smoking is a primary influence on future drug use, while the correlated liabilities model argues that smoking and other drug use are predicated on genetic or environmental factors.

Cessation

Smoking cessation, referred to as "quitting" is the action leading towards abstinence of tobacco smoking. There are a number of methods such as cold turkey, nicotine replacement therapy, antidepressants, hypnosis, self-help, and support groups.

See also

Cigarette smoking among college students

Cigarette smoking for weight loss

One hitter (smoking)

References

Bibliography

External links

Tobacco History Links — repository from Tobacco.org

Surgeon General: Tobacco Cessation

CDC: Smoking & Tobacco Use

WHO: Tobacco Free Initiative

Category:Smoking Category:Tobacco Category:Habits Category:IARC Group 1 carcinogens

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name	Myocardial infarction
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Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, results from the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (cholesterol and fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and ensuing oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (''infarction'') of heart muscle tissue (''myocardium'').

Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety (often described as a sense of impending doom). Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue. Approximately one-quarter of all myocardial infarctions are "silent", that is without chest pain or other symptoms.

Among the diagnostic tests available to detect heart muscle damage are an electrocardiogram (ECG), echocardiography, cardiac MRI and various blood tests. The most often used blood markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels. Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual nitroglycerin.

Most cases of STEMI (ST elevation MI) are treated with thrombolysis or percutaneous coronary intervention (PCI). NSTEMI (non-ST elevation MI) should be managed with medication, although PCI is often performed during hospital admission. In people who have multiple blockages and who are relatively stable, or in a few emergency cases, bypass surgery may be an option, especially in diabetics.

Ischemic heart disease (which includes myocardial infarction, angina pectoris and heart failure when preceded by myocardial infarction) was the leading cause of death for both men and women worldwide in 2004. Important risk factors are previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (triglycerides, low-density lipoprotein) and low levels of high density lipoprotein (HDL), diabetes, high blood pressure, obesity, chronic kidney disease, heart failure, excessive alcohol consumption, the abuse of certain drugs (such as cocaine and methamphetamine), and chronic high stress levels.

Classification

There are two basic types of acute myocardial infarction: Transmural: associated with atherosclerosis involving major coronary artery. It can be subclassified into anterior, posterior, inferior, lateral or septal. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply. Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia.

In the clinical context, a myocardial infarction can be further subclassified into a ST elevation MI (STEMI) versus a non-ST elevation MI (non-STEMI) based on ECG changes.

The phrase ''heart attack'' is sometimes used incorrectly to describe sudden cardiac death, which may or may not be the result of acute myocardial infarction. A heart attack is different from, but can be the cause of cardiac arrest, which is the stopping of the heartbeat, and cardiac arrhythmia, an abnormal heartbeat. It is also distinct from heart failure, in which the pumping action of the heart is impaired; however severe myocardial infarction may lead to heart failure.

A 2007 consensus document classifies myocardial infarction into five main types:

Type 1 – Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection

Type 2 – Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension

Type 3 – Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood

Type 4 – Associated with coronary angioplasty or stents:

* Type 4a – Myocardial infarction associated with PCI

* Type 4b – Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy

Type 5 – Myocardial infarction associated with CABG

Signs and symptoms

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium, where it may mimic heartburn. Levine's sign, in which the patient localizes the chest pain by clenching their fist over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value.

Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.

Women and older patients report atypical symptoms more frequently than their male and younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men). The most common symptoms of MI in women include dyspnea (shortness of breath), weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms that may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men.

Approximately one-fourth of all myocardial infarctions are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. A silent course is more common in the elderly, in patients with diabetes mellitus and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient. In diabetics, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.

Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.

The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, and esophageal rupture. Other non-catastrophic differentials include gastroesophageal reflux and Tietze's syndrome.

Causes

Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if the exertion is more intense than the individual usually performs. The period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are physically very fit. For those in poor physical condition, the rate differential is over 35-fold higher. One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat, which, as has been observed with intravascular ultrasound, increases mechanical "shear stress" on atheromas and the likelihood of plaque rupture.

Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between ''Chlamydophila pneumoniae'' infection and atherosclerosis. While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor. Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.

There is an association of an increased incidence of a heart attack in the morning hours, more specifically around 9 a.m. Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation.

Risk factors

In general, risk factors for atherosclerosis are risk factors for myocardial infarction:

Age — Men acquire an independent risk factor at age 45, Women acquire an independent risk factor at age 55; in addition, individuals acquire another independent risk factor if they have a first-degree male relative (brother, father) who suffered a coronary vascular event at or before age 55. Another independent risk factor is acquired if one has a first-degree female relative (mother, sister) who suffered a coronary vascular event at age 65 or younger.

Males are more at risk than females.

Diabetes (with or without insulin resistance)

High blood pressure

Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high Triglycerides

Tobacco smoking including secondhand smoke

Air pollution

Family history of ischaemic heart disease (IHD)

Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).

Hyperhomocysteinemia (high homocysteine)

Stress — Occupations with high stress index are known to have susceptibility for atherosclerosis

Alcohol — Studies show that prolonged exposure to high quantities of alcohol can increase the risk of heart attack

Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile. Non-modifiable risk factors include age, sex, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition.

Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation are also correlated with a higher risk of MI. To understand epidemiological study results, it is important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.

Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.

Inflammation is known to be an important step in the process of atherosclerotic plaque formation. C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation. Elevated CRP blood levels, especially measured with high-sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes. Moreover, some drugs for MI might also reduce CRP levels. The use of high-sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion in patients who already present with other risk factors or known coronary artery disease. Whether CRP plays a direct role in atherosclerosis remains uncertain.

Inflammation in periodontal disease may be linked to coronary heart disease, and, since periodontitis is very common, this could have great consequences for public health. Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease. Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines; thus, periodontitis may mediate its effect on MI risk via other risk factors. Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells. A role for specific periodontal bacteria has been suggested but remains to be established. There is some evidence that influenza may trigger an acute myocardial infarction.

Baldness, hair greying, a diagonal earlobe crease (Frank's sign) and possibly other skin features have been suggested as independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.

Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with CT scans. Several studies have shown that coronary calcium can provide predictive information beyond that of classical risk factors.

The European Society of Cardiology and the European Association for Cardiovascular Prevention and Rehabilitation have developed an interactive tool for prediction and managing the risk of heart attack and stroke in Europe. HeartScore is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. The Heartscore Programme is available in 12 languages and offers web-based or PC version.

Pathophysiology

Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated myocardial infarction and ST-elevated myocardial infarction, which are most frequently (but not always) a manifestation of coronary artery disease. The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades. Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).

If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the occluded coronary artery die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction. As a result, the patient's heart will be permanently damaged. This myocardial scarring also puts the patient at risk for potentially life threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences.

Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (''V-Fib''/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life-threatening arrhythmia is ventricular tachycardia (''V-Tach''/VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct.

The cardiac defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.

Diagnosis

The diagnosis of myocardial infarction can be made after assessing patient's complaints and physical status. ECG changes, coronary angiogram and levels of cardiac markers help to confirm the diagnosis. ECG gives valuable clues to identify the site of myocardial damage while coronary angiogram allows visualization of narrowing or obstructions in the heart vessels. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.

A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist. In stable patients whose symptoms have resolved by the time of evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmocologic stress. Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned.

WHO criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied: # Clinical history of ischaemic type chest pain lasting for more than 20 minutes # Changes in serial ECG tracings # Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin

The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI.

Prevention

The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for those with heart disease, and limitation of alcohol intake. People are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:

Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased. Beta blocker therapy such as metoprolol or carvedilol should be commenced. These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia. β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI. ACE inhibitor therapy should be commenced 24–48 hours post-MI in hemodynamically-stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI. Statin therapy has been shown to reduce mortality and morbidity post-MI. The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids. The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above. Spironolactone is another option that is sometimes preferable to eplerenone due to cost. Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease. Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality post-MI. While the mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that the survival benefit is due to electrical stabilization and the prevention of ventricular fibrillation. However, further studies in a high-risk subset have not shown a clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids.

Blood donation may reduce the risk of heart disease for men, but the link has not been firmly established.

A Cochrane review found that giving heparin to people with heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of suffering from minor bleeding.

Management

An MI is a medical emergency that requires immediate medical attention. Treatment attempts to salvage as much myocardium as possible and to prevent further complications, hence the phrase "time is muscle". Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI. A 2009 and 2010 review of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use. Other analgesics such as nitrous oxide are of unknown benefit. Percutaneous coronary intervention (PCI) or fibrinolysis are recommended in those with an STEMI.

Prognosis

The prognosis post myocardial infarction varies greatly, depending on a person's health, the extent of the heart damage and the treatment given. For the period 2005–2008 in the United States, the median mortality at 30 days was 16.6% with a range from 10.9% to 24.9% depending on the hospital. Using variables available in the emergency room, people with a higher risk of adverse outcome can be identified. One study found that 0.4% of patients with a low-risk profile died after 90 days, whereas in high-risk people it was 21.1%.

Some of the more reproduced risk-stratifying factors include: age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular disease and elevation of cardiac markers. Assessment of left ventricular ejection fraction may increase the predictive power. The prognostic importance of Q-waves is debated. Prognosis is significantly worsened if a mechanical complication such as papillary muscle or myocardial free wall rupture occur. Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.

Complications

Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). Acute complications may include heart failure if the damaged heart is no longer able to adequately pump blood around the body; aneurysm or rupture of the myocardium; mitral regurgitation, in particular if the infarction causes dysfunction of the papillary muscle; and arrhythmias, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation and heart block. Longer-term complications include heart failure, atrial fibrillation, and the increased risk of a second myocardial infarction.

Epidemiology

Myocardial infarction is a common presentation of ischemic heart disease. The WHO estimated in 2002, that 12.6 percent of worldwide deaths were from ischemic heart disease with it the leading cause of death in developed countries, and third to AIDS and lower respiratory infections in developing countries. Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.

Coronary heart disease is responsible for 1 in 5 deaths in the United States. It is becoming more common in the developing world such that, in India, cardiovascular disease (CVD) is the leading cause of death. The deaths due to CVD in India were 32% of all deaths in 2007 and are expected to rise from 1.17 million in 1990 and 1.59 million in 2000 to 2.03 million in 2010. Although a relatively new epidemic in India, it has quickly become a major health issue with deaths due to CVD expected to double during 1985–2015. Mortality estimates due to CVD vary widely by state, ranging from 10% in Meghalaya to 49% in Punjab (percentage of all deaths). Punjab (49%), Goa (42%), Tamil Nadu (36%) and Andhra Pradesh (31%) have the highest CVD related mortality estimates. State-wise differences are correlated with prevalence of specific dietary risk factors in the states. Moderate physical exercise is associated with reduced incidence of CVD in India (those that exercise have less than half the risk of those that do not).

Legal implications

At common law, in general a myocardial infarction is a disease, but may sometimes be an injury. This has implications for no-fault insurance schemes such as workers' compensation. In general, a heart attack is not covered; however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion. In addition, in some jurisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person having suffered from a myocardial infarction may be prevented from participating in activity that puts other people's lives at risk, for example driving a car or flying an airplane.

Research

Patients who receive stem cell treatment by coronary artery injections of stem cells derived from their own bone marrow after a myocardial infarction (MI) show improvements in left ventricular ejection fraction and end-diastolic volume not seen with placebo. The larger the initial infarct size, the greater the effect of the infusion. Clinical trials of progenitor cell infusion as a treatment approach to ST elevation MI are proceeding.

There are currently 3 biomaterial and tissue engineering approaches for the treatment of MI, but these are in an even earlier stage of medical research, so many questions and issues must be addressed before they can be applied to patients. The first involves polymeric left ventricular restraints in the prevention of heart failure. The second utilizes ''in vitro'' engineered cardiac tissue, which is subsequently implanted ''in vivo''. The final approach entails injecting cells and/or a scaffold into the myocardium to create ''in situ'' engineered cardiac tissue.

References

External links

American Heart Association's Heart Attack web site – Information and resources for preventing, recognizing and treating heart attack.

Heart Attack – overview of resources from MedlinePlus

Category:Aging-associated diseases Category:Causes of death Category:Ischemic heart diseases Category:Medical emergencies

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Old Toby (died 1858), whose name was Pikee Queenah (Swooping Eagle) was war chief of the Tuziyammo (Big Lodge) band of Western Shoshone and a Shoshone dog soldier.

Guide

He served as a guide for the later part of Lewis and Clark Expedition in 1805, as did Tetoharsky, and Twisted Hair. He guided Clark's exploration of the Salmon River and led the entire party from the Lemhi River Valley at Salmon, Idaho, over the Bitterroot Mountains to the Bitterroot Valley, and then over the Lolo Trail to the Clearwater River country above Lewiston, Idaho.

He left the expedition and returned home. Nez Perce Indians relayed that he stole horses and returned home. He died of typhoid in 1858.

Name

Thomas Rees' journal gives his name as Tobe, an abbreviation of Tosa-tive koo-be, meaning "furnished white white-man brains," referring to his work as their guide. He was simply called Toby, but the moniker "Old Toby" was added later in popular literature.

Legacy

A monument was erected is his honor in the 1930s but demolished during construction of US Highway 93. A new monument was erected in his honor in North Fork, Idaho, near Highway 93 and the Salmon River Road in 2009.

References

Category:Year of birth missing Category:1858 deaths Category:Lewis and Clark Expedition people Category:Shoshone people