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Tobacco
History
History of tobacco
Biology
Nicotiana (Nicotiana tabacum) Tobacco diseases Types of tobacco
Social impact
Health effects Prevalence of consumption Tobacco advertising Tobacco politics Tobacco smoking
Production
Cultivation of tobacco Curing of tobacco Tobacco industry Tobacco products
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Tobacco is an agricultural product processed from the leaves of plants in the genus Nicotiana. It can be consumed, used as a pesticide and, in the form of nicotine tartrate, used in some medicines.^[1] It is most commonly used as a drug, and is a valuable cash crop for countries such as Cuba, China and the United States. Tobacco is a name for any plant of the genus Nicotiana of the Solanaceae family (nightshade family) and for the product manufactured from the leaf and used in cigars and cigarettes, snuff, and pipe and chewing tobacco. Tobacco plants are also used in plant bioengineering, and some of the 60 species are grown as ornamentals. The chief commercial species, N. tabacum, is believed native to tropical America, like most nicotiana plants, but has been so long cultivated that it is no longer known in the wild. N. rustica, a mild-flavored, fast-burning species, was the tobacco originally raised in Virginia, but it is now grown chiefly in Turkey, India, and Russia. The alkaloid nicotine is the most characteristic constituent of tobacco and is responsible for its addictive nature. The harmful effects of tobacco derive from the thousands of different compounds generated in the smoke, including polycyclic aromatic hydrocarbons (such as benzpyrene), formaldehyde, cadmium, nickel, arsenic, radioactive polonium-210, tobacco-specific nitrosamines (TSNAs), phenols, and many others.^[2]

In consumption it most commonly appears in the forms of smoking, chewing, snuffing, or dipping tobacco. Tobacco had long been in use as an entheogen in the Americas, but upon the arrival of Europeans in North America, it quickly became popularized as a trade item and a widely-abused drug. This popularization led to the development of the southern economy of the United States until it gave way to cotton. Following the American Civil War, a change in demand and a change in labor force allowed for the development of the cigarette. This new product quickly led to the growth of tobacco companies.

There are more than 70 species of tobacco in the plant genus Nicotiana. The word nicotiana (as well as nicotine) is in honor of Jean Nicot, French ambassador to Portugal, who in 1559 sent it as a medicine to the court of Catherine de Medici.^[3]

Because of the powerfully addictive properties of nicotine, tolerance and dependence develop. Absorption quantity, frequency, and speed of tobacco consumption are believed to be directly related to biological strength of nicotine dependence, addiction, and tolerance.^[4][5] The usage of tobacco is an activity that is practiced by some 1.1 billion people, and up to 1/3 of the adult population.^[6] The World Health Organization(WHO) reports it to be the leading preventable cause of death worldwide and estimates that it currently causes 5.4 million deaths per year.^[7] Rates of smoking have leveled off or declined in developed countries, but continue to rise in developing countries.

Tobacco is cultivated similarly to other agricultural products. Seeds are sown in cold frames or hotbeds to prevent attacks from insects, and then transplanted into the fields. Tobacco is an annual crop, which is usually harvested mechanically or by hand. After harvest, tobacco is stored for curing, which allows for the slow oxidation and degradation of carotenoids. This allows for the agricultural product to take on properties that are usually attributed to the "smoothness" of the smoke. Following this, tobacco is packed into its various forms of consumption, which include smoking, chewing, snuffing, and so on. Most cigarettes incorporate flue-cured tobacco, which produces a milder, more inhalable smoke. Use of low pH, inhalable, flue cured tobacco is one of the principal reasons smoking causes lung cancer and other diseases association with smoke inhalation.^[8]

Tobacco can also be pressed into plugs and sliced into flakes.

A historic kiln in Myrtleford, Victoria, Australia.

Basma tobacco leaves drying in the sun at Pomak village in Xanthi, Greece.

Etymology[link]

The Spanish and Portuguese word tabaco is thought to have originated in Taino, the Arawakan language of the Caribbean. In Taino, it was said to refer either to a roll of tobacco leaves (according to Bartolomé de las Casas, 1552), or to the tabago, a kind of Y-shaped pipe for sniffing tobacco smoke (according to Oviedo; with the leaves themselves being referred to as cohiba).^[9]

However, similar words in Spanish, Portuguese and Italian were commonly used from 1410 to define medicinal herbs, originating from the Arabic طبق tabbaq, a word reportedly dating to the 9th century, as the name of various herbs.^[10]

History[link]

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Early developments[link]

The earliest depiction of a European man smoking, from Tabacco by Anthony Chute.

Tobacco had already long been used in the Americas when European settlers arrived and introduced the practice to Europe, where it became popular. Many Native American tribes traditionally used tobacco. Eastern North American tribes carried large amounts of tobacco in pouches as a readily accepted trade item, and often smoked it in peace pipes, either in defined sacred ceremonies, or to seal a bargain,^[11] and they smoked it at such occasions in all stages of life, even in childhood.^[12] It was believed that tobacco is a gift from the Creator, and that the exhaled tobacco smoke carries one's thoughts and prayers to heaven.^[13]

Before the development of lighter Virginia and White Burley strains of tobacco, the smoke was too harsh to be inhaled traditionally by Native Americans in ceremonial use or by Europeans who used it in the form of pipes and cigars.^[14] Inhaling "rough" tobacco without seriously damaging the lungs in the short term required smoking only small quantities at a time using a pipe like the midwakh or kiseru or smoking newly invented waterpipes such as the bong or the hookah (See Thuoc lao for a modern continuance of this practice). Inhaling smoke was already common in the East with the introduction of cannabis and opium millennia before.

Popularization[link]

An Illustration from Frederick William Fairholt's Tobacco, its History and Association, 1859.

Following the arrival of the Europeans, tobacco became increasingly popular as a trade item. It fostered the economy for the southern United States until it was replaced by cotton. Following the American civil war, a change in demand and a change in labor force allowed inventor James Bonsack to create a machine that automated cigarette production.

This increase in production allowed tremendous growth in the tobacco industry until the scientific revelations of the mid-20th century.

Contemporary[link]

Following the scientific revelations of the mid-20th century, tobacco became condemned as a health hazard, and eventually became encompassed as a cause for cancer, as well as other respiratory and circulatory diseases. In the United States, this led to the Tobacco Master Settlement Agreement (MSA), which settled the lawsuit in exchange for a combination of yearly payments to the states and voluntary restrictions on advertising and marketing of tobacco products.

In the 1970s, Brown & Williamson cross-bred a strain of tobacco to produce Y1. This strain of tobacco contained an unusually high amount of nicotine, nearly doubling its content from 3.2-3.5% to 6.5%. In the 1990s, this prompted the Food and Drug Administration (FDA) to use this strain as evidence that tobacco companies were intentionally manipulating the nicotine content of cigarettes.

In 2003, in response to growth of tobacco use in developing countries, the World Health Organization (WHO)^[15] successfully rallied 168 countries to sign the Framework Convention on Tobacco Control. The Convention is designed to push for effective legislation and its enforcement in all countries to reduce the harmful effects of tobacco. This led to the development of tobacco cessation products.

Biology[link]

Nicotiana[link]

Nicotine is the compound responsible for the addictive nature of Tobacco use.

There are many species of tobacco in the genus of herbs Nicotiana. It is part of the nightshade family (Solanaceae) indigenous to North and South America, Australia, South West Africa and the South Pacific.

Many plants contain nicotine, a powerful neurotoxin to insects. However, tobaccos contain a higher concentration of nicotine than most other plants. Unlike many other Solanaceae, they do not contain tropane alkaloids, which are often poisonous to humans and other animals.

Despite containing enough nicotine and other compounds such as germacrene and anabasine and other piperidine alkaloids (varying between species) to deter most herbivores,^[16] a number of such animals have evolved the ability to feed on Nicotiana species without being harmed. Nonetheless, tobacco is unpalatable to many species, and accordingly some tobacco plants (chiefly tree tobacco, N. glauca) have become established as invasive weeds in some places.

Types[link]

There are a number of types of tobacco including, but are not limited to:

• Aromatic fire-cured is cured by smoke from open fires. In the United States, it is grown in northern middle Tennessee, central Kentucky and in Virginia. Fire-cured tobacco grown in Kentucky and Tennessee are used in some chewing tobaccos, moist snuff, some cigarettes, and as a condiment in pipe tobacco blends. Another fire-cured tobacco is Latakia, which is produced from oriental varieties of N. tabacum. The leaves are cured and smoked over smoldering fires of local hardwoods and aromatic shrubs in Cyprus and Syria.
• Brightleaf tobacco, Brightleaf is commonly known as "Virginia tobacco", often regardless of the state where they are planted. Prior to the American Civil War, most tobacco grown in the US was fire-cured dark-leaf. This type of tobacco was planted in fertile lowlands, used a robust variety of leaf, and was either fire cured or air cured. Most Canadian cigarettes are made from 100% pure Virginia tobacco.^[17]
• Burley tobacco, is an air-cured tobacco used primarily for cigarette production. In the U.S., burley tobacco plants are started from palletized seeds placed in polystyrene trays floated on a bed of fertilized water in March or April.
• Cavendish is more a process of curing and a method of cutting tobacco than a type. The processing and the cut are used to bring out the natural sweet taste in the tobacco. Cavendish can be produced from any tobacco type, but is usually one of, or a blend of Kentucky, Virginia, and burley, and is most commonly used for pipe tobacco and cigars.
• Criollo tobacco is a type of tobacco, primarily used in the making of cigars. It was, by most accounts, one of the original Cuban tobaccos that emerged around the time of Columbus.
• Dokha, is a tobacco originally grown in Iran, mixed with leaves, bark, and herbs for smoking in a midwakh.
• Turkish tobacco, is a sun-cured, highly aromatic, small-leafed variety (Nicotiana tabacum) that is grown in Turkey, Greece, Bulgaria, and Macedonia. Originally grown in regions historically part of the Ottoman Empire, it is also known as "oriental". Many of the early brands of cigarettes were made mostly or entirely of Turkish tobacco; today, its main use is in blends of pipe and especially cigarette tobacco (a typical American cigarette is a blend of bright Virginia, burley and Turkish).
• Perique, a farmer called Pierre Chenet is credited with first turning this local tobacco into the Perique in 1824 through the technique of pressure-fermentation. Considered the truffle of pipe tobaccos, it is used as a component in many blended pipe tobaccos, but is too strong to be smoked pure. At one time, the freshly moist Perique was also chewed, but none is now sold for this purpose. It is typically blended with pure Virginia to lend spice, strength, and coolness to the blend.
• Shade tobacco, is cultivated in Connecticut and Massachusetts. Early Connecticut colonists acquired from the Native Americans the habit of smoking tobacco in pipes, and began cultivating the plant commercially, even though the Puritans referred to it as the "evil weed". The industry has weathered some major catastrophes, including a devastating hailstorm in 1929, and an epidemic of brown spot fungus in 2000, but is now in danger of disappearing altogether, given the value of the land to real estate speculators.
• White burley, in 1865, George Webb of Brown County, Ohio planted red burley seeds he had purchased, and found that a few of the seedlings had a whitish, sickly look. The air-cured leaf was found to be more mild than other types of tobacco.
• Wild tobacco, is native to the southwestern United States, Mexico, and parts of South America. Its botanical name is Nicotiana rustica.
• Y1 is a strain of tobacco cross-bred by Brown & Williamson in the 1970s to obtain an unusually high nicotine content. In the 1990s, the United States Food and Drug Administration (FDA) used it as evidence that tobacco companies were intentionally manipulating the nicotine content of cigarettes.^[18]

Impact[link]

Social[link]

This section requires expansion with: information expanding the effects of tobacco on cultural practices.

Smoking in public was for a long time something reserved for men, and when done by women was sometimes associated with promiscuity.^{[citation needed]} In Japan, during the Edo period, prostitutes and their clients often approached one another under the guise of offering a smoke. The same was true in 19th century Europe.^[19]

Following the American Civil War the usage of tobacco, primarily in cigars, became associated with masculinity and power, and is an iconic image associated with the stereotypical capitalist. Today, tobacco is often rejected; this has spawned quitting associations and anti-smoking campaigns. Bhutan is the only country in the world where tobacco sales are illegal.^[20]

Demographic[link]

Research is limited mainly to tobacco smoking, which has been studied more extensively than any other form of consumption. As of 2000, smoking is practiced by some 1.22 billion people, of which men are more likely to smoke than women^[21] (however the gender gap declines with age),^[22][23] poor more likely than rich, and people in developing countries or transitional economies more likely than people in developed countries.^[24] As of 2004, the World Health Organization (WHO) reports that of the 58.8 million deaths occurring globally,^[25] 5.4 million are tobacco-attributed.^[26]

Health[link]

Data from The Lancet suggests tobacco is ranked the 3rd most addictive and 14th most harmful of 20 commonly-used drugs.^[27]

The harms caused by using tobacco tobacco include 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 cancers).

The World Health Organization estimates that tobacco caused 5.4 million deaths in 2004^[28] and 100 million deaths over the course of the 20th century.^[29] 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."^[30]

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.^[31] In the developing world, tobacco consumption is rising by 3.4% per year.^[32]

When the market for tobacco reduced in the West, the industry looked to India and China for 'emerging markets'. In response, various activists in these markets have campaigned against tobacco products. One example is Dr. Sharad Vaidya, a cancer surgeon in India who helped to add the study of tobacco's health effects to school curricula, to establish legislation banning public smoking, to stop sports sponsorship, and to prohibit sale to those under 21 years of age.

China is the world's largest manufacturer of cigarettes, producing about 2.4 trillion per year or 40 percent of the world's total. ^[33]Changes have been made to eliminate advertising, post health warnings, and ban smoking from public buildings. Many doctors, however, smoke and neglect to warn their patients that smoking increases their risk for disease. Judith Mackay, a Hong Kong-based physician, has been a relentless and effective campaigner, assisting Chinese health officials in the effort to reduce smoking and its immense health, social, and economic costs. Among her projects is the Tobacco Atlas. Her work caused Time Magazine to name her to its 2007 list of the most influential figures across the globe. In a 2010 talk at the USC U.S.-China Institute, Mackay summarized the progress that's been made in China and the challenges that remain.^[34]

Economic[link]

This section requires expansion with: discussion of the impact on the poor, taxation, and so forth.

"Much of the disease burden and premature mortality attributable to tobacco use disproportionately affect the poor", and of the 1.22 billion smokers, 1 billion of them live in developing or transitional economies.^[24]

In Indonesia, the lowest income group spends 15% of its total expenditures on tobacco. In Egypt, more than 10% of households expenditure in low-income homes is on tobacco. The poorest 20% of households in Mexico spend 11% of their income on tobacco.^[35]

Production[link]

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Cultivation[link]

Tobacco plants growing in a field in Intercourse, Pennsylvania

Tobacco is cultivated similarly to other agricultural products. Seeds were at first quickly scattered onto the soil. However, young plants came under increasing attack from flea beetles (Epitrix cucumeris or Epitrix pubescens), which caused destruction of half the tobacco crops in United States in 1876. By 1890 successful experiments were conducted that placed the plant in a frame covered by thin cotton fabric. Today, tobacco is sown in cold frames or hotbeds, as their germination is activated by light.

In the United States, tobacco is often fertilized with the mineral apatite, which partially starves the plant of nitrogen, to produce a more desired flavor. Apatite, however, contains radium, lead 210, and polonium 210—which are known radioactive carcinogens.

After the plants are about eight inches tall, they are transplanted into the fields. Farmers used to have to wait for rainy weather to plant. A hole is created in the tilled earth with a tobacco peg, either a curved wooden tool or deer antler. After making two holes to the right and left - you would move forward two feet, select plants from your bag and repeat. Various mechanical tobacco planters like Bemis, New Idea Setter, and New Holland Transplanter were invented in the late 19th and 20th centuries to automate the process: making the hole, watering it, guiding the plant in — all in one motion.

Tobacco is cultivated annually, and can be harvested in several ways. In the oldest method still used today, the entire plant is harvested at once by cutting off the stalk at the ground with a tobacco knife. It is then speared onto sticks, four to six plants a stick and hung in a curing barn. In the 19th century, bright tobacco began to be harvested by pulling individual leaves off the stalk as they ripened. The leaves ripen from the ground upwards, so a field of tobacco may go through several so-called "pullings," more commonly known as cropping. Before this the crop needs to be topped when the pink flowers develop. Topping always refers to the removal of the tobacco flower before the leaves are systematically removed and, eventually, entirely harvested. As the industrial revolution took hold, harvesting wagons used to transport leaves were equipped with man-powered stringers, an apparatus that used twine to attach leaves to a pole. In modern times, large fields are harvested mechanically, although topping the flower and in some cases the plucking of immature leaves is still done by hand. Most tobacco in the U.S. is grown in Kentucky, Virginia and North Carolina.

Curing[link]

Tobacco barn in Simsbury, Connecticut used for air curing of shade tobacco

Sun-cured tobacco, Bastam, Iran.

Curing and subsequent aging allow for the slow oxidation and degradation of carotenoids in tobacco leaf. This produces certain compounds in the tobacco leaves, and gives a sweet hay, tea, rose oil, or fruity aromatic flavor that contributes to the "smoothness" of the smoke. Starch is converted to sugar, which glycates protein, and is oxidized into advanced glycation endproducts (AGEs), a caramelization process that also adds flavor. Inhalation of these AGEs in tobacco smoke contributes to atherosclerosis and cancer.^[36] Levels of AGE's is dependent on the curing method used.

Tobacco can be cured through several methods, including:

• Air cured tobacco is hung in well-ventilated barns and allowed to dry over a period of four to eight weeks. Air-cured tobacco is low in sugar, which gives the tobacco smoke a light, mild flavor, and high in nicotine. Cigar and burley tobaccos are air cured.
• Fire cured tobacco is hung in large barns where fires of hardwoods are kept on continuous or intermittent low smoulder and takes between three days and ten weeks, depending on the process and the tobacco. Fire curing produces a tobacco low in sugar and high in nicotine. Pipe tobacco, chewing tobacco, and snuff are fire cured.
• Flue cured tobacco was originally strung onto tobacco sticks, which were hung from tier-poles in curing barns (Aus: kilns, also traditionally called Oasts). These barns have flues run from externally-fed fire boxes, heat-curing the tobacco without exposing it to smoke, slowly raising the temperature over the course of the curing. The process generally takes about a week. This method produces cigarette tobacco that is high in sugar and has medium to high levels of nicotine.
• Sun-cured tobacco dries uncovered in the sun. This method is used in Turkey, Greece and other Mediterranean countries to produce oriental tobacco. Sun-cured tobacco is low in sugar and nicotine and is used in cigarettes.

Consumption[link]

Tobacco is consumed in many forms and through a number of different methods. Below are examples including, but not limited to, such forms and usage.

• Beedi are thin, often flavored, south Asian cigarettes made of tobacco wrapped in a tendu leaf, and secured with colored thread at one end.
• Chewing tobacco is the oldest way of consuming tobacco leaves. It is consumed orally, in two forms: through sweetened strands, or in a shredded form. When consuming the long sweetened strands, the tobacco is lightly chewed and compacted into a ball. When consuming the shredded tobacco, small amounts are placed at the bottom lip, between the gum and the teeth, where it is gently compacted, thus it can often be called dipping tobacco. Both methods stimulate the saliva glands, which led to the development of the spittoon.
• Cigars are tightly rolled bundles of dried and fermented tobacco, which is ignited so its smoke may be drawn into the smoker's mouth.
• Cigarettes are a product consumed through inhalation of smoke and manufactured from cured and finely cut tobacco leaves and reconstituted tobacco, often combined with other additives, then rolled or stuffed into a paper cylinder.
• Creamy snuffs are tobacco paste, consisting of tobacco, clove oil, glycerin, spearmint, menthol, and camphor, and sold in a toothpaste tube. It is marketed mainly to women in India, and is known by the brand names Ipco (made by Asha Industries), Denobac, Tona, Ganesh. It is locally known as "mishri" in some parts of Maharashtra.
• Dipping tobaccos are a form of smokeless tobacco. Dip is occasionally referred to as "chew", and because of this, it is commonly confused with chewing tobacco, which encompasses a wider range of products. A small clump of dip is 'pinched' out of the tin and placed between the lower or upper lip and gums.
• Gutka is a preparation of crushed betel nut, tobacco, and sweet or savory flavorings. It is manufactured in India and exported to a few other countries. A mild stimulant, it is sold across India in small, individual-size packets.
• Hookah is a single or multi-stemmed (often glass-based) water pipe for smoking. Originally from India, 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 or moassel, a mixture of tobacco, flavouring and honey or glycerin.
• Kreteks 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.
• Roll-Your-Own, often called rollies or roll ups, 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 to make.
• 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.
• Snuff is a generic term for fine-ground smokeless tobacco products. Originally the term referred only to dry snuff, a fine tan dust popular mainly in the 18th century. Snuff powder originated in the UK town of Great Harwood, and was famously ground in the town's monument prior to local distribution and transport further up north to Scotland. There are two major varieties: European (dry) and American (moist)—though American snuff is often called dipping tobacco.
• Snus is a steam-cured moist powder tobacco product that is not fermented, and does not induce salivation. It is consumed by placing it in the mouth against the gums for an extended period of time. It is a form of snuff used in a manner similar to American dipping tobacco, but does not require regular spitting.
• Topical tobacco paste is sometimes recommended as a treatment for wasp, hornet, fire ant, scorpion, and bee stings.^[37] An amount equivalent to the contents of a cigarette is mashed in a cup with about a 0.5 to 1 teaspoon of water to make a paste that is then applied to the affected area.
• Tobacco water is a traditional organic insecticide used in domestic gardening. Tobacco dust can be used similarly. It is produced by boiling strong tobacco in water, or by steeping the tobacco in water for a longer period. When cooled, the mixture can be applied as a spray, or 'painted' on to the leaves of garden plants, where it kills insects. Tobacco is however banned from use as pesticide in certified organic production.^{[by whom?]}

Global production[link]

Trends[link]

Production of tobacco leaf increased by 40% between 1971, during which 4.2 million tons of leaf were produced, and 1997, during which 5.9 million tons of leaf were produced.^[38] According to the Food and Agriculture organization of the UN, tobacco leaf production was expected to hit 7.1 million tons by 2010. This number is a bit lower than the record high production of 1992, during which 7.5 million tons of leaf were produced.^[39] The production growth was almost entirely due to increased productivity by developing nations, where production increased by 128%.^[40] During that same time period, production in developing countries actually decreased.^[39] China’s increase in tobacco production was the single biggest factor in the increase in world production. China’s share of the world market increased from 17% in 1971 to 47% in 1997.^[38] This growth can be partially explained by the existence of a high import tariff on foreign tobacco entering China. While this tariff has been reduced from 64% in 1999 to 10% in 2004,^[41] it still has led to local, Chinese cigarettes being preferred over foreign cigarettes because of their lower cost.

Every year 6.7 million tons of tobacco are produced throughout the world. The top producers of tobacco are China (39.6%), India (8.3%), Brazil (7.0%) and the United States (4.6%).^[42]

Major producers[link]

China[link]

Around the peak of global tobacco production there were 20 million rural Chinese households producing tobacco on 2.1 million hectares of land.^[43] While it is the major crop for millions of Chinese farmers, growing tobacco is not as profitable as cotton or sugar cane. This is because the Chinese government sets the market price. While this price is guaranteed, it is lower than the natural market price, because of the lack of market risk. To further control tobacco in their borders, China founded a State Tobacco Monopoly Administration (STMA) in 1982. STMA control tobacco production, marketing, imports and exports and contributes 12% to the nation's national income.^[44] As noted above, despite the income generated for the state by profits from state-owned tobacco companies and the taxes paid by companies and retailers, China's government has acted to reduce tobacco use.^[45]

Pakistan[link]

Each year 5% of the total land of Pakistan is cultivated for tobacco. It is widely grown in Southern Punjab and Khyber Pakhtunkhwa province of Pakistan.

Brazil[link]

In Brazil around 135,000 family farmers cite tobacco production as their main economic activity.^[43] Tobacco has never exceeded 0.7% of the country’s total cultivated area.^[46] In the southern regions of Brazil, Virginia and Amarelinho flue-cured tobacco as well as Burley and Galpao Comun air-cured tobacco are produced. These types of tobacco are used for cigarettes. In the northeast, darker, air- and sun-cured tobacco is grown. These types of tobacco are used for cigars, twists and dark-cigarettes.^[46] Brazil’s government has made attempts to reduce the production of tobacco, but has not had a successful systematic anti-tobacco farming initiative. Brazil’s government, however, provides small loans for family farms, including those that grow tobacco, through the Programa Nacional de Fortalecimiento da Agricultura Familiar (PRONAF).^[47]

India[link]

India's Tobacco Board is headquartered in Guntur in the state of Andhra Pradesh.^[48] India has 96,865 registered tobacco farmers^[49] and many more who are not registered. Around 0.25% of India’s cultivated land is used for tobacco production.^[50]

Since 1947, the Indian Government has supported growth in the tobacco industry. India has seven tobacco research centers that are located in Madras (now known as Chennai, Tamil Nadu), Andhra Pradesh, Punjab, Bihar, Mysore, West Bengal, and Rajamundry.^[49] Rajahmundry houses the core research institute. The government has set up a Central Tobacco Promotion Council, which works to increase exports of Indian tobacco.

The Indian Government and several states have taken multiple measures to reduce Cigarette smoking. Smoking in public places is banned in many states, it is not allowed to be portrayed in movies, warnings are posted on cigarette packs.

Minor producer[link]

Tobacco plantation, Pinar del Río, Cuba

Philippines[link]

Tobacco in the Philippines remained highly concentrated in 2009 and dominated by cigarette manufacturers Fortune Tobacco Corporation and Philip Morris International. The strength of these companies is due to their extensive distribution networks which encompass both traditional and non-traditional retail channels as well as their ability to offer their products at affordable prices. Top player Fortune Tobacco Corp maintained its leadership position throughout the review period as mass market cigarette smokers continued to purchase its economy cigarette brands, particularly leading brand Fortune International.^[51]

Cigarette prices in the Philippines are low, with the price of Marlboro (cigarette) being the second lowest for all ASEAN nations. The cigarette market has been dominated by menthol brands for several decades, although non-menthol volume has been steadily improving in recent years. La Suerte Cigar and Cigarette Company and the Fortune Tobacco Corporation (FTC) have been the two leading producers, and have had licensing agreements with PMI and RJ Reynolds (RJR) respectively. FTC commands a 67% market share, while La Suerte holds a 25% share.

Problems in tobacco production[link]

Child labor[link]

The International Labour Office reported that the most child-laborers work in agriculture, which is one of the most hazardous types of work.^[52] The tobacco industry houses some of these working children. There is widespread use of children on farms in Argentina, Brazil, China, India, Indonesia, Malawi and Zimbabwe.^[53] While some of these children work with their families on small family-owned farms, others work on large plantations. In late 2009 reports were released by the London-based human-rights group Plan International, claiming that child labor was common on Malawi (producer of 1.8% of the world’s tobacco^[38]) tobacco farms. The organization interviewed 44 teens, who worked full-time on farms during the 2007-2008 growing season. The child-laborers complained of low pay, long hours as well as physical and sexual abuse by their supervisors.^[54] They also reported suffering from “green tobacco sickness,” a form of nicotine poisoning. When wet leaves are handled, nicotine from the leaves gets absorbed in the skin and causes nausea, vomiting and dizziness. Children were exposed to 50-cigarettes worth of nicotine through direct contact with tobacco leaves. This level of nicotine in children can permanently alter brain structure and function.^[52]

Economy[link]

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Tobacco Harvesting, Viñales Valley, Cuba

The cultivation of tobacco can be economically detrimental to developing countries. When resources are put into tobacco production they are taken away from food production. Large amounts of firewood that could be used domestically for fuel and heating are instead used for the curing of tobacco.

A large percent of the profits from tobacco production go to large tobacco companies rather than local tobacco farmers. Also many countries have government subsides for tobacco farming, which do not make economic sense.^[55] Major tobacco companies have encouraged global tobacco production. Philip Morris, British American Tobacco and Japan Tobacco each own or lease tobacco manufacturing facilities in at least 50 countries and buy crude tobacco leaf from at least 12 more countries.^[56] This encouragement, along with government subsidies has led to a glut in the tobacco market. This surplus has resulted in lower prices, which are devastating to small-scale tobacco farmers. According to the World Bank, between 1985 and 2000 the inflation-adjusted price of tobacco dropped 37%.^[57]

Environment[link]

Tobacco production requires the use of a large amount of pesticides; tobacco companies recommend up to 16 separate applications of pesticides just in the period between planting the seeds in greenhouses and transplanting the young plants to the field.^[58] Pesticide use has been worsened by the desire to produce larger crops in less time because of the decreasing market value of tobacco. Pesticides often harm tobacco farmers because they are unaware of the health effects and the proper safety protocol for working with pesticides. These pesticides, as well as fertilizers, end up in the soil, the waterway and the food chain.^[59] Coupled with child labor, pesticides pose an even greater threat. Early exposure to pesticides may increase a child's lifelong cancer risk as well as harm his or her nervous and immune systems.^[60]

Tobacco is a crop that extracts nutrients, such as phosphorus, nitrogen and potassium, from the soil at a rate higher than any other major crop.^[61] This leads to dependence on fertilizers.

Furthermore, the wood used for the curing of tobacco in some places leads to deforestation. While some big tobacco producers such as China and the United States have access to petroleum, coal and natural gas, which can be used as alternatives to wood, most developing countries still rely on wood in the curing process.^[61] Brazil alone uses the wood of 60 million trees per year for curing, packaging and rolling cigarettes.^[58]

Art[link]

This section requires expansion.

Advertising[link]

Tobacco advertising is the advertising of tobacco products by the tobacco industry through a variety of media including sponsorship, particularly of sporting events. It is now one of the most highly regulated forms of marketing. Some or all forms of tobacco advertising are banned in many countries.

Many colleges have anti-tobacco programs where students fight for their right not to be exposed to tobacco advertising and smoke.^[62]

Belomorkanal - Russian cigarettes   Hans Rudi Erdt: Problem Cigarettes, 1912   French Painted Mural Advertisement   Tobacco display in Munich   Advertisement for "Murad" Turkish cigarettes 1918   Advertisement for "Egyptian Deities" cigarettes 1919

Cinema[link]

• Sommersby
• Thank You for Smoking
• The Insider

Gallery[link]

Broadleaf tobacco inspected in Chatham, Virginia, USA.   Tobacco field in northern Poland   Flowers of tobacco plant in northern Poland in September   Tobacco flowers of tobacco plant in Rolesville, North Carolina, USA.   Tobacco field in Rolesville, North Carolina, USA.   Tobacco grown in Havana, Cuba, c. 1921-1939

References[link]

Notes[link]

Bibliography[link]

Further reading[link]

External links[link]

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Myocardial infarction
Classification and external resources
Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA), right coronary artery = RCA
ICD-10	I21-I22
ICD-9	410
DiseasesDB	8664
MedlinePlus	000195
eMedicine	med/1567 emerg/327 ped/2520
MeSH	D009203

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).^[1] Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue.^[2] A sizeable proportion of myocardial infarctions (22–64%)^[3] 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.^[4]

Most cases of myocardial infarction with ST elevation on ECG (STEMI) are treated with reperfusion therapy, such as percutaneous coronary intervention (PCI) or thrombolysis.^[5] Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although PCI may be required if the patient's risk warrants it.^[6] People who have multiple blockages of their coronary arteries, particularly if they also have diabetes mellitus, may benefit from bypass surgery (CABG),^[7][8]. The European Society of Cardiology guidelines in 2011 proposed treating the blockage causing the myocardial infarction by PCI and performing CABG later when the patient is more stable.^[7] Rarely CABG may be preferred in the acute phase of myocardial infarction, for example when PCI has failed or is contraindicated.^[7]

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.^[9] Important risk factors are previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood pressure, lack of physical activity and obesity, chronic kidney disease, excessive alcohol consumption, the abuse of illicit drugs (such as cocaine and amphetamines), and chronic high stress levels.^[10][11][12]

Classification[link]

There are two basic types of acute myocardial infarction based on pathology:

• Transmural: associated with atherosclerosis involving a 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.^[13]
• 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.^[13]

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.^[14]

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.^[7]

A 2007 consensus document classifies myocardial infarction into five main types:^[15]

• 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[link]

Rough diagram of pain zones in myocardial infarction; dark red: most typical area, light red: other possible areas; view of the chest

Back view

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.^[16] 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,^[7][17] 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.^[18]

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),^[1] weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system^[19] 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.^[7]

Women and older patients report atypical symptoms more frequently than their male and younger counterparts.^[20] Women also report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men).^[20] 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.^[21]

At least one-fourth of all myocardial infarctions are silent, without chest pain or other symptoms, ^[22][3] with silent myocardial infarcations being more common in younger people. These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. Estimates of the prevalence of silent myocardial infarctions vary between 22 and 64% ^[3]. A silent course is more common in the elderly^[3], in patients with diabetes mellitus^[23] and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient.^[24] In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.^[23]

Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.^[25]

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.^[26]

Causes[link]

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.^[27] 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.^[27] For those in poor physical condition, the rate differential is over 35-fold higher.^[27] 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.^[27]

Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.^[28] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.^[28] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.^[29]

There is an association of an increased incidence of a heart attack in the morning hours, more specifically around 9 a.m.^[30][31][32] Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation.^[33]

Risk factors[link]

Myocardial infarction results from atherosclerosis.^[7] Risk factors for myocardial infarction include:

• Age^[10]
• Gender: At any given age men are more at risk than women, particularly before the menopause,^[27] but because in general women live longer than men ischemic heart disease causes slightly more total deaths in women.^[10]
• Diabetes mellitus type 1 or Diabetes mellitus type 2 ^[34]
• High blood pressure^[35]
• Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides^[35]
• Tobacco smoking, including secondhand smoke^[35]
• Short term exposure to air pollution including: carbon monoxide, nitrogen dioxide, and sulfur dioxide but not ozone.^[36]
• Family history of ischaemic heart disease or myocardial infarction particularly if one has a first-degree relative (father, brother, mother, sister) who suffered a 'premature' myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women).^[10]
• Obesity^[37] (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).
• Lack of physical activity.^[10]
• Psychosocial factors including, low socio-economic status, social isolation, negative emotions and stress increase the risk of myocardial infarction and are associated with worse outcomes after myocardial infarction. 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.^[38]
• Alcohol — Studies show that prolonged exposure to high quantities of alcohol can increase the risk of heart attack.
• Oral contraceptive pill – 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.^[39]
• Hyperhomocysteinemia (high homocysteine)in homocysteinuria is associated with premature atherosclerosis^[40], whether elevated homocysteine in the normal range is causal is contentious.^[41]

Inflammation is known to be an important step in the process of atherosclerotic plaque formation.^[42] 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.^[42] Moreover, some drugs for MI might also reduce CRP levels.^[42] 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.^[43] Whether CRP plays a direct role in atherosclerosis remains uncertain.^[42] 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.^[44] Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease.^[45] Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines;^[46] thus, periodontitis may mediate its effect on MI risk via other risk factors.^[47] Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells.^[48][49] A role for specific periodontal bacteria has been suggested but remains to be established.^[50] There is some evidence that influenza may trigger an acute myocardial infarction.^[51]

Baldness, hair greying, a diagonal earlobe crease (Frank's sign^[52]) and possibly other skin features have been suggested as independent risk factors for MI.^[53] Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.^[54]

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.^[55][56][57]

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.^[58] Non-modifiable risk factors include age, sex, and family history of an early heart attack, which is thought of as reflecting a genetic predisposition.^[27] 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.^[38]

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.^[59]

Pathophysiology[link]

A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, causing catastrophic thrombus formation, totally occluding the artery and preventing blood flow downstream.

Drawing of the heart showing anterior left ventricle wall infarction

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.^[14] 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.^[60][61] 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.^[62] Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis.^[63] 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).^[60][61]

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.^[64] 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[link]

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.^[65] 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.^[66] 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 pharmacologic stress.^[66][67] 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.^[68]

WHO criteria^[69] 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:

1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. 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.^[70] 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[link]

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:^[71][72]

• 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.^[73]
• Beta blocker therapy such as metoprolol or carvedilol should be commenced.^[74] These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia.^[75] 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.^[76]
• Statin therapy has been shown to reduce mortality and morbidity post-MI.^[77][78] 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.^[79]
• 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.^[80] 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.^[81] Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality post-MI.^[82] 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.^[83] 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.^[84][85]

Blood donation may reduce the risk of heart disease for men,^[86] 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.^[87]

Management[link]

An MI requires immediate medical attention. Treatment attempts to salvage as much myocardium as possible and to prevent further complications, hence the phrase "time is muscle".^[88] 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.^[89] 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.^[90][91] Other analgesics such as nitrous oxide are of unknown benefit.^[6] Percutaneous coronary intervention (PCI) or fibrinolysis are recommended in those with an STEMI.

Prognosis[link]

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.^[92] 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%.^[93]

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.^[93][94][95] Assessment of left ventricular ejection fraction may increase the predictive power.^[96] The prognostic importance of Q-waves is debated.^[97] Prognosis is significantly worsened if a mechanical complication such as papillary muscle or myocardial free wall rupture occurs.^[98] Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.^[99]

Complications[link]

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[link]

Myocardial infarction is a common presentation of ischemic heart disease/coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease;^[9] with it being the leading cause of death in high or middle income countries and second only to lower respiratory infections in lower income countries.^[9] Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.^[100]

Rates of death from ischemic heart disease have slowed or declined in most high income countries, although cardiovascular disease still accounted for 1 in 3 of all deaths in the USA in 2008.^[101] In contrast, ischemic heart disease is becoming a more common cause of death in the developing world. For example in India, ischemic heart disease had become the leading cause of death by 2004 accounting for 1.46 million deaths (14% of total deaths) and deaths due to ischemic heart disease were expected to double during 1985–2015.^[102] Globally it is predicted that disability adjusted life years (DALYs) lost to ischemic heart disease will account for 5.5% of total DALYs in 2030, making it the second most important cause of disability (after unipolar depressive disorder), as well as the leading cause of death by this date.^[9]

Legal implications[link]

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;^[103] however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion.^[104] 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.^[105]

Research[link]

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.^[106]

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.^[107]

References[link]