Myocardial infarction
| 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). In the diagram, RCA is the right coronary artery.
|
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| ICD-10 | I21-I22 |
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
| Patient UK | Myocardial infarction |
| MeSH | D009203 |
A person having an acute MI usually has sudden chest pain that is felt behind the sternum and sometimes travels to the left arm or the left side of the neck. Additionally, the person may have shortness of breath, sweating, nausea, vomiting, abnormal heartbeats, and anxiety. Women experience fewer of these symptoms than men, but usually have shortness of breath, weakness, a feeling of indigestion, and fatigue.[1] In many cases, in some estimates as high as 64%, the person does not have chest pain or other symptoms.[2] These are called "silent" myocardial infarctions.
Important risks are previous cardiovascular disease, old age, tobacco smoking, abnormal blood levels of certain lipids, diabetes, high blood pressure, lack of physical activity, obesity, chronic kidney disease, excessive alcohol consumption, and the use of cocaine and amphetamines.[3][4] The main way to determine if a person has had a myocardial infarction are electrocardiograms (ECGs) that trace the electrical signals in the heart and testing the blood for substances associated with damage to the heart muscle. ECG testing is used to differentiate between two types of myocardial infarction based on the appearance of the tracing. An ST section of the tracing higher than the baseline is called an ST elevation MI (STEMI) which usually requires more aggressive treatment. If this is not the case, the diagnosis is confirmed with a blood test (usually troponin).
Immediate treatments for a suspected MI often include aspirin, which prevents further blood from clotting; nitroglycerin, sometimes given to treat chest pain; and oxygen.[5] STEMI is treated by restoring circulation to the heart, called reperfusion therapy, and typical methods are angioplasty, where the arteries are pushed open, and thrombolysis, where the blockage is removed using medications.[6] Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although angioplasty may be required if the person is considered to be at high risk.[7] People who have multiple blockages of their coronary arteries, particularly if they also have diabetes, may also be treated with bypass surgery (CABG).[8][9] Ischemic heart disease, which includes MI, angina, and heart failure when it happens after MI, was the leading cause of death for both men and women worldwide in 2011.[10][11]
Signs and symptoms
Rough diagram of pain zones in myocardial infarction; dark red: most
typical area, light red: other possible areas; view of the chest
Back view
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),[15] weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system[16] which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate blood flow to the brain and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in MIs.[8]
Female, elderly, and diabetic patients report atypical symptoms more frequently than their male and younger counterparts.[17][18] Women also report more numerous symptoms compared with men (2.6 on average vs. 1.8 symptoms in men).[17] The most common symptoms of MI in women include dyspnea, 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.[19] Women may also experience back or jaw pain during an episode.[20]
At least one-fourth of all MIs are silent, without chest pain or other symptoms.[2][21] 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 MIs vary between 22 and 64%.[2] A silent course is more common in the elderly,[2] in patients with diabetes mellitus[22] and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient.[23] In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.[22]
Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.[24]
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 noncatastrophic differentials include gastroesophageal reflux and Tietze's syndrome.[25]
Causes
Many of the risk factors for myocardial infarction are modifiable and thus many cases may be preventable.Lifestyle
Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease.[26] Lack of exercise has been linked to 7-12% of cases.[26][27] Less common causes include stress-related causes such as job stress, which accounts for about 3% of cases,[26] and chronic high stress levels.[28]Tobacco smoking, including secondhand smoke[29] Short-term exposure to air pollution, including carbon monoxide, nitrogen dioxide, and sulfur dioxide, but not ozone.[30] Lack of physical activity,[3] psychosocial factors including, low socioeconomic status, social isolation and negative emotions increase the risk of and are associated with worse outcomes after MI. 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.[31] Alcohol — prolonged exposure to high quantities of alcohol can increase the risk of heart attack.
There is little evidence that reducing dietary saturated fat or increasing polyunsaturated fat intake affects heart attack risk.[32] Trans fats do appear to increase risk.[32]
Disease
Diabetes mellitus (type 1 or 2),[33] high blood pressure,[29] dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides[29] Obesity[34] (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).A number of acute and chronic infections including: Chlamydophila pneumoniae, influenza, Helicobacter pylori, and Porphyromonas gingivalis among others have been linked to atherosclerosis and myocardial infarction.[35] As of 2013, there is no evidence of benefit from antibiotics or vaccination, however, calling the association into question.[35][36]
Genetic
Genome-wide association studies have found 27 genetic variants that are associated with an increased risk of myocardial infarction.[37] The 9p21 genomic locus (containing CDKN2A,2B) has the strongest association with MI.[37] The majority of these variants are in regions that have not been previously implicated in coronary artery disease. The following genes have an association with MI: PCSK9, SORT1, MIA3, WDR12, MRAS, PHACTR1, LPA, TCF21, MTHFDSL, ZC3HC1, CDKN2A, 2B, ABO, PDGF0, APOA5, MNF1ASM283, COL4A1, HHIPC1, SMAD3, ADAMTS7, RAS1, SMG6, SMG6, SNF8, LDLR, SLC5A3, MRPS6, KCNE2.[37]Other
At any given age, men are more at risk than women, particularly before menopause,[38] but because in general women live longer than men, ischemic heart disease causes slightly more total deaths in women.[3] Family history of ischaemic heart disease or MI, 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).[3]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]
An increased incidence of a heart attack is associated with time of day especially in the morning hours, more specifically around 9 am.[40][41][42]
Old age increases risk of a heart attack.[3]
Pathophysiology
See also: Acute coronary syndrome
The animation shows how plaque buildup or a coronary artery spasm can lead to a heart attack and how blocked blood flow in a coronary artery can lead to a heart attack.
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
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 their place. Recent studies indicate that another form of cell death, apoptosis, also plays a role in the process of tissue damage subsequent to MI.[48] 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 can cause sudden cardiac death. However, VT 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 device was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient 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.
Myocardial infarction results from atherosclerosis.[8] Inflammation is known to be an important step in the process of atherosclerotic plaque formation.[49] C-reactive protein (CRP) is a sensitive but nonspecific 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.[49] Moreover, some drugs for MI might also reduce CRP levels.[49] 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.[50] Whether CRP plays a direct role in atherosclerosis remains uncertain.[49]
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.[51][52][53]
Hyperhomocysteinemia (high blood levels of the amino acid homocysteine) in homocysteinuria is associated with premature atherosclerosis;[54] whether elevated homocysteine in the normal range is causal is controversial.[55]
Pathological types
The two main types of acute myocardial infarction, based on pathology, are:- Transmural AMI is 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.[56] In addition, on ECG, ST elevation and Q waves are seen.
- Subendocardial AMI involves a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia.[56] In addition, ST depression is seen on ECG.
Diagnosis
Main article: Myocardial infarction diagnosis
A cardiac troponin
rise accompanied by either typical symptoms, pathological Q waves, ST
elevation or depression, or coronary intervention is diagnostic of MI.[57]WHO criteria[58] formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with MI if two (probable) or three (definite) of the following criteria are satisfied:
- Clinical history of ischemic type chest pain lasting for more than 20 minutes
- Changes in serial ECG tracings
- Rise and fall of serum cardiac biomarkers
Classification
Myocardial infarctions are generally classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI).[43] A STEMI is the combination of symptoms related to poor oxygenation of the heart with elevation of the ST segments on the electrocardiogram followed by an increase in proteins in the blood related to heart muscles death.[59] If used, they should be started in the first 24 hours.[59] They should not be used in those who have recently taken cocaine.[60] They make up abut 25 to 40 percent of cases.[59]The phrase "heart attack" is often used non-specifically to refer to a myocardial infarction and to sudden cardiac death. An MI is different from, but can cause cardiac arrest, which is the stopping of the heartbeat. It is also distinct from heart failure, in which the pumping action of the heart is impaired. However, an MI may lead to heart failure.[8]
A 2007 consensus document classifies MI into five main types:[61]
- Type 1 – spontaneous MI related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
- Type 2 – MI secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension
- Type 3 – sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by new ST elevation, or new left bundle branch block (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 – MI associated with percutaneous coronary intervention (PCI)
- Type 4b – MI associated with stent thrombosis as documented by angiography or at autopsy
- Type 5 – MI associated with CABG
Electrocardiogram
For a person to qualify as having a STEMI, in addition to reported angina, the ECG must show new ST elevation in two or more adjacent ECG leads.[59] This must be greater than 2 mm (0.2 mV) for males and greater than 1.5 mm (0.15mV) in females if in leads V2 and V3 or greater than 1 mm (0.1 mV) if it is in other ECG leads.[59] A left bundle branch block that is believed to be new used to be considered the same as ST elevation; however, this is no longer the case.[59] In early STEMIs there may just be peaked T waves with ST elevation developing later.[59]Cardiac biomarkers
While there are a number of different biomarkers, troponins are considered to be the best[59] and reliance on older tests (such as CK-MB) or myoglobin is discouraged.[62] Copeptin may be useful to rule out MI rapidly when used along with troponin.[63]Imaging
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 an MI. Echo may be performed in equivocal cases by the on-call cardiologist.[64] 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 physiological or pharmacological stress.[64] Thallium may also be used to determine viability of tissue, distinguishing whether nonfunctional myocardium is actually dead or merely in a state of hibernation or of being stunned.[65] Medical societies recommend that the physician confirm a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis.[66] Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging.[66] Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a patient's history, physical exam, ECG, and cardiac biomarkers suggest the likelihood of a problem.[66]Prevention
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This section requires expansion. (November 2014) |
On a population level, public health measures may be used to reduce unhealthy diets (excessive salt, saturated fat and trans fat) including food labelling and marketing requirements as well as requirements for catering and restaurants, and stimulating physical activity. This may be part of regional cardiovascular disease prevention programmes, or through the health impact assessment of regional and local plans and policies.[67]
Lifestyle
People considered at high risk of cardiovascular disease or with previous cardiovascular problems are advised to keep a diet where less than 30% of the energy intake derives from fat, a diet that contains less than 7% of the energy intake in the form saturated fat, and a diet that contains less than 300 mg/day of cholesterol.[68] Replacing saturated with mono- polyunsaturated fat is also recommended,[68] as the consumption of polyunsaturated fat instead of saturated fat can decrease coronary heart disease.[69] Olive oil, rapeseed oil and related products are to be used instead of saturated fat.[68] Other recommendations include: increased intake of wholegrain starch, reduced sugar intake (particularly of refined sugar), consumption of 5 portions of fruit and vegetables daily, consumption of 2 or more portions of fish per week, and 4-5 portions of unsalted nuts, seeds or legumes per week.[68] Vitamins and mineral supplements are of no proven benefit,[70] and neither are plant stanols or sterols.[68]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 intensity aerobic exercise a week.[68] Keeping a healthy weight, drinking alcohol within the recommended limits, and smoking cessation are measures that may reduce the risk of cardiovascular disease.[68]
Medication
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.[71][72] Nevertheless, many clinical practice guidelines continue to recommend aspirin for primary prevention,[73] and some researchers feel that those with very high cardiovascular risk but low risk of bleeding should continue to receive aspirin.[74]Cholesterol-lowering drugs from the statin class may be used in those at an elevated risk of cardiovascular disease; this can be calculated with validated risk prediction tools such as QRISK2.[68]
Management
Main article: Management of acute coronary syndrome
An MI requires immediate medical attention. Treatment attempts to
save as much viable heart muscle as possible and to prevent further
complications, hence the phrase "time is [heart] muscle".[75]
Aspirin and nitroglycerin may be administered. Nitroglycerin
(administered under the tongue or intravenously) may be administered to
improve the blood supply to the heart.[62] Morphine may be used if nitroglycerin is not effective.[62] Other analgesics such as nitrous oxide are of unknown benefit.[7]In the past, high flow oxygen was recommended for everyone with possible myocardial infarction.[62] More recently, routine use was found to lead to increased mortality and infarct size.[76][77] Therefore, oxygen is currently only used if oxygen levels are found to be low or someone is in respiratory distress.[62]
STEMI
The current definitive treatment modalities for MI with ECG evidence of ST elevation (STEMI) include percutaneous coronary intervention, thrombolysis or both. Thrombolysis can either be administered in the pre-hospital or in-hospital setting. There is inconclusive evidence whether pre-hospital thrombolysis reduces death in people with STEMI compared to in-hospital thrombolysis.[78] Pre-hospital thrombolysis reduces time to receipt of thrombolytic treatment, based on studies conducted in higher income countries.[78]Primary percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a hospital in a timely manner.[79] If PCI cannot be performed within 90 to 120 minutes then fibrinolysis, preferably within 30 minutes, is recommended.[80][81] If after fibrinolysis, significant cardiogenic shock, continued severe chest pain, or less than a 50% improvement in ST elevation after 90 minutes occurs, then rescue PCI is indicated emergently.[81][82] After PCI, people are generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and clopidogrel).[83]
NSTEMI
In the absence of ST elevation, formal diagnosis of MI is delayed until a blood test for biomarkers (usually troponin) can be performed; this is 3-6 hours after the onset of symptoms. The scenario is referred to as "non-ST elevation acute coronary syndrome" (NSTEACS). In the meantime, the calculated risk of further cardiovascular events (e.g. using the GRACE score)[84] and the presence of other ECG changes and clinical features[62] determines ongoing management.People with an acute coronary syndrome where no ST elevation is demonstrated (non-ST elevation ACS or NSTEACS) are treated with aspirin.[62][84] Clopidogrel is added in many cases, particularly if the risk of cardiovascular events is felt to be high and early PCI is being considered.[84][62] Depending on whether early PCI is planned, an inhibitor of antithrombin (fondaparinux or low molecular weight heparin) may be added.[84] In very high-risk scenarios, inhibitors of the platelet glycoprotein αIIbβ3a receptor such as eptifibatide or tirofiban may be used.[84][62]
Heparins in those who have had an NSTEMI or unstable angina do not change the risk of death.[85] They do decrease the risk of having a further myocardial infarction.[85]
P2Y12 inhibitors such as clopidogrel or ticagrelor do not change the risk of death when given to people with a suspected NSTEMI prior to PCI. They do however increase the risk of bleeding and decrease the risk of further cardiovascular problems. Thus their routine use prior to PCI is of questionable value.[86]
Cardiac rehabilitation
Cardiac rehabilitation benefits many who have experienced myocardial infarction, even if there has been substantial heart damage and resultant left ventricular failure; ideally other medical conditions that could interfere with participation should be managed optimally. It should start soon after discharge from hospital. The programme may include lifestyle advice, exercise, social support, as well as recommendations about driving, flying, sport participation, stress management, and sexual intercourse.[87]Secondary prevention
A number of lifestyle recommendations are available to those who have experienced myocardial infarction. This includes the adoption of a Mediterranean-type diet, maintaining alcohol intake within recommended limits, exercising to the point of mild breathlessness for 20-30 minutes every day, stopping smoking, and trying to achieve a healthy weight.[87]People are usually started on several long-term medications after an MI, with the aim of preventing further cardiovascular events such as MIs, congestive heart failure, or strokes.
- Aspirin as well as an another antiplatelet agent such as clopidogrel or ticagrelor ("dual antiplatelet therapy" or DAPT) is continued for up to twelve months, followed by asprin indefinitely.[87] If someone has another medical condition that requires anticoagulation (e.g. with warfarin) this may need to be adjusted based on risk of further cardiac events as well as bleeding risk.[87]
- Beta blocker therapy such as metoprolol or carvedilol should be started within 24 hours, provided there is no acute heart failure or heart block.[62][59][87] The dose should be increased to the highest tolerated.[87]
- ACE inhibitor therapy should be commenced when stable and continued indefinitely at the highest tolerated dose. Those who cannot tolerate ACE inhibitors may be treated with angiotensin II receptor antagonist.[87]
- Statin therapy has been shown to reduce mortality and morbidity.[88] The protective effects of statins may be due to more than their LDL lowering effects. The general consensus is that statins have the ability to stabilize plaques and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.[89]
- Aldosterone antagonists (spironolactone or eplerenone) may be used if there is evidence of left ventricular dysfunction after an MI, ideally after commencing an ACE inhibitor.[87]
- Previous studies suggesting a benefit from omega-3 fatty acid supplementation has not been confirmed.[87]
Prognosis
The prognosis after MI varies greatly depending on a person's health, the extent of the heart damage, and the treatment given.In those who have an STEMI in the United States, between 5 to 6 percent die before leaving hospital and 7 to 18 percent die within a year.[59]
Using variables available in the emergency room, people with a higher risk of adverse outcome can be identified. One study found 0.4% of patients with a low-risk profile died after 90 days, whereas in high-risk people it was 21.1%.[90]
Some risk factors for death 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.[90][91][92] Assessment of left ventricular ejection fraction may increase the predictive power.[93] Prognosis is worse if a mechanical complication such as papillary muscle or myocardial free wall rupture occurs.[94] Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.[95]
Complications
Main article: Myocardial infarction complications
Complications may occur immediately following the heart attack (in
the acute phase), or may need time to develop (a chronic problem). Acute
complications may include heart failure if the damaged heart is no
longer able to pump blood adequately around the body; aneurysm or
rupture of the myocardium; mitral regurgitation, in particular if the infarction causes dysfunction of the papillary muscle; Dressler's syndrome; 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 MI.Epidemiology
Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease;[11] 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.[11] Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year.[96] STEMIs occur about twice as often in men as women.[59]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 USA in 2008.[97] In contrast, IHD is becoming a more common cause of death in the developing world. For example in India, 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.[98] 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 (after unipolar depressive disorder), as well as the leading cause of death by this date.[11]
Society and culture
In the United States, women who have had an MI are often treated with fewer medical interventions than men.[59]Economics
In 2011, AMI was one of the top five most expensive conditions seen during inpatient hospitalizations in the U.S., with an aggregate cost of about $11.5 billion for 612,000 hospital stays.[99]Legal implications
At common law, in general, a myocardial infarction is a disease, but may sometimes be an injury. This can create coverage issues in administration of no-fault insurance schemes such as workers' compensation. In general, a heart attack is not covered;[100] however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion.[101] 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 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.[102]Research
Patients who receive stem cell treatment by coronary artery injections of stem cells derived from their own bone marrow after an 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 STEMI are underway.[103]Currently, three biomaterial and tissue engineering approaches are used for the treatment of post-MI conditions, but these are in an even earlier stage of medical research. 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 uses 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.[104]
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