A myocardial infarction occurs when anatheroscleroticplaque slowly builds up in the inner lining of acoronary artery and then suddenly ruptures, causing catastrophicthrombus formation, totally occluding the artery and preventing blood flow downstream to the heart muscle.
Treatment of an MI is time-critical.[16]Aspirin is an appropriate immediate treatment for a suspected MI.[9]Nitroglycerin oropioids may be used to help with chest pain; however, they do not improve overall outcomes.[8][9]Supplemental oxygen is recommended in those withlow oxygen levels or shortness of breath.[9] In a STEMI, treatments attempt to restore blood flow to the heart and includepercutaneous coronary intervention (PCI), where the arteries are pushed open and may bestented, orthrombolysis, where the blockage is removed using medications.[8] People who have anon-ST elevation myocardial infarction (NSTEMI) are often managed with the blood thinnerheparin, with the additional use of PCI in those at high risk.[9] In people with blockages of multiple coronary arteries and diabetes,coronary artery bypass surgery (CABG) may be recommended rather thanangioplasty.[17] After an MI, lifestyle modifications, along with long-term treatment with aspirin,beta blockers andstatins, are typically recommended.[8]
Worldwide, about 15.9 million myocardial infarctions occurred in 2015.[10] More than 3 million people had an ST elevation MI, and more than 4 million had an NSTEMI.[18] STEMIs occur about twice as often in men as women.[19] About one million people have an MI each year in the United States.[3] In the developed world, the risk of death in those who have had a STEMI is about 10%.[8] Rates of MI for a given age have decreased globally between 1990 and 2010.[20] In 2011, an MI was one of the top five most expensive conditions during inpatient hospitalizations in the US, with a cost of about $11.5 billion for 612,000 hospital stays.[21]
Myocardial infarction (MI) refers to tissue death (infarction) of the heart muscle (myocardium) caused byischemia, the lack of oxygen delivery to myocardial tissue. It is a type ofacute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart.[22] Unlike the other type of acute coronary syndrome,unstable angina, a myocardialinfarction occurs when there iscell death, which can be estimated by measuring by ablood test forbiomarkers (the cardiac proteintroponin).[23] When there is evidence of an MI, it may be classified as an ST elevation myocardial infarction (STEMI) or Non-ST elevation myocardial infarction (NSTEMI) based on the results of anECG.[24]
The phrase "heart attack" is often used non-specifically to refer to myocardial infarction. An MI is different from—but can cause—cardiac arrest, where the heart is not contracting at all or so poorly that all vital organs cease to function, thus leading to death.[25] It is also distinct fromheart failure, in which the pumping action of the heart is impaired. However, an MI may lead to heart failure.[26]
Signs and symptoms
Areas where pain is experienced in myocardial infarction, showing common (dark red) and less common (light red) areas on the chest (top) and back (bottom).
Chest pain that may or may not radiate to other parts of the body is the most typical and significant symptom of myocardial infarction. It might be accompanied by other symptoms such as sweating.[27]
Pain
Chest pain is one of the most common symptoms of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and upperabdomen.[28][29] The pain most suggestive of an acute MI, with the highestlikelihood ratio, is pain radiating to the right arm and shoulder.[30][29] Similarly, chest pain similar to a previous heart attack is also suggestive.[31] The pain associated with MI is usually diffuse, does not change with position, and lasts for more than 20 minutes.[24] It might be described as pressure, tightness, knifelike, tearing, burning sensation (all these are also manifested during other diseases). It could be felt as an unexplained anxiety, and pain might be absent altogether.[29]Levine's sign, in which a person localizes the chest pain by clenching one or both fists over theirsternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed it had a poorpositive predictive value.[32]
Typically, chest pain because of ischemia, be it unstable angina or myocardial infarction, lessens with the use ofnitroglycerin, but nitroglycerin may also relieve chest pain arising from non-cardiac causes.[33]
Other
Chest pain may be accompanied bysweating, nausea or vomiting, andfainting,[24][30] and these symptoms may also occur without any pain at all.[28] Dizziness or lightheadedness is common and occurs due to reduction in oxygen and blood to the brain. In females, the most common symptoms of myocardial infarction include shortness of breath, weakness, andfatigue.[34] Females are more likely to have unusual or unexplained tiredness and nausea or vomiting as symptoms.[35] Females having heart attacks are more likely to have palpitations, back pain, labored breath, vomiting, and left arm pain than males, although the studies showing these differences had high variability.[36] Females are less likely to report chest pain during a heart attack and more likely to report nausea, jaw pain, neck pain, cough, and fatigue, although these findings are inconsistent across studies.[37] Females with heart attacks also had more indigestion,dizziness,loss of appetite, and loss of consciousness.[38]Shortness of breath is a common, and sometimes the only symptom, occurring when damage to the heart limits theoutput of theleft ventricle, with breathlessness arising either fromlow oxygen in the blood orpulmonary edema.[28][39]
"Silent" myocardial infarctions can happen without any symptoms at all.[12] These cases can be discovered later onelectrocardiograms, using blood enzyme tests, or atautopsy after a person has died. Such silent myocardial infarctions represent between 22 and 64% of all infarctions,[12] and are more common in theelderly,[12] in those withdiabetes mellitus[16] and afterheart transplantation. In people with diabetes, differences inpain threshold,autonomic neuropathy, andpsychological factors have been cited as possible explanations for the lack of symptoms.[42] In heart transplantation, thedonor heart is not fully innervated by the nervous system of the recipient.[43]
Many risk factors for myocardial infarction are potentially modifiable, with the most important beingtobacco smoking (includingsecondhand smoke).[16] Smoking appears to be the cause of about 36% and obesity the cause of 20% ofcoronary artery disease.[47] Lack of physical activity has been linked to 7–12% of cases.[47][48] Less common causes include stress-related causes such asjob stress, which accounts for about 3% of cases,[47] and chronic high stress levels.[49]
Diet
There is varying evidence about the importance ofsaturated fat in the development of myocardial infarctions. Eating polyunsaturated fat instead ofsaturated fats has been shown in studies to be associated with a decreased risk of myocardial infarction,[50] while other studies find little evidence that reducing dietary saturated fat or increasingpolyunsaturated fat intake affects heart attack risk.[51][52] Dietary cholesterol does not appear to have a significant effect on blood cholesterol and thus recommendations about its consumption may not be needed.[53]Trans fats do appear to increase risk.[51] Acute and prolonged intake of high quantities of alcoholic drinks (3–4 or more daily) increases the risk of a heart attack.[54]
Genetics
Family history ofischemic heart disease or MI, particularly if one has a male first-degree relative (father, brother) who had a myocardial infarction before age 55 years, or a female first-degree relative (mother, sister) less than age 65 increases a person's risk of MI.[45]
The risk of having a myocardial infarction increases with older age, low physical activity, and lowsocioeconomic status.[45] Heart attacks appear to occur more commonly in the morning hours, especially between 6AM and noon.[56] Evidence suggests that heart attacks are at least three times more likely to occur in the morning than in the late evening.[57]Shift work is also associated with a higher risk of MI.[58] One analysis has found an increase in heart attacks immediately following the start ofdaylight saving time.[59]
Endometriosis in women under the age of 40 is an identified risk factor.[62]
Air pollution is also an important modifiable risk. Short-term exposure to air pollution such ascarbon monoxide,nitrogen dioxide, andsulfur dioxide (but notozone) has been associated with MI and other acute cardiovascular events.[63] For sudden cardiac deaths, every increment of 30 units in Pollutant Standards Index correlated with an 8% increased risk of out-of-hospital cardiac arrest on the day of exposure.[64] Extremes of temperature are also associated.[65]
Calcium deposits in the coronary arteries can be detected withCT scans. Calcium seen in coronary arteries can provide predictive information beyond that of classical risk factors.[68]High blood levels of the amino acid homocysteine is associated with premature atherosclerosis;[69] whether elevated homocysteine in the normal range is causal is controversial.[70]
The animation shows plaque buildup or acoronary artery spasm can lead to a heart attack and how blocked blood flow in a coronary artery can lead to a heart attack.
The most common cause of a myocardial infarction is the rupture of an atherosclerotic plaque on anartery supplying heart muscle.[41][72] Plaques can become unstable, rupture, and additionally promote the formation of ablood clot that blocks the artery; this can occur in minutes. Blockage of an artery can lead to tissue death in tissue being supplied by that artery.[73] Atherosclerotic plaques are often present for decades before they result in symptoms.[73]
The gradual buildup ofcholesterol and fibrous tissue in plaques in the wall of thecoronary arteries or other arteries, typically over decades, is termedatherosclerosis.[74] Atherosclerosis is characterized by progressive inflammation of the walls of the arteries.[73] Inflammatory cells, particularlymacrophages, move into affected arterial walls. Over time, they become laden with cholesterol products, particularlyLDL, and becomefoam cells. Acholesterol core forms as foam cells die. In response togrowth factors secreted by macrophages,smooth muscle and other cells move into the plaque and act to stabilize it. A stable plaque may have a thick fibrous cap withcalcification. If there is ongoing inflammation, the cap may be thin or ulcerate. Exposed to the pressure associated with blood flow, plaques, especially those with a thin lining, may rupture and trigger the formation of a blood clot (thrombus).[73] The cholesterol crystals have been associated with plaque rupture through mechanical injury and inflammation.[75]
Cross section showing anterior left ventricle wall infarction
If impaired blood flow to the heart lasts long enough, it triggers a process called theischemic cascade; the heart cells in the territory of the blocked coronary artery die (infarction), chiefly throughnecrosis, and do not grow back. Acollagenscar forms in their place.[73] When an artery is blocked, cells lackoxygen, needed to produceATP inmitochondria. ATP is required for the maintenance of electrolyte balance, particularly through theNa/K ATPase. This leads to an ischemic cascade of intracellular changes, necrosis andapoptosis of affected cells.[76]
Cells in the area with the worst blood supply, just below the inner surface of the heart (endocardium), are most susceptible to damage.[77][78] Ischemia first affects this region, thesubendocardial region, and tissue begins to die within 15–30 minutes of loss of blood supply.[79] The dead tissue is surrounded by a zone of potentially reversible ischemia that progresses to become a full-thicknesstransmural infarct.[76][79] The initial "wave" of infarction can take place over 3–4 hours.[73][76] These changes are seen ongross pathology and cannot be predicted by the presence or absence of Q waves on an ECG.[78] The position, size and extent of an infarct depends on the affected artery, totality of the blockage, duration of the blockage, the presence ofcollateral blood vessels, oxygen demand, and success of interventional procedures.[28][72]
Injury to the myocardium also occurs during re-perfusion. This might manifest as ventricular arrhythmia. The re-perfusion injury is a consequence of the calcium and sodium uptake from the cardiac cells and the release of oxygen radicals during reperfusion. No-reflow phenomenon—when blood is still unable to be distributed to the affected myocardium despite clearing the occlusion—also contributes to myocardial injury. Topical endothelial swelling is one of many factors contributing to this phenomenon.[81]
A myocardial infarction, according to established consensus, is defined by elevated cardiacbiomarkers with a rising or falling trend and at least one of the following:[82]
"STEMI" redirects here. For the Christian evangelist organization, seeStephen Tong § Ministry.
A myocardial infarction is usually clinically classified as an ST-elevation MI (STEMI) or a non-ST elevation MI (NSTEMI). These are based onST elevation, a portion of a heartbeat graphically recorded on anECG.[24] STEMIs make up about 25–40% of myocardial infarctions.[19] A more explicit classification system, based on international consensus in 2012, also exists. This classifies myocardial infarctions into five types:[24]
Spontaneous MI related to plaque erosion and/or rupture fissuring, or dissection
MI related to ischemia, such as from increased oxygen demand or decreased supply, e.g., coronary artery spasm, coronary embolism, anemia, arrhythmias, high blood pressure, or low blood pressure
Sudden unexpected cardiac death, including cardiac arrest, where symptoms may suggest MI, an ECG may be taken with suggestive changes, or a blood clot is found in a coronary artery by angiography and/or at autopsy, but where blood samples could not be obtained, or at a time before the appearance of cardiac biomarkers in the blood
There are many differentbiomarkers used to determine the presence of cardiac muscle damage.Troponins, measured through a blood test, are considered to be the best,[19] and are preferred because they have greatersensitivity and specificity for measuring injury to the heart muscle than other tests.[72] A rise in troponin occurs within 2–3 hours of injury to the heart muscle, and peaks within 1–2 days. The level of the troponin, as well as a change over time, are useful in measuring and diagnosing or excluding myocardial infarctions, and the diagnostic accuracy of troponin testing is improving over time.[72] One high-sensitivity cardiac troponin can rule out a heart attack as long as the ECG is normal.[83][84]
Other tests, such asCK-MB ormyoglobin, are discouraged.[85] CK-MB is not as specific as troponins for acute myocardial injury, and may be elevated with past cardiac surgery, inflammation or electrical cardioversion; it rises within 4–8 hours and returns to normal within 2–3 days.[28]Copeptin may be useful to rule out MI rapidly when used along with troponin.[86]
Electrocardiogram
A 12-lead ECG showing an inferior STEMI due to reduced perfusion through theright coronary artery. Elevation of theST segment can be seen in leads II, III and aVF.
Electrocardiograms (ECGs) are a series of leads placed on a person's chest that measure electrical activity associated with contraction of the heart muscle.[87] The taking of an ECG is an important part of the workup of an AMI,[24] and ECGs are often not just taken once but may be repeated over minutes to hours, or in response to changes in signs or symptoms.[24]
ECG readouts produce a waveform with different labeled features.[87] In addition to a rise in biomarkers, a rise in theST segment, changes in the shape or flipping ofT waves, newQ waves, or a newleft bundle branch block can be used to diagnose an AMI.[24] In addition,ST elevation can be used to diagnose an ST segment myocardial infarction (STEMI). A rise must be new in V2 and V3 ≥2 mm (0,2 mV) for males or ≥1.5 mm (0.15 mV) for females or ≥1 mm (0.1 mV) in two otheradjacent chest or limb leads.[19][24] ST elevation is associated with infarction, and may be preceded by changes indicating ischemia, such as ST depression or inversion of the T waves.[87] Abnormalities can help differentiate the location of an infarct, based on the leads that are affected by changes.[16] Early STEMIs may be preceded by peaked T waves.[19] Other ECG abnormalities relating to complications of acute myocardial infarctions may also be evident, such asatrial orventricular fibrillation.[88]
Imaging
ECG : AMI with ST elevation in V2-4
Noninvasive imaging plays an important role in the diagnosis and characterisation of myocardial infarction.[24] Tests such aschest X-rays can be used to explore and exclude alternate causes of a person's symptoms.[24]Echocardiography may assist in modifying clinical suspicion of ongoing myocardial infarction in patients that can't be ruled out or ruled in following initialECG andTroponin testing.[89]Myocardial perfusion imaging has no role in the acute diagnostic algorithm; however, it can confirm a clinical suspicion of Chronic Coronary Syndrome when the patient's history,physical examination (includingcardiac examination) ECG, and cardiac biomarkers suggest coronary artery disease.[90]
Medical societies and professional guidelines recommend that the physician confirm a person is at high risk for Chronic Coronary Syndrome before conducting diagnostic non-invasive imaging tests to make a diagnosis,[90][92][89] as such tests are unlikely to change management and result in increased costs.[90] Patients who have a normal ECG and who are able to exercise, for example, most likely do not merit routine imaging.[90]
Poor movement of the heart due to an MI as seen on ultrasound[93]
Pulmonary edema due to an MI as seen on ultrasound[93]
There is a large crossover between the lifestyle and activity recommendations to prevent a myocardial infarction, and those that may be adopted assecondary prevention after an initial myocardial infarction,[72] because of shared risk factors and an aim to reduce atherosclerosis affecting heart vessels.[28] Theinfluenza vaccine also appear to protect against myocardial infarction with a benefit of 15 to 45%.[97]
Primary prevention
Lifestyle
Physical activity can reduce the risk of cardiovascular disease, and people at risk are advised to engage in 150 minutes of moderate or 75 minutes of vigorous intensityaerobic exercise a week.[98] Keeping a healthy weight, drinking alcohol within the recommended limits, andquitting smoking reduce the risk of cardiovascular disease.[98]
Substitutingunsaturated fats such asolive oil andrapeseed oil instead of saturated fats may reduce the risk of myocardial infarction,[50] although there is not universal agreement.[51] Dietary modifications are recommended by some national authorities, with recommendations including increasing the intake of wholegrain starch, reducing sugar intake (particularly of refined sugar), consuming five portions of fruit and vegetables daily, consuming two or more portions of fish per week, and consuming 4–5 portions of unsaltednuts,seeds, orlegumes per week.[98] The dietary pattern with the greatest support is theMediterranean diet.[99]Vitamins and mineral supplements are of no proven benefit,[100] and neither are plantstanols orsterols.[98]
Public health measures may also act at a population level to reduce the risk of myocardial infarction, for example by reducing unhealthy diets (excessive salt, saturated fat, and trans-fat) including food labeling and marketing requirements as well as requirements for catering and restaurants and stimulating physical activity. This may be part of regional cardiovascular disease prevention programs or through thehealth impact assessment of regional and local plans and policies.[101]
Most guidelines recommend combining different preventive strategies. A 2015 Cochrane Review found some evidence that such an approach might help with blood pressure, body mass index and waist circumference. However, there was insufficient evidence to show an effect on mortality or actual cardio-vascular events.[102]
Medication
Statins, drugs that act to lower blood cholesterol, decrease the incidence and mortality rates of myocardial infarctions.[103] They are often recommended in those at an elevated risk of cardiovascular diseases.[98]
Aspirin has been studied extensively in people considered at increased risk of myocardial infarction. Based on numerous studies in different groups (e.g. people with or without diabetes), there does not appear to be a benefit strong enough to outweigh the risk of excessive bleeding.[104][105] Nevertheless, manyclinical practice guidelines continue to recommend aspirin for primary prevention,[106] and some researchers feel that those with very high cardiovascular risk but low risk of bleeding should continue to receive aspirin.[107]
Secondary prevention
There is a large crossover between the lifestyle and activity recommendations to prevent a myocardial infarction, and those that may be adopted assecondary prevention after an initial myocardial infarct.[72] Recommendations includestopping smoking, a gradual return to exercise, eating a healthydiet, low insaturated fat and low incholesterol,drinking alcohol within recommended limits, exercising, and trying to achieve a healthy weight.[72][108] Exercise is both safe and effective even if people have had stents or heart failure,[109] and is recommended to start gradually after 1–2 weeks.[72] Counselling should be provided relating to medications used, and for warning signs of depression.[72] Previous studies suggested a benefit fromomega-3 fatty acid supplementation but this has not been confirmed.[108]
Medications
Following a heart attack, nitrates, when taken for two days, andACE-inhibitors decrease the risk of death.[110] Other medications include:
Aspirin is continued indefinitely, as well as another antiplatelet agent such as clopidogrel or ticagrelor ("dual antiplatelet therapy" or DAPT) for up to twelve months.[108] If someone has another medical condition that requires anticoagulation (e.g. withwarfarin) this may need to be adjusted based on risk of further cardiac events as well as bleeding risk.[108] In those who have had a stent, more than 12 months of clopidogrel plus aspirin does not affect the risk of death.[111]
Beta blocker therapy such asmetoprolol orcarvedilol is recommended to be started within 24 hours, provided there is no acute heart failure orheart block.[19][85] The dose should be increased to the highest tolerated.[108] Contrary to most guidelines, the use of beta blockers does not appear to affect the risk of death,[112][113] possibly because other treatments for MI have improved. When beta blocker medication is given within the first 24–72 hours of a STEMI no lives are saved. However, 1 in 200 people were prevented from a repeat heart attack, and another 1 in 200 from having an abnormal heart rhythm. Additionally, for 1 in 91 the medication causes atemporary decrease in the heart's ability to pump blood.[114]
Statin therapy has been shown to reduce mortality and subsequent cardiac events and should be commenced to lower LDL cholesterol. Other medications, such asezetimibe, may also be added with this goal in mind.[72]
Adefibrillator, an electric device connected to the heart and surgically inserted under the skin, may be recommended. This is particularly if there are any ongoing signs of heart failure, with a lowleft ventricular ejection fraction and a New York Heart Association grade II or III after 40 days of the infarction.[72] Defibrillators detect potentially fatal arrhythmia and deliver an electrical shock to the person to depolarize a critical mass of the heart muscle.[116]
A myocardial infarction requires immediate medical attention. Treatment aims to preserve as much heart muscle as possible, and to prevent further complications.[28] Treatment depends on whether the myocardial infarction is a STEMI or NSTEMI.[72] Treatment in general aims to unblock blood vessels, reduce blood clot enlargement, reduce ischemia, and modify risk factors with the aim of preventing future MIs.[28] In addition, the main treatment for myocardial infarctions with ECG evidence of ST elevation (STEMI) includethrombolysis orpercutaneous coronary intervention, although PCI is also ideally conducted within 1–3 days for NSTEMI.[72] In addition toclinical judgement, risk stratification may be used to guide treatment, such as with theTIMI andGRACE scoring systems.[16][72][118]
Pain
The pain associated with myocardial infarction is often treated withnitroglycerin, avasodilator, oropioid medications such asmorphine.[28] Nitroglycerin (givenunder the tongue orinjected into a vein) may improve blood supply to the heart.[28] It is an important part of therapy for its pain relief effects, though there is no proven benefit tomortality.[28][119] Morphine or other opioid medications may also be used, and are effective for the pain associated with STEMI.[28] There is poor evidence that morphine shows any benefit tooverall outcomes, and there is some evidence of potential harm.[120][121]
Antithrombotics
Aspirin, anantiplatelet drug, is given as aloading dose to reduce the clot size and reduce further clotting in the affected artery.[28][72] It is known to decrease mortality associated with acute myocardial infarction by at least 50%.[72]P2Y12 inhibitors such asclopidogrel,prasugrel andticagrelor are given concurrently, also as aloading dose, with the dose depending on whether further surgical management or fibrinolysis is planned.[72] Prasugrel and ticagrelor are recommended in European and American guidelines, as they are active more quickly and consistently than clopidogrel.[72] P2Y12 inhibitors are recommended in both NSTEMI and STEMI, including in PCI, with evidence also to suggest improved mortality.[72]Heparins, particularly in the unfractionated form, act at several points in theclotting cascade, help to prevent the enlargement of a clot, and are also given in myocardial infarction, owing to evidence suggesting improved mortality rates.[72] In very high-risk scenarios,inhibitors of the platelet glycoprotein αIIbβ3a receptor such aseptifibatide ortirofiban may be used.[72]
There is varying evidence on the mortality benefits in NSTEMI. A 2014 review of P2Y12 inhibitors such asclopidogrel found they do not change the risk of death when given to people with a suspected NSTEMI prior to PCI,[122] nor do heparins change the risk of death.[123] They do decrease the risk of having a further myocardial infarction.[72][123]
Angiogram
Inserting a stent to widen the artery.
Primarypercutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner, ideally within 90–120 minutes of contact with a medical provider.[72][124] Some recommend it is also done in NSTEMI within 1–3 days, particularly when considered high-risk.[72] A 2017 review, however, did not find a difference between early versus later PCI in NSTEMI.[125]
If PCI cannot be performed within 90 to 120 minutes in STEMI then fibrinolysis, preferably within 30 minutes of arrival to hospital, is recommended.[72][128] If a person has had symptoms for 12 to 24 hours evidence for effectiveness of thrombolysis is less and if they have had symptoms for more than 24 hours it is not recommended.[129] Thrombolysis involves the administration of medication that activates theenzymes that normally dissolve blood clots. These medications includetissue plasminogen activator,reteplase,streptokinase, andtenecteplase.[28] Thrombolysis is not recommended in a number of situations, particularly when associated with a high risk of bleeding or the potential for problematic bleeding, such as active bleeding, paststrokes or bleeds into the brain, or severehypertension. Situations in which thrombolysis may be considered, but with caution, include recent surgery, use of anticoagulants, pregnancy, and proclivity to bleeding.[28] Major risks of thrombolysis are major bleeding andintracranial bleeding.[28] Pre-hospital thrombolysis reduces time to thrombolytic treatment, based on studies conducted in higher income countries; however, it is unclear whether this has an impact on mortality rates.[130]
Other
In the past, high flow oxygen was recommended for everyone with a possible myocardial infarction.[85] More recently, no evidence was found for routine use in those with normal oxygen levels and there is potential harm from the intervention.[131][132][133][134][135] Therefore, oxygen is currently only recommended if oxygen levels are found to be low or if someone is in respiratory distress.[28][85]
If despite thrombolysis there is significantcardiogenic shock, continued severe chest pain, or less than a 50% improvement inST elevation on the ECG recording after 90 minutes, then rescue PCI is indicated emergently.[136][137]
Those who have hadcardiac arrest may benefit fromtargeted temperature management with evaluation for implementation of hypothermia protocols. Furthermore, those with cardiac arrest, and ST elevation at any time, should usually have angiography.[19]Aldosterone antagonists appear to be useful in people who have had an STEMI and do not have heart failure.[138]
Rehabilitation and exercise
Cardiac rehabilitation benefits many who have experienced myocardial infarction,[72] even if there has been substantial heart damage and resultantleft ventricular failure. It should start soon after discharge from the hospital. The program may include lifestyle advice, exercise, social support, as well as recommendations about driving, flying, sports participation, stress management, and sexual intercourse.[108] Returning to sexual activity after myocardial infarction is a major concern for most patients, and is an important area to be discussed in the provision of holistic care.[139][140]
In the short-term, exercise-based cardiovascular rehabilitation programs may reduce the risk of a myocardial infarction, reduces a large number of hospitalizations from all causes, reduces hospital costs, improveshealth-related quality of life, and has a small effect onall-cause mortality.[141] Longer-term studies indicate that exercise-based cardiovascular rehabilitation programs may reduce cardiovascular mortality and myocardial infarction.
Prognosis
The prognosis after myocardial infarction varies greatly depending on the extent and location of the affected heart muscle, and the development and management of complications.[16] Prognosis is worse with older age and social isolation.[16] Anterior infarcts, persistent ventricular tachycardia or fibrillation, development ofheart blocks, and left ventricular impairment are all associated with poorer prognosis.[16] Without treatment, about a quarter of those affected by MI die within minutes and about forty percent within the first month.[16] Morbidity and mortality from myocardial infarction has, however, improved over the years due to earlier and better treatment:[30] in those who have a STEMI in the United States, between 5 and 6 percent die before leaving the hospital and 7 to 18 percent die within a year.[19]
It is unusual for babies to experience a myocardial infarction, but when they do, about half die.[142] In the short-term, neonatal survivors seem to have a normal quality of life.[142]
Complications may occur immediately following the myocardial infarction or may take time to develop.Disturbances of heart rhythms, includingatrial fibrillation,ventricular tachycardia andfibrillation andheart block can arise as a result of ischemia, cardiac scarring, and infarct location.[16][72]Stroke is also a risk, either as a result ofclots transmitted from the heart during PCI, as a result of bleeding following anticoagulation, or as a result of disturbances in the heart's ability to pump effectively as a result of the infarction.[72]Regurgitation of blood through the mitral valve is possible, particularly if the infarction causes dysfunction of the papillary muscle.[72]Cardiogenic shock as a result of the heart being unable to adequately pump blood may develop, dependent on infarct size, and is most likely to occur within the days following an acute myocardial infarction. Cardiogenic shock is the largest cause of in-hospital mortality.[30][72] Rupture of the ventricular dividing wall or left ventricular wall may occur within the initial weeks.[72]Dressler's syndrome, a reaction following larger infarcts and a cause ofpericarditis is also possible.[72]
Heart failure may develop as a long-term consequence, with an impaired ability of heart muscle to pump, scarring, and an increase in the size of the existing muscle.Aneurysm of the left ventricle myocardium develops in about 10% of MI and is itself a risk factor for heart failure, ventricular arrhythmia, and the development ofclots.[16]
Myocardial infarction is a common presentation ofcoronary artery disease. TheWorld Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease;[146] with it being the leading cause of death in high- or middle-income countries and second only tolower respiratory infections inlower-income countries.[146] Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year.[18] STEMIs occur about twice as often in men as women.[19]
Rates of death from ischemic heart disease (IHD) have slowed or declined in most high-income countries, although cardiovascular disease still accounted for one in three of all deaths in the US in 2008.[147] For example, rates of death from cardiovascular disease have decreased almost a third between 2001 and 2011 in the United States.[148]
In contrast, IHD is becoming a more common cause of death in the developing world. For example, inIndia, IHD had become the leading cause of death by 2004, accounting for 1.46 million deaths (14% of total deaths) and deaths due to IHD were expected to double during 1985–2015.[149] Globally,disability adjusted life years (DALYs) lost to ischemic heart disease are predicted to account for 5.5% of total DALYs in 2030, making it the second-most-important cause of disability (afterunipolar depressive disorder), as well as the leading cause of death by this date.[146]
Race: In the U.S.African Americans have a greater burden of myocardial infarction and other cardiovascular events. On a population level, there is a higher overallprevalence of risk factors that are unrecognized and therefore not treated, which places these individuals at a greater likelihood of experiencing adverse outcomes and therefore potentially highermorbidity andmortality.[155] Similarly, South Asians (including South Asians that have migrated to other countries around the world) experience higher rates of acute myocardial infarctions at younger ages, which can be largely explained by a higher prevalence of risk factors at younger ages.[156]
Socioeconomic status: Among individuals who live in the low-socioeconomic (SES) areas, which is close to 25% of the US population, myocardial infarctions (MIs) occurred twice as often compared with people who lived in higher SES areas.[157]
Immigration status: In 2018 many lawfully presentimmigrants who were eligible for coverage remained uninsured because immigrant families faced a range of enrollment barriers, including fear, confusion about eligibility policies, difficulty navigating the enrollment process, andlanguage andliteracy challenges. Uninsuredundocumented immigrants are ineligible for coverage options due to their immigration status.[158]
Health care access: Lack ofhealth insurance and financial concerns about accessing care were associated with delays in seeking emergency care for acute myocardial infarction which can have significant, adverse consequences on patient outcomes.[159]
Education: Researchers found that compared to people withgraduate degrees, those with lower educational attainment appeared to have a higherrisk of heart attack, dying from acardiovascular event, and overall death.[160]
Society and culture
Depictions of heart attacks in popular media often include collapsing or loss of consciousness which are not common symptoms; these depictions contribute to widespread misunderstanding about the symptoms of myocardial infarctions, which in turn contributes to people not getting care when they should.[161]
Legal implications
Atcommon law, in general, a myocardial infarction is adisease but may sometimes be aninjury. This can create coverage issues in the administration of no-fault insurance schemes such asworkers' compensation. In general, a heart attack is not covered;[162] however, it may be awork-related injury if it results, for example, from unusual emotional stress or unusual exertion.[163] In addition, in some jurisdictions, heart attacks had by persons in particular occupations such aspolice officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person having had an MI may be prevented from participating in activity that puts other people's lives at risk, for example driving a car or flying an airplane.[164]
^Coventry LL, Finn J, Bremner AP (2011). "Sex differences in symptom presentation in acute myocardial infarction: a systematic review and meta-analysis".Heart & Lung.40 (6):477–91.doi:10.1016/j.hrtlng.2011.05.001.PMID22000678.
^"Electrocardiogram".NHLBI, NIH. 9 December 2016.Archived from the original on 11 April 2017. Retrieved10 April 2017.
^abcdefghijklmnColledge NR, Walker BR, Ralston SH, Davidson LS (2010).Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill Livingstone/Elsevier. pp. 588–599.ISBN978-0-7020-3085-7.
^abcdKasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J (2015).Harrison's Principles of Internal Medicine. McGraw Hill Education. pp. 98–99.ISBN978-0-07-180215-4.OCLC923181481.
^Gupta R, Munoz R (August 2016). "Evaluation and Management of Chest Pain in the Elderly".Emergency Medicine Clinics of North America.34 (3):523–42.doi:10.1016/j.emc.2016.04.006.PMID27475013.
^Marcus GM, Cohen J, Varosy PD, Vessey J, Rose E, Massie BM, et al. (January 2007). "The utility of gestures in patients with chest discomfort".The American Journal of Medicine.120 (1):83–9.doi:10.1016/j.amjmed.2006.05.045.PMID17208083.
^Canto JG, Goldberg RJ, Hand MM, Bonow RO, Sopko G, Pepine CJ, Long T (December 2007). "Symptom presentation of females with acute coronary syndromes: myth vs reality".Archives of Internal Medicine.167 (22):2405–2413.doi:10.1001/archinte.167.22.2405.PMID18071161.
^Coventry LL, Finn J, Bremner AP (November–December 2011). "Sex differences in symptom presentation in acute myocardial infarction: a systematic review and meta-analysis".Heart & Lung.40 (6):477–491.doi:10.1016/j.hrtlng.2011.05.001.PMID22000678.
^Chen W, Woods SL, Puntillo KA (July–August 2005). "Sex differences in symptoms associated with acute myocardial infarction: a review of the research".Heart & Lung.34 (4):240–247.doi:10.1016/j.hrtlng.2004.12.004.PMID16027643.
^DeVon HA, Zerwic JJ (July–August 2002). "Symptoms of acute coronary syndromes: are there gender differences? A review of the literature".Heart & Lung.31 (4):235–245.doi:10.1067/mhl.2002.126105.PMID12122387.
^Ashton R, Raman D."Dyspnea".www.clevelandclinicmeded.com. Cleveland Clinic.Archived from the original on 11 July 2017. Retrieved24 May 2017.
^Davis TM, Fortun P, Mulder J, Davis WA, Bruce DG (March 2004). "Silent myocardial infarction and its prognosis in a community-based cohort of Type 2 diabetic patients: the Fremantle Diabetes Study".Diabetologia.47 (3):395–399.doi:10.1007/s00125-004-1344-4.PMID14963648.S2CID12567614.
^Rubin E, Gorstein F, Rubin R, Schwarting R, Strayer D (2001).Rubin's Pathology — Clinicopathological Foundations of Medicine. Maryland: Lippincott Williams & Wilkins. p. 549.ISBN978-0-7817-4733-2.
^abcChowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. (March 2014). "Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis".Annals of Internal Medicine.160 (6):398–406.doi:10.7326/M13-1788.PMID24723079.
^Mustafic H, Jabre P, Caussin C, Murad MH, Escolano S, Tafflet M, et al. (February 2012). "Main air pollutants and myocardial infarction: a systematic review and meta-analysis".JAMA.307 (7):713–21.doi:10.1001/jama.2012.126.PMID22337682.
^Ho AF, Wah W, Earnest A, Ng YY, Xie Z, Shahidah N, et al. (November 2018). "Health impacts of the Southeast Asian haze problem – A time-stratified case crossover study of the relationship between ambient air pollution and sudden cardiac deaths in Singapore".International Journal of Cardiology.271:352–358.doi:10.1016/j.ijcard.2018.04.070.PMID30223374.S2CID52282745.
^Chatzidimitriou D, Kirmizis D, Gavriilaki E, Chatzidimitriou M, Malisiovas N (October 2012). "Atherosclerosis and infection: is the jury still not in?".Future Microbiology.7 (10):1217–30.doi:10.2217/fmb.12.87.PMID23030426.
^Sánchez-Manubens J, Bou R, Anton J (February 2014). "Diagnosis and classification of Kawasaki disease".Journal of Autoimmunity.48–49:113–7.doi:10.1016/j.jaut.2014.01.010.PMID24485156.
^Clarke R, Halsey J, Bennett D, Lewington S (February 2011). "Homocysteine and vascular disease: review of published results of the homocysteine-lowering trials".Journal of Inherited Metabolic Disease.34 (1):83–91.doi:10.1007/s10545-010-9235-y.PMID21069462.S2CID8714058.
^Lonn E (September 2007). "Homocysteine in the prevention of ischemic heart disease, stroke and venous thromboembolism: therapeutic target or just another distraction?".Current Opinion in Hematology.14 (5):481–7.doi:10.1097/MOH.0b013e3282c48bd8.PMID17934354.S2CID8734056.
^abcdefColledge NR, Walker BR, Ralston SH, Davidson LS (2010).Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill Livingstone/Elsevier. pp. 577–9.ISBN978-0-7020-3085-7.
^abBolooki HM, Askari A (August 2010)."Acute Myocardial Infarction".www.clevelandclinicmeded.com.Archived from the original on 28 April 2017. Retrieved24 May 2017.
^abAaronson PI, Ward JP, Connolly MJ (2013).The cardiovascular system at a glance (4th ed.). Chichester, West Sussex: Wiley-Blackwell. pp. 88–89.ISBN978-0-470-65594-8.
^Kutty RS, Jones N, Moorjani N (November 2013). "Mechanical complications of acute myocardial infarction".Cardiology Clinics (Review).31 (4):519–31,vii–viii.doi:10.1016/j.ccl.2013.07.004.PMID24188218.
^Lipinski MJ, Escárcega RO, D'Ascenzo F, Magalhães MA, Baker NC, Torguson R, et al. (May 2014). "A systematic review and collaborative meta-analysis to determine the incremental value of copeptin for rapid rule-out of acute myocardial infarction".The American Journal of Cardiology.113 (9):1581–91.doi:10.1016/j.amjcard.2014.01.436.PMID24731654.
^abcColledge NR, Walker BR, Ralston SH, Davidson LS (2010).Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill Livingstone/Elsevier. pp. 529–30.ISBN978-0-7020-3085-7.
^Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J (2015).Harrison's principles of internal medicine. McGraw Hill Education. p. 1457.ISBN978-0-07-180215-4.OCLC923181481.
^abcColledge NR, Walker BR, Ralston SH, Davidson LS (2010).Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill Livingstone/Elsevier. pp. 535, 539.ISBN978-0-7020-3085-7.
^Stradling C, Hamid M, Taheri S, Thomas GN (2014). "A review of dietary influences on cardiovascular health: part 2: dietary patterns".Cardiovascular & Hematological Disorders Drug Targets.14 (1):50–63.doi:10.2174/1871529x14666140701095426.PMID24993125.
^Fortmann SP, Burda BU, Senger CA, Lin JS, Whitlock EP (December 2013). "Vitamin and mineral supplements in the primary prevention of cardiovascular disease and cancer: An updated systematic evidence review for the U.S. Preventive Services Task Force".Annals of Internal Medicine.159 (12):824–34.doi:10.7326/0003-4819-159-12-201312170-00729.PMID24217421.S2CID17366251.
^Hodis HN, Mack WJ (July 2014). "Hormone replacement therapy and the association with coronary heart disease and overall mortality: clinical application of the timing hypothesis".The Journal of Steroid Biochemistry and Molecular Biology.142:68–75.doi:10.1016/j.jsbmb.2013.06.011.PMID23851166.S2CID30838065.
^Perez MI, Musini VM, Wright JM (October 2009). "Effect of early treatment with anti-hypertensive drugs on short and long-term mortality in patients with an acute cardiovascular event".The Cochrane Database of Systematic Reviews (4): CD006743.doi:10.1002/14651858.CD006743.pub2.PMID19821384.
^Jobs A, Mehta SR, Montalescot G, Vicaut E, Van't Hof AW, Badings EA, et al. (August 2017). "Optimal timing of an invasive strategy in patients with non-ST-elevation acute coronary syndrome: a meta-analysis of randomised trials".Lancet.390 (10096):737–746.doi:10.1016/S0140-6736(17)31490-3.PMID28778541.S2CID4489347.
^Sepehrvand N, James SK, Stub D, Khoshnood A, Ezekowitz JA, Hofmann R (October 2018). "Effects of supplemental oxygen therapy in patients with suspected acute myocardial infarction: a meta-analysis of randomised clinical trials".Heart.104 (20):1691–1698.doi:10.1136/heartjnl-2018-313089.PMID29599378.S2CID4472549.
^Rahim L, Allana S, Steinke EE, Ali F, Khan AH (November 2017). "Level of knowledge among cardiac nurses regarding sexual counseling of post-MI patients in three tertiary care hospitals in Pakistan".Heart & Lung.46 (6):412–416.doi:10.1016/j.hrtlng.2017.09.002.PMID28988654.S2CID4277993.
^abPapneja K, Chan AK, Mondal TK, Paes B (March 2017). "Myocardial Infarction in Neonates: A Review of an Entity with Significant Morbidity and Mortality".Pediatric Cardiology.38 (3):427–441.doi:10.1007/s00246-016-1556-7.PMID28238152.S2CID20779415.
^Weir RA, McMurray JJ, Velazquez EJ (May 2006). "Epidemiology of heart failure and left ventricular systolic dysfunction after acute myocardial infarction: prevalence, clinical characteristics, and prognostic importance".The American Journal of Cardiology.97 (10A):13F –25F.doi:10.1016/j.amjcard.2006.03.005.PMID16698331.
^abcWorld Health Organization (2008).The Global Burden of Disease: 2004 Update. Geneva: World Health Organization.ISBN978-92-4-156371-0.
^Gupta R, Joshi P, Mohan V, Reddy KS, Yusuf S (January 2008). "Epidemiology and causation of coronary heart disease and stroke in India".Heart.94 (1):16–26.doi:10.1136/hrt.2007.132951.PMID18083949.S2CID27117207.
Min Cho S, et al. (2021). "Machine learning compared with conventional statistical models for predicting myocardial infarction readmission and mortality: a systematic review".Canadian Journal of Cardiology.37 (8). Elsevier:1207–1214.doi:10.1016/j.cjca.2021.02.020.PMID33677098.S2CID232141652.
