Euthanasia (from the Greek: εὐθανασία meaning "good death": εὖ, eu (well or good) + θάνατος, thanatos (death)) refers to the practice of intentionally ending a life in order to relieve pain and suffering.

There are different euthanasia laws in each country. The British House of Lords Select Committee on Medical Ethics defines euthanasia as "a deliberate intervention undertaken with the express intention of ending a life, to relieve intractable suffering".^[1] In the Netherlands, euthanasia is understood as "termination of life by a doctor at the request of a patient".^[2]

Euthanasia is categorized in different ways, which include voluntary, non-voluntary, or involuntary. Voluntary euthanasia is legal in some countries and U.S. states. Non-voluntary euthanasia is illegal in all countries. However, in the Netherlands, physicians can avoid prosecution by following well described and strict conditions when non-voluntary euthanasia is performed on infants.^[3] Involuntary euthanasia is usually considered murder.^[4]

Euthanasia is the most active area of research in contemporary bioethics.^[5]

Definition[link]

Like other terms borrowed from history, "euthanasia" has had different meanings depending on usage. The first apparent usage of the term "euthanasia" belongs to the historian Suetonius who described how the Emperor Augustus, "dying quickly and without suffering in the arms of his wife, Livia, experienced the 'euthanasia' he had wished for."^[6] The word "euthanasia" was first used in a medical context by Francis Bacon in the 17th century, to refer to an easy, painless, happy death, during which it was a "physician's responsibility to alleviate the 'physical sufferings' of the body." Bacon referred to an "outward euthanasia"—the term "outward" he used to distinguish from a spiritual concept—the euthanasia "which regards the preparation of the soul."^[7]

In current usage, one approach to defining euthanasia has been to mirror Suetonius, regarding it as the "painless inducement of a quick death".^[8] However, it is argued that this approach fails to properly define euthanasia, as it leaves open a number of possible actions which would meet the requirements of the definition, but would not be seen as euthanasia. In particular, these include situations where a person kills another, painlessly, but for no reason beyond that of personal gain; or accidental deaths which are quick and painless, but not intentional.^[9][10]

Thus another approach is to incorporate the notion of suffering into the definition.^[9] The definition offered by the Oxford English Dictionary incorporates suffering as a necessary condition, with "the painless killing of a patient suffering from an incurable and painful disease or in an irreversible coma",^[11] and this approach can be seen as a part of other works, such as Marvin Khol and Paul Kurtz's "a mode or act of inducing or permitting death painlessly as a relief from suffering".^[12] However, focusing on this approach to defining euthanasia may also lead to counterexamples: such definitions may encompass killing a person suffering from an incurable disease for personal gain (such as to claim an inheritance), and commentators such as Tom Beauchamp & Arnold Davidson have argued that doing such would constitute "murder simpliciter" rather than euthanasia.^[9]

The third element incorporated into many definitions is that of intentionality – the death must be intended, rather than being accidental, and the intent of the action must be a "merciful death".^[9] Michael Wreen argued that “the principal thing that distinguishes euthanasia from intentional killing simpliciter is the agent's motive: it must be a good motive insofar as the good of the person killed is concerned”,^[13] a view mirrored by Heather Draper, who also spoke to the importance of motive, arguing that "the motive forms a crucial part of arguments for euthanasia, because it must be in the best interests of the person on the receiving end."^[10] Definitions such as that offered by the House of Lords Select Committee on Medical Ethics take this path, where euthanasia is defined as "a deliberate intervention undertaken with the express intention of ending a life, to relieve intractable suffering."^[1] Beauchamp & Davidson also highlight Baruch Brody's "an act of euthanasia is one in which one person ... (A) kills another person (B) for the benefit of the second person, who actually does benefit from being killed".^[14]

Draper argued that any definition of euthanasia must incorporate four elements: an agent and a subject; an intention; a causal proximity, such that the actions of the agent lead to the outcome; and an outcome. Based on this, she offered a definition incorporating those elements, stating that euthanasia "must be defined as death that results from the intention of one person to kill another person, using the most gentle and painless means possible, that is motivated solely by the best interests of the person who dies."^[15] Prior to Draper, Beauchamp & Davidson had also offered a definition which includes these elements, although they offered a somewhat longer account, and one that specifically discounts fetuses in order to distinguish between abortions and euthanasia:^[16]

"In summary, we have argued ... that the death of a human being, A, is an instance of euthanasia if and only if (1) A's death is intended by at least one other human being, B, where B is either the cause of death or a causally relevant feature of the event resulting in death (whether by action or by omission); (2) there is either sufficient current evidence for B to believe that A is acutely suffering or irreversibly comatose, or there is sufficient current evidence related to A's present condition such that one or more known causal laws supports B's belief that A will be in a condition of acute suffering or irreversible comatoseness; (3) (a) B's primary reason for intending A's death is cessation of A's (actual or predicted future) suffering or irreversible comatoseness, where B does not intend A's death for a different primary reason, though there may be other relevant reasons, and (b) there is sufficient current evidence for either A or B that causal means to A's death will not produce any more suffering than would be produced for A if B were not to intervene; (4) the causal means to the event of A's death are chosen by A or B to be as painless as possible, unless either A or B has an overriding reason for a more painful causal means, where the reason for choosing the latter causal means does not conflict with the evidence in 3b; (5) A is a nonfetal organism."^[17]

Wreen, in part responding to Beauchamp & Davidson, offered a six part definition:

"Person A committed an act of euthanasia if and only if (1) A killed B or let her die; (2) A intended to kill B; (3) the intention specified in (2) was at least partial cause of the action specified in (1); (4) the causal journey from the intention specified in (2) to the action specified in (1) is more or less in accordance with A's plan of action; (5) A's killing of B is a voluntary action; (6) the motive for the action specified in (1), the motive standing behind the intention specified in (2), is the good of the person killed."^[18]

Wreen also considered a seventh requirement: "(7) The good specified in (6) is, or at least includes, the avoidance of evil", although as Wreen noted in the paper, he was not convinced that the restriction was required.^[19]

In discussing his definition, Wreen noted the difficulty of justifying euthanasia when faced with the notion of the subject's "right to life". In response, Wreen argued that euthanasia has to be voluntary, and that "involuntary euthanasia is, as such, a great wrong".^[19] Other commentators incorporate consent more directly into their definitions. For example, in a discussion of euthanasia presented in 2003 by the European Association of Palliative Care (EPAC) Ethics Task Force, the authors offered: "Medicalized killing of a person without the person's consent, whether nonvoluntary (where the person in unable to consent) or involuntary (against the person's will) is not euthanasia: it is murder. Hence, euthanasia can be voluntary only."^[20] Although the EPAC Ethics Task Force argued that both non-voluntary and involuntary euthanasia could not be included in the definition of euthanasia, there is discussion in the literature about excluding one but not the other.^[19]

Classification of euthanasia[link]

Euthanasia may be classified according to whether a person gives informed consent into three types: voluntary, non-voluntary and involuntary.^[21][22]

There is a debate within the medical and bioethics literature about whether or not the non-voluntary (and by extension, involuntary) killing of patients can be regarded as euthanasia, irrespective of intent or the patient's circumstances. In the definitions offered by Beauchamp & Davidson and, later, by Wreen, consent on the part of the patient was not considered to be one of their criteria, although it may have been required to justify euthanasia.^[9][23] However, others see consent as essential.

Voluntary euthanasia[link]

Euthanasia conducted with the consent of the patient is termed voluntary euthanasia. Active voluntary euthanasia is legal in Belgium, Luxembourg and the Netherlands. Passive voluntary euthanasia is legal throughout the U.S. per Cruzan v. Director, Missouri Department of Health. When the patient brings about his or her own death with the assistance of a physician, the term assisted suicide is often used instead. Assisted suicide is legal in Switzerland and the U.S. states of Oregon, Washington and Montana.

Non-voluntary euthanasia[link]

Euthanasia conducted where the consent of the patient is unavailable is termed non-voluntary euthanasia. Examples include child euthanasia, which is illegal worldwide but decriminalised under certain specific circumstances in the Netherlands under the Groningen Protocol.

Involuntary euthanasia[link]

Euthanasia conducted against the will of the patient is termed involuntary euthanasia.

Procedural decision[link]

Voluntary, non-voluntary and involuntary euthanasia can all be further divided into passive or active variants.^[24] A number of authors consider these terms to be misleading and unhelpful.^[1]

Passive euthanasia[link]

Passive euthanasia entails the withholding of common treatments, such as antibiotics, necessary for the continuance of life.^[1]

Active euthanasia[link]

Active euthanasia entails the use of lethal substances or forces, such as administering a lethal injection, to kill and is the most controversial means.

History[link]

According to the historian N. D. A. Kemp, the origin of the contemporary debate on euthanasia started in 1870.^[25] Nevertheless, euthanasia was debated and practiced long before that date. Euthanasia was practised in Ancient Greece and Rome: for example, hemlock was employed as a means of hastening death on the island of Kea, a technique also employed in Marseilles and by Socrates in Athens. Euthanasia, in the sense of the deliberate hastening of a person's death, was supported by Socrates, Plato and Seneca the Elder in the ancient world, although Hippocrates appears to have spoken against the practice, writing "I will not prescribe a deadly drug to please someone, nor give advice that may cause his death" (noting there is some debate in the literature about whether or not this was intended to encompass euthanasia).^[26][27][28]

Euthanasia was strongly opposed in the Judeo-Christian tradition. Thomas Aquinas opposed both and argued that the practice of euthanasia contradicted our natural human instincts of survival.,^[29] as did Francois Ranchin (1565–1641), a French physician and professor of medicine, and Michael Boudewijns (1601–1681), a physician and teacher.^[27]:208[30] Nevertheless, there were voices arguing for euthanasia, such as John Donne in 1624,^[31] and euthanasia continued to be practised. Thus in 1678, the publication of Caspar Questel's De pulvinari morientibus non subtrahend, ("On the pillow of which the dying should not be deprived"), initiated debate on the topic. Questel described various customs which were employed at the time to hasten the death of the dying, (including the sudden removal of a pillow, which was believed to accelerate death), and argued against their use, as doing so was "against the laws of God and Nature".^{[27]:209–211} This view was shared by many who followed, including Philipp Jakob Spener, Veit Riedlin and Johann Georg Krünitz.^[27]:211 In spite of opposition, euthanasia continued to be practised, involving techniques such as bleeding, suffocation and removing people from their beds to be placed on the cold ground.^{[27]:211–214}

Suicide and euthanasia were more acceptable under Protestantism and during the Age of Enlightenment,^[30] and Thomas More wrote of euthanasia in Utopia, although it is not clear if More was intending to endorse the practise.^{[27]:208–209} Other cultures have taken different approaches: for example, in Japan suicide has not traditionally been viewed as a sin, and accordingly the perceptions of euthanasia are different from those in other parts of the world.^[32]

Beginnings of the contemporary euthanasia debate[link]

In the mid-1800s, the use of morphine to treat "the pains of death" emerged, with John Warren recommending its use in 1848. A similar use of chloroform was revealed by Joseph Bullar in 1866. However, in neither case was it recommended that the use should be to hasten death. In 1870 Samuel Williams, a schoolteacher, initiated the contemporary euthanasia debate through a speech given at the Birmingham Speculative Club, which was subsequently published in a one-off publication entitled Essays of the Birmingham Speculative Club, the collected works of a number of members of an amateur philosophical society.^[33]:794 Williams' proposal was to use chloroform to deliberately hasten the death of terminally ill patients:

That in all cases of hopeless and painful illness, it should be the recognized duty of the medical attendant, whenever so desired by the patient, to administer choloroform or such other anaesthetic as may by-and-bye supersede chloroform – so as to destroy consciousness at once, and put the sufferer to a quick and painless death; all needful precautions being adopted to prevent any possible abuse of such duty; and means being taken to establish, beyond the possibility of doubt or question, that the remedy was applied at the express wish of the patient.

—Samuel Williams (1872) ,  Euthanasia Williams and Northgate: London.^[33]:794

The essay was favourably reviewed in The Saturday Review, and an editorial speaking against the essay appeared in The Spectator.^[25] From there it proved to be influential, and other writers came out in support of such views: Lionel Tollemache wrote in favour of euthanasia, as did Annie Besant, the essayist and reformer who later became involved with the National Secular Society, considering it a duty to society to "die voluntarily and painlessly" when one reaches the point of becoming a 'burden'.^[25][34] Popular Science also analyzed the issue in May 1873, assessing both sides of the argument.^[35] Nevertheless, Kemp notes that at the time, medical doctors did not participate in the discussion; it was "essentially a philosophical enterprise... tied inextricably to a number of objections to the Christian doctrine of the sanctity of human life".^[25]

Early euthanasia movement in the United States[link]

Felix Adler, circa 1913, the first prominent American to argue for permitting suicide in cases of chronic illness

The rise of the euthanasia movement in the United States coincided with the so-called Gilded Age – a time of social and technological change that encompassed an "individualistic conservatism that praised laissez faire economics, scientific method, and rationalism", along with major depressions, industrialisation and conflict between corporations and labor unions.^[33]:794 It was also a time that saw the development of the modern hospital system, seen as a factor in the emergence of the euthanasia debate.^[36]

Robert Ingersoll argued for euthanasia, stating in 1894 that where someone is suffering from a terminal illness, such as terminal cancer, they should have a right to end their pain through suicide. Felix Adler offered a similar approach, although, unlike Ingersoll, Adler did not reject religion, instead arguing from an Ethical Culture framework. In 1891, Alder argued that those suffering from overwhelming pain should have the right to commit suicide, and, furthermore, that it should be permissible for a doctor to assist – thus making Adler the first "prominent American" to argue for suicide in cases where people were suffering from chronic illness.^[37] Both Ingersoll and Adler argued for voluntary euthanasia of adults suffering from terminal ailments.^[37] However, Dowbiggin argues that by breaking down prior moral objections to euthanasia and suicide, Ingersoll and Adler made it possible for others to stretch the definition of euthanasia.^[38]

America also saw the first attempt to legalise euthanasia, when Henry Hunt introduced legislation into the General Assembly of Ohio in 1906.^[39]:614 Hunt did so at the behest of Anna Hall, a wealthy heiress who was a major figure in the euthanasia movement during the early 20th century in the United States. Hall had watched her mother die after an extended battle with liver cancer, and had dedicated herself to ensuring that others would not have to endure the same suffering. Towards this end she engaged in an extensive letter writing campaign, recruited Lurana Sheldon and Maud Ballington Booth, and organised a debate on euthanasia at the annual meeting of the American Humane Association in 1905 – described by Jacob Appel as the first significant public debate on the topic in the 20th century.^{[39]:614–616} Hunt's bill called for the administration of an anesthetic to bring about a patient's death, so long as the person is of lawful age and sound mind, and was suffering from a fatal injury, an irrecoverable illness or great physical pain. It also required that the case be heard by a physician, required informed consent in front of three witnesses, and then required the attendance of three physicians who had to agree that the patient's recovery was impossible. A motion to reject the bill outright was voted down, but the bill itself failed to pass, 79 to 23.^{[33]:796[39]:618–619}

Along with the Ohio euthanasia proposal, 1906 also witnessed the creation of a second bill: Assemblyman Ross Gregory introduced a proposal to permit euthanasia to the Iowa legislature. However, the Iowa legislation was far broader in scope than that offered in Ohio. It allowed for the death of any person of at least ten years of age who suffered from an ailment that would prove fatal and cause extreme pain, should they be of sound mind and express a desire to artificially hasten their death. In addition, it allowed for infants to be euthanised if they were sufficiently deformed, and permitted guardians to request euthanasia on behalf of their wards. The proposed legislation also imposed penalties on physicians who refused to perform euthanasia when requested: a 6–12 month prison term and a fine of between $200 and $1000 dollars. Unsurprisingly, the proposal proved to be controversial.^{[39]:619–621} It engendered considerable debate but failed to pass, having been withdrawn from consideration after being passed to the Committee on Public Health.^[39]:623

After 1906 the euthanasia debate reduced in intensity, resurfacing periodically but not returning to the same level of debate until the 1930s in the United Kingdom.^[33]:796

1930s[link]

In January 1936, King George V was given a fatal dose of morphine and cocaine in order to hasten his death. At the time he was suffering from cardiorespiratory failure, and the decision to end his life was made by his physician, Lord Dawson.^[40] Although this remained a secret for over 50 years, the death of George V coincided with proposed legislation in the House of Lords to legalise euthanasia. The legislation came through the British Volunteer Euthanasia Legalisation Society (now known as Dignity in Dying),^[41] which was formed in 1935, although its formation can be traced back to a 1931 speech by Dr Charles Killick Millard.^[25]

Euthanasia opponent Ian Dowbiggin argues that the early membership of the Euthanasia Society of America (ESA) reflected how many perceived euthanasia at the time, often seeing it as a eugenics matter rather than an issue concerning individual rights.^[37] Dowbiggin argues that not every eugenist joined the ESA "solely for eugenic reasons", but he postulates that there were clear ideological connections between the eugenics and euthanasia movements.^[37]

A 24 July 1939 killing of a severely disabled infant in Nazi Germany was described in a BBC "Genocide Under the Nazis Timeline" as the first "state-sponsored euthanasia".^[42] Parties that consented to the killing included Hitler's office, the parents, and the Reich Committee for the Scientific Registration of Serious and Congenitally Based Illnesses.^[42] The Telegraph noted that the killing of the disabled infant—whose name was Gerhard Kretschmar, born blind, with missing limbs, subject to convulsions, and reportedly "an idiot"— provided "the rationale for a secret Nazi decree that led to 'mercy killings' of almost 300,000 mentally and physically handicapped people".^[43] While Kretchmar's killing received parental consent, afterwards, most of the 5,000 to 8,000 killed children were forcibly taken from their parents.^[42][43]

Nazi Euthanasia Program (Action T4)[link]

The neutrality of this article is disputed. Please see the discussion on the talk page. Please do not remove this message until the dispute is resolved. (December 2011)

Nazi poster that reads "60,000 Reichsmark is the lifetime cost to the community of this genetic defective. Member of the [German] race, that's your money".^[44]

The "euthanasia campaign" of mass murder gathered momentum on 14 January 1940 when the "handicapped" were killed with gas vans and killing centres, eventually leading to the deaths of 70,000 adult Germans.^[45] Professor Robert Jay Lifton, author of The Nazi Doctors and a leading authority on the T4 program, contrasts this program with what he considers to be a genuine euthanasia. He explains that the Nazi version of "euthanasia" was based on the work of Adolf Jost, who published The Right to Death (Das Recht auf den Tod) in 1895. Lifton writes: "Jost argued that control over the death of the individual must ultimately belong to the social organism, the state. This concept is in direct opposition to the Anglo-American concept of euthanasia, which emphasizes the individual's 'right to die' or 'right to death' or 'right to his or her own death,' as the ultimate human claim. In contrast, Jost was pointing to the state's right to kill. [...] Ultimately the argument was biological: 'The rights to death [are] the key to the fitness of life.' The state must own death—must kill—in order to keep the social organism alive and healthy."^[46]

In modern terms, the use of "euthanasia" in the context of Action T4 is seen to be a euphemism to disguise a program of genocide, in which people were killed on the grounds "disabilities, religious beliefs, and discordant individual values".^[47] Compared to the discussions of euthanasia that emerged post-war, the Nazi program may have been worded in terms that appear similar to the modern use of the euthanasia, but there was no "mercy" and the patients were not necessarily terminally ill.^[47] Despite these differences, historian and euthanasia opponent Ian Dowbiggin writes that "the origins of Nazi euthanasia, like those of the American euthanasia movement, predate the Third Reich and were intertwined with the history of eugenics and social Darwinism, and with efforts to discredit traditional morality and ethics."^[37]:65

Euthanasia debate[link]

Historically, the euthanasia debate has tended to focus on a number of key concerns. According to euthanasia opponent Ezekiel Emanuel, proponents of euthanasia have presented four main arguments: a) that people have a right to self-determination, and thus should be allowed to choose their own fate; b) assisting a subject to die might be a better choice than requiring that they continue to suffer; c) the distinction between passive euthanasia, which is often permitted, and active euthanasia, which is not, is not substantive (or that the underlying principle–the doctrine of double effect–is unreasonable or unsound); and d) permitting euthanasia will not necessarily lead to unacceptable consequences. Pro-euthanasia activists often point to countries like the Netherlands and Belgium, and states like Oregon, where it has been made legal to argue that it is mostly unproblematic.

Similarly, Emanuel argues that there are four major arguments presented by opponents of euthanasia: a) not all deaths are painful; b) alternatives, such as cessation of active treatment, combined with the use of effective pain relief, are available; c) the distinction between active and passive euthanasia is morally significant; and d) legalising euthanasia will place society on a slippery slope,^[48] which will lead to unacceptable consequences.^[33]:797–8

Legal status[link]

The examples and perspective in this section may not represent a worldwide view of the subject. Please improve this article and discuss the issue on the talk page. (November 2011)

West's Encyclopedia of American Law states that "a 'mercy killing' or euthanasia is generally considered to be a criminal homicide"^[49] and is normally used as a synonym of homicide committed at a request made by the patient.^[50]

The judicial sense of the term "homicide" includes any intervention undertaken with the express intention of ending a life, even to relieve intractable suffering.^[50][51][52] Not all homicide is unlawful.^[53] Two designations of homicide that carry no criminal punishment are justifiable and excusable homicide.^[53] In most countries this is not the status of euthanasia. The term "euthanasia" is usually confined to the active variety; the University of Washington website states that "euthanasia generally means that the physician would act directly, for instance by giving a lethal injection, to end the patient's life".^[54] Physician-assisted suicide is thus not classified as euthanasia by the US State of Oregon, where it is legal under the Oregon Death with Dignity Act, and despite its name, it is not legally classified as suicide either.^[55] Unlike physician-assisted suicide, withholding or withdrawing life-sustaining treatments with patient consent (voluntary) is almost unanimously considered, at least in the United States, to be legal.^[56] The use of pain medication in order to relieve suffering, even if it hastens death, has been held as legal in several court decisions.^[54]

Some governments around the world have legalized voluntary euthanasia but generally it remains as a criminal homicide. In the Netherlands and Belgium, where euthanasia has been legalized, it still remains homicide although it is not prosecuted and not punishable if the perpetrator (the doctor) meets certain legal exceptions.^{[57][58][59][60]}

Physician sentiment[link]

A survey in the United States of more than 10,000 physicians came to the result that approximately 16% of physicians would ever consider halting life-sustaining therapy because the family demands it, even if believed that it was premature. Approximately 55% would not, and for the remaining 29%, it would depend on circumstances.^[61]

This study also stated that approximately 46% of physicians agree that physician-assisted suicide should be allowed in some cases; 41% do not, and the remaining 14% think it depends.^[61]

In the United Kingdom, the pro-assisted dying group Dignity in Dying cite conflicting research on attitudes by doctors to assisted dying: with a 2009 Palliative Medicine-published survey showing 64% support (to 34% oppose) for assisted dying in cases where a patient has an incurable and painful disease, while 49% of doctors in a study published in BMC Medical Ethics oppose changing the law on assisted dying to 39% in favour.^[62]

See also[link]

• Animal euthanasia
• Child euthanasia
• Child euthanasia in Nazi Germany
• Coup de grâce
• Dysthanasia
• Euthanasia and the slippery slope
• Medical law
• Palliative sedation
• Principle of double effect
• Terri Schiavo case

References[link]

External links[link]

Look up euthanasia in Wiktionary, the free dictionary.

Wikinews has news related to: Euthanasia

• Physician assisted death from The Hastings Center

Further reading[link]

Wikiquote has a collection of quotations related to: Euthanasia

• Rachels, James (1986). The end of life: Euthanasia and Morality. Oxford University Press. ISBN 978-0-19-286070-5. 
• Torr, James D. (2000). Euthanasia: opposing viewpoints. San Diego: Greenhaven Press. ISBN 0-7377-0127-7. 
• Nitschke, Philip; Fiona Stewart, Philip Nitschke & Fiona Stewart (2006). The Peaceful Pill Handbook. Exit International US Ltd. ISBN 978-0-9788788-0-1. 

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]