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Myocardial infarction

2007 Schools Wikipedia Selection. Related subjects: Health and medicine

   CAPTION: Myocardial infarction
   Classifications 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 (LAC, right coronary artery = RAC).
   ICD- 10 I 21.- I 22.
   ICD- 9 410
   DiseasesDB 8664
   MedlinePlus 000195
   eMedicine med/1567  emerg/327 ped/2520

   Acute myocardial infarction (AMI or MI), commonly known as a heart
   attack, is a disease that occurs when the blood supply to a part of the
   heart is interrupted. The resulting oxygen shortage causes damage and
   potential death of heart tissue. It is a medical emergency, and the
   leading cause of death for both men and women all over the world.
   Important risk factors are older age, smoking, high LDL ("bad
   cholesterol") and low HDL ("good cholesterol"), diabetes, high blood
   pressure, and obesity.

   The term myocardial infarction is derived from myocardium (the heart
   muscle) and infarction (tissue death due to oxygen starvation). The
   phrase "heart attack" sometimes refers to heart problems other than MI,
   such as unstable angina pectoris and sudden cardiac death.

   Myocardial infarctions are usually accompanied by characteristic severe
   chest pain and autonomic phenomena such as looking pale, sweating and
   feeling sick.

   Initial treatment measures for someone suspected of suffering from an
   acute myocardial infarction include oxygen, aspirin, glyceryl
   trinitrate and pain relief. While these are being administered,
   diagnostic tests are often performed, including serial
   electrocardiograms (ECG, EKG), X-rays and blood tests. Further
   treatment may include either medications to break down blood clots that
   block the blood flow to the heart, or mechanically restoring the flow
   by dilatation or bypass surgery of the blocked coronary artery.
   Coronary care unit admission allows rapid and safe treatment of
   complications such as abnormal heart rhythms.

Epidemiology

   Myocardial infarction is a common presentation of ischemic heart
   disease. The WHO estimated that in 2002, 12.6% of deaths worldwide were
   from ischemic heart disease. Ischemic heart disease is the leading
   cause of death in develop countries, but in developing countries it
   third to AIDS and lower respiratory infections.

   In the United States, diseases of the heart are the leading cause of
   death, causing a higher mortality than cancer ( malignant neoplasms).
   Coronary heart disease is responsible for 1 in every 5 deaths in the
   U.S.. Some 7,200,000 men and 6,000,000 women are living with some form
   of coronary heart disease. 1,200,000 people suffer a (new or recurrent)
   coronary attack every year, and about 40% of them die as a result of
   the attack. This roughly means that every 65 seconds, an American dies
   of a coronary event.

Risk factors

   Risk factors for atherosclerosis may also be risk factors for coronary
   artery disease:
     * older age
     * male gender
     * cigarette smoking
     * hypercholesterolemia (more accurately hyperlipoproteinemia,
       especially high low density lipoprotein and low high density
       lipoprotein)
     * diabetes (with or without insulin resistance)
     * high blood pressure
     * obesity (defined by a body mass index of more than 30 kg/m^2, or
       alternatively by waist circumference or waist-hip ratio).

   These major factors are most often modifiable, so heart attacks can
   generally be prevented by a healthier lifestyle. Physical activity is
   associated with a lower risk profile. Non-modifiable factors besides
   age and gender include a family history of an early heart attack
   (before the age of 60), which is thought of as reflecting a genetic
   predisposition.

   Socioeconomic factors such as a shorter education and lower income
   (particularly in women), as well as living with a partner attribute to
   the risk of MI. To understand epidemiological study results, it's
   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 it's effect on income and marital status.

   Women who use oral contraceptives have a modestly increased risk of
   myocardial infarction, especially if they also have other risk factors,
   such as smoking.

   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. Inflammation is known to be an important step
   in the process of atherosclerotic plaque formation. Moreover, some
   drugs for MI might also reduce CRP levels. The use of high sensitivity
   CRP assays as a means of screening the general population is advised
   against, but it may be used optionally at the physician's discretion,
   in patients who already present with other risk factors or known
   coronary artery disease. Whether CRP plays a direct role in
   atherosclerosis remains uncertain.

   Baldness, hair greying, a diagonal earlobe crease and possibly other
   skin features are independent risk factors for MI. Their role remains
   controversial; a common denominator of these signs and the risk of MI
   is supposed, possibly genetic.

Pathophysiology

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

   The term "myocardial infarction" literally means that there is
   destruction of heart muscle cells due to a lack of oxygen. If these
   cells are not supplied with sufficient oxygen by the coronary arteries
   to meet their metabolic demands, they die by a process called
   infarction. Not all "heart attacks" lead to loss of heart muscle,
   particularly if the heart attack is aborted.

   The decrease in blood supply has several consequences. Heart muscle
   which has lost blood flow long enough, e.g. 10–15 minutes, undergoes
   the ischemic cascade, dies (this is called necrosis) and does not grow
   back. A collagen scar, which does not have the ability to contract,
   forms in its place. Thus the heart ends up permanently weaker as a pump
   for the remainder of the individual's life. Recent studies indicate
   that apoptosis also plays a role in the process of tissue damage
   subsequent to myocardial infarction.

   Injured, but still living, heart muscle conducts the electrical
   impulses which initiate each heart beat much more slowly. The speed can
   become so slow that the spreading impulse is preserved long enough for
   the uninjured muscle to complete contraction; now the slowed electrical
   signal, still travelling within the injured area, can re-enter and
   trigger the healthy muscle (termed re-entry) to beat again too soon for
   the heart to relax long enough and receive any blood return from the
   veins. If this re-entry process results in sustained heart rates in the
   200 to over 400 beats per minute range, a phenomenon called ventricular
   tachycardia (V-Tach) or ventricular fibrillation (V-Fib), then the
   rapid heart rate prevents the heart from pumping blood effectively.
   Heart output and blood pressure falls to near zero and the individual
   quickly dies. This is the most common mechanism of the sudden death
   that can result from a myocardial infarction.

   The cardiac defibrillator device was specifically designed for stopping
   these too rapid heart rates. If used properly, it stops and resets the
   electrical impulses in all heart cells —in effect " rebooting" the
   heart— thereby stimulating the entire heart muscle to contract together
   in synchrony, hopefully stopping continuation of the re-entry process.
   If used within one minute of onset of V-Tach or V-Fib, the
   defibrillator has a high success rate in stopping these often fatal
   arrhythmias allowing a functional heart rhythm to return.

Causes

   The most common cause of heart attack by far is atherosclerosis, a
   gradual buildup of cholesterol and fibrous tissue in plaques in the
   wall of arteries (in this case, the coronary arteries), typically over
   decades. Blood stream column irregularities visible on angiographies
   reflect artery lumen narrowing as a result of decades of advancing
   atherosclerosis. Plaques can become unstable, rupture, and additionally
   promote a thrombus (blood clot) that occludes the artery; this can
   occur in minutes. When a severe enough plaque rupture occurs in the
   coronary vasculature, it leads to myocardial infarction (necrosis of
   downstream myocardium).

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

   Increased spasm/contraction of coronary arteries and left ventricular
   hypertrophy in association with cocaine abuse can also precipitate
   myocardial infarction.

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

Classification

   According to the ICD-10's chapter on cardiovascular disease, myocardial
   infarction is a form of ischemic heart disease. The latter comprises
   several forms of angina pectoris, acute myocardial infarction (AMI),
   subsequent myocardial infarction, certain complications, other acute
   ischemic heart diseases (such as the postmyocardial infarction
   syndrome), and chronic ischemic heart disease (which includes, for
   example, coronary atherosclerosis, old MI, ischemic cardiomyopathy and
   silent myocardial ischemia). The term coronary heart disease refers to
   heart diseases that originate from atherosclerosis of the coronary
   arteries. Many people have this condition without symptoms, but as it
   progresses it can cause myocardial infarction or angina pectoris.

   Electrocardiography (ECG) allows to distinguish between different
   subtypes of myocardial infarction (ST-elevation myocardial infarction,
   STEMI and non-ST-elevation myocardial infarction, NSTEMI, discussed
   below).

   Depending on the location of the obstruction in the coronary
   circulation, different zones of the heart can become injured. Using the
   anatomical terms of location, one can describe anterior, inferior,
   lateral, apical and septal infarctions (and combinations, such as
   anteroinferior, anterolateral, and so on). For example, an occlusion of
   the left anterior descending coronary artery will result in an anterior
   wall myocardial infarct.

   Another distinction is whether a MI is subendocardial, affecting only
   the inner third to one half of the heart muscle, or transmural,
   damaging (almost) the entire wall of the heart. The inner part of the
   heart muscle is more vulnerable to oxygen shortage, because the
   coronary arteries run inward from the epicardium to the endocardium,
   and because the blood flow through the heart muscle is hindered by the
   heart contraction.

   The phrases transmural and subendocardial infarction used to be
   considered synonymous with Q-wave and non-Q-wave myocardial infarction
   respectively, based on the presence or absence of Q waves on the ECG.
   It has since been shown that there is no clear correlation between the
   presence of Q waves with a transmural infarction and the absence of Q
   waves with a subendocardial infarction, but Q waves are associated with
   larger infarctions, while the lack of Q waves is associated with
   smaller infarctions. The presence or abscence of Q-waves also has
   clinical importance, with improved outcomes associated with a lack of Q
   waves.

Symptoms

   Rough diagram of pain zones in myocardial infarction (dark red = most
   typical area, light red = other possible areas, view of the chest).
   Enlarge
   Rough diagram of pain zones in myocardial infarction (dark red = most
   typical area, light red = other possible areas, view of the chest).
   Back view.
   Enlarge
   Back view.

   The onset of symptoms in myocardial infarction (MI) is usually gradual,
   over several minutes, and rarely instantaneous. Chest pain is the most
   common symptom of acute myocardial infarction and is often described as
   a sensation of tightness, pressure, or squeezing. Chest pain due to
   ischemia (a lack of blood and hence oxygen supply) of the heart muscle
   is termed angina pectoris. Pain radiates most often to the left arm,
   but may also radiate to the lower jaw, neck, right arm, back, and
   epigastrium, where it may mimic heartburn. Any group of symptoms
   compatible with a sudden interruption of the blood flow to the heart
   are called an acute coronary syndrome.

   Shortness of breath ( dyspnea) occurs when the damage to the heart
   limits the output of the left ventricle, causing left ventricular
   failure and consequent pulmonary edema. Other symptoms include
   diaphoresis (an excessive form of sweating), weakness,
   light-headedness, nausea, vomiting, and palpitations. Loss of
   consciousness and even sudden death can occur in myocardial infarctions
   and are poor prognostic indicators.

   Women often experience different symptoms than men. 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 which may manifest as long as one month
   before the actual clinically manifested ischemic event. In women, chest
   pain may be less predictive of coronary ischemia than in men.

   Approximately half of all MI patients have experienced warning symptoms
   such as chest pain prior to the infarction.

   Approximately one third of all myocardial infarctions are silent,
   without chest pain or other symptoms. These cases can be discovered
   later on electrocardiograms or at autopsy without a prior history of
   related complaints. A silent course is more common in the elderly, in
   patients with diabetes mellitus and after heart transplantation,
   probably because the donor heart is not connected to nerves of the
   host. In diabetics, differences in pain threshold, autonomic
   neuropathy, and psychological factors have been cited as possible
   explanations for the lack of symptoms.

Diagnosis

   The diagnosis of myocardial infarction is made by integrating the
   history of the presenting illness and physical examination with
   electrocardiogram findings and cardiac markers ( blood tests for heart
   muscle cell damage). A coronary angiogram allows to visualize
   narrowings or obstructions on the heart vessels, and therapeutic
   measures can follow immediately. 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 on admittance to an
   emergency department. New regional wall motion abnormalities on an
   echocardiogram are also suggestive of a myocardial infarction and are
   sometimes performed in equivocal cases. Technetium and thallium can be
   used in nuclear medicine to visualize areas of reduced blood flow and
   tissue viability, respectively. Technetium is used in a MUGA scan.

Diagnostic criteria

   WHO criteria 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 enzymes (biomarkers) such as
       creatine kinase, troponin I, and lactate dehydrogenase isozymes
       specific for the heart.

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

Physical examination

   The general appearance of patients may vary according to the
   experienced symptoms; the patient may be comfortable, or restless and
   in severe distress with an increased respiratory rate. A cool and pale
   skin is common and points to vasoconstriction. Some patients have
   low-grade fever (38–39 °C). Blood pressure may be elevated or
   decreased, and the pulse can be become irregular.

   If heart failure ensues, elevated jugular venous pressure and
   hepatojugular reflux, or swelling of the legs due to peripheral edema
   may be found on inspection. Rarely, a cardiac bulge with a pace
   different from the pulse rhythm can be felt on precordial examination.
   Various abnormalities can be found on auscultation, such as a third and
   fourth heart sound, systolic murmurs, paradoxical splitting of the
   second heart sound, a pericardial friction rub and rales over the lung.
   12-lead electrocardiogram (ECG) with ST-segment elevation in leads II,
   III and aVF, suggestive of an inferior acute myocardial infarction
   (AMI).
   Enlarge
   12-lead electrocardiogram (ECG) with ST-segment elevation in leads II,
   III and aVF, suggestive of an inferior acute myocardial infarction
   (AMI).

Electrocardiogram

   The earliest electrocardiographic (ECG or EKG) finding resulting from
   acute myocardial infarction is the hyperacute T wave. In practice this
   is rarely seen, because it only exists for 5-30 minutes after the onset
   of infarction. Findings suggestive of MI are elevations of the ST
   segment and changes in the T wave. ST segment elevation is usually
   evident within hours of the onset of symptoms. Later, there can be loss
   of R wave height and development of pathological Q waves. The T waves
   invert which may persist for many months or even permanently.

   In addition, the presence of a new left bundle branch block in the
   appropriate clinical setting is also indicative of an acute myocardial
   infarction. After a myocardial infarction, changes can often be seen on
   the ECG called Q waves, representing scarred heart tissue. However, a
   normal ECG/EKG does not rule out a myocardial infarction.

   The ST segment elevation distinguishes between:
     * STEMI ("ST-Elevation Myocardial Infarction")
     * NSTEMI ("Non-ST-Elevation Myocardial Infarction") -- diagnosed when
       cardiac enzymes are elevated.

   The leads with abnormalities on the ECG may help identify the location:

Cardiac markers

   Cardiac markers or cardiac enzymes are proteins from cardiac tissue
   found in the blood. These proteins are released into the bloodstream
   when damage to the heart occurs, as in the case of a myocardial
   infarction. Until the 1980s, the enzymes SGOT and LDH were used to
   assess cardiac injury. Then it was found that disproportional elevation
   of the MB subtype of the enzyme creatine kinase (CK) was very specific
   for myocardial injury. Current guidelines are generally in favour of
   troponin sub-units I or T, which are very specific for the heart muscle
   and are thought to rise before permanent injury develops. Elevated
   troponins in the setting of chest pain may accurately predict a high
   likelihood of a myocardial infarction in the near future.

   The diagnosis of myocardial infarction requires two out of three
   components (history, ECG, and enzymes). When damage to the heart
   occurs, levels of cardiac markers rise over time, which is why blood
   tests for them are taken over a 24 hour period. Because these enzyme
   levels are not elevated immediately following a heart attack, patients
   presenting with chest pain are generally treated with the assumption
   that a myocardial infarction has occurred and then evaluated for a more
   precise diagnosis.

Angiography

   Angiogram of the coronary arteries.
   Enlarge
   Angiogram of the coronary arteries.

   In difficult cases or in situations where intervention to restore blood
   flow is appropriate, coronary angiography can be performed. A catheter
   is inserted into an artery (usually the femoral artery) and pushed to
   the vessels supplying the heart. Obstructed or narrowed arteries can be
   identified, and angioplasty applied as a therapeutic measure (see
   below). Angioplasty requires extensive skill, especially in emergency
   settings, and may not always be available out of hours. It is commonly
   performed by interventional cardiologists.

Histopathology

   Microscopy image (magn. ca 100x, H&E stain) from autopsy specimen of
   myocardial infarct (7 days of duration).
   Enlarge
   Microscopy image (magn. ca 100x, H&E stain) from autopsy specimen of
   myocardial infarct (7 days of duration).

   Histopathological examination of the heart may reveal infarction at
   autopsy. Under the microscope, myocardial infarction presents as a
   circumscribed area of ischemic, coagulative necrosis (cell death). On
   gross examination, the infarct is not identifiable within the first 12
   hours.

   Although earlier changes can be discerned using electron microscopy,
   one of the earliest changes under a normal microscope are so-called
   wavy fibers. Subsequently, the myocyte cytoplasm becomes more
   eosinophilic (pink) and the cells lose their transversal striations,
   with typical changes and eventually loss of the cell nucleus. The
   interstitium at the margin of the infarcted area is initially
   infiltrated with neutrophils, then with lymphocytes and macrophages,
   who phagocytose ("eat") the myocyte debris. The necrotic area is
   surrounded and progressively invaded by granulation tissue, which will
   replace the infarct with a fibrous ( collagenous) scar (which are
   typical steps in wound healing). The interstitial space (the space
   between cells outside of blood vessels) may be infiltrated with red
   blood cells.

   These features can be recognized in cases where the perfusion was not
   restored; reperfused infarcts can have other hallmarks, such as
   contraction band necrosis.

First aid

   As myocardial infarction is a common medical emergency, and the signs
   are often part of first aid courses. The emergency action principles
   also apply in the case of myocardial infarction.

Automatic external defibrillation (AED)

   Since the publication of data showing that the availability of
   automated external defibrillators (AEDs) in public places may
   significantly increase chances of survival, many of these have been
   installed in public buildings, public transport facilities, and in
   non-ambulance emergency vehicles (e.g. police cars and fire engines).
   AEDs analyze the heart's rhythm and determine whether the rhythm is
   amenable to defibrillation ("shockable"), as in ventricular tachycardia
   and ventricular fibrillation.

Emergency services

   Emergency services may recommend the patient to take nitroglycerin
   tablets or patches, in case these are available, particularly if they
   had prior heart attacks or angina.

   In an ambulance, an intravenous line is established, and the patient is
   transported immediately if breathing and pulse are present. Oxygen
   first aid is provided and the patient is calmed. Close cardiac
   monitoring (with an electrocardiogram) is initiated if available.

   If the patient has lost breathing or circulation advanced cardiac life
   support (including defibrillation) may be necessary and (at the
   paramedic level) injection of medications may be given per protocol.
   CPR is performed if there is no satisfactory cardiac output.

   About 20% of patients die before they reach the hospital — the cause of
   death is often ventricular fibrillation.

Wilderness first aid

   In wilderness first aid, a possible heart attack justifies evacuation
   by the fastest available means, including MEDEVAC, even in the earliest
   or precursor stages. The patient will rapidly be incapable of further
   exertion and have to be carried out.

Air travel

   Certified personel traveling by commercial aircraft may be able to
   assist an MI patient by using the on-board first aid kit, which may
   contain some cardiac drugs (such as glyceryl trinitrate spray, aspirin,
   or opioid painkillers) and oxygen. Pilots may divert the flight to land
   at a nearby airport. Cardiac monitors are being introduced by some
   airlines, and they can be used by both on-board and ground-based
   physicians.

Treatment

   A heart attack is a medical emergency which demands both immediate
   attention and activation of the emergency medical services. The
   ultimate goal of the management in the acute phase of the disease is to
   salvage as much myocardium as possible and prevent further
   complications. As time passes, the risk of damage to the heart muscle
   increases; hence the phrase that in myocardial infarction, "time is
   muscle", and time wasted is muscle lost.

   The treatments itself may have complications. If attempts to restore
   the blood flow are initiated after a critical period of only a few
   hours, the result is reperfusion injury instead of amelioration. Other
   treatment modalities may also cause complications; the use of
   antithrombotics for example carries an increased risk of bleeding.

First line

   In the hospital, oxygen, aspirin, glyceryl trinitrate (nitroglycerin)
   and analgesia (usually morphine, hence the popular mnemonic MONA,
   morphine, oxygen, nitro, aspirin) are administered as soon as possible.
   In many areas, first responders can be trained to administer these
   prior to arrival at the hospital.

   Of the first line agents used, the only one which has been proven to
   decrease mortality is aspirin.

Reperfusion

   Individuals with ST elevation (known as ST elevation myocardial
   infarctions or STEMIs) are typically offered urgent therapies to
   restore blood flow to the infarct zone (reperfusion). These include
   thrombolytic agents, percutaneous coronary intervention or bypass
   surgery. Individuals without ST elevations (known as non-ST elevation
   myocardial infarctions or NSTEMIs) are often stabilized with
   antiplatelet drugs and anticoagulated. If there condition remains (
   hemodynamically) stable, they can be offered either late coronary
   angiography with subsequent restoration of blood flow
   (revascularization), or non-invasive stress testing to determine if
   there is significant ischemia that would benefit from
   revascularization.

   The basis for this distinction in treatment regimens is that ST segment
   elevations on an ECG are typically due to complete occlusion of a
   coronary artery. On the other hand, in NSTEMIs there is typically a
   sudden narrowing of a coronary artery with preserved (but diminished)
   flow to the distal myocardium. Anticoagulation and antiplatelet agents
   are given to prevent the narrowed artery from occluding.

   At least 10% of patients with STEMI don't develop myocardial necrosis
   (as evidenced by a rise in cardiac markers) after reperfusion therapy.
   Such a succesfull restoration of flow to the infarct-related artery
   during an acute myocardial infarction is known as "aborting" the
   myocardial infarction. If treated within the hour, about 25% of STEMIs
   can be aborted.

Thrombolytic therapy

   Thrombolytic drugs are indicated for the treatment of STEMIs if they
   can be administered within 12 hours of the onset of symptoms. Their
   effectiveness is highest in the first 2 hours after the artery is
   occluded and rapidly decreases after that. After 12 hours, it is
   generally believed that the risks associated with thrombolytic agents
   outweigh any benefit they may have to open up the infarct-related
   artery. Because irreversible ischemic injury occurs within 2–4 hours of
   the infarction, there is a limited window of time available for
   reperfusion to work. When reperfusion occurs later, this may result in
   reperfusion injury.

   Thrombolytic agents include streptokinase, urokinase, and alteplase
   (recombinant tissue plasminogen activator, rtPA). More recently,
   thrombolytic agents similar in structure to rtPA such as reteplase and
   tenecteplase have been used. These newer agents boast efficacy at least
   as good as rtPA with significantly easier administration. The
   thrombolytic agent used in a particular individual is based on
   institution preference and the age of the patient.

   Depending on the thrombolytic agent being used, adjuvant
   anticoagulation with heparin or low molecular weight heparin may be of
   benefit. With tPA and related agents (reteplase and tenecteplase),
   heparin is needed to maintain coronary artery patency. Because of the
   anticoagulant effect of fibrinogen depletion with streptokinase and
   urokinase treatment, it is less necessary there.

   Thrombolytic therapy to abort a myocardial infarction is not always
   effective, and has a 10-20% failure rate. In cases of failure of the
   thrombolytic agent to open the infarct-related coronary artery, the
   patient is then either treated conservatively with anticoagulants and
   allowed to "complete the infarction" or percutaneous coronary
   intervention (PCI, see below) is then performed. Percutaneous coronary
   intervention in this setting is known as "rescue PCI" or "salvage PCI".
   Complications, particularly bleeding, are significantly higher with
   rescue PCI than with primary PCI due to the action of the thrombolytic
   agent.

Percutaneous coronary intervention

   Although clinical trials suggest better outcomes compared to
   thrombolytic therapy, logistic and economic obstacles seem to hinder a
   more widespread application of percutaneous coronary intervention (PCI)
   via cardiac catheterization. The use of percutaneous coronary
   intervention as a therapy to abort a myocardial infarction is known as
   primary PCI. The goal of primary PCI is to open the artery as soon as
   possible, and preferably within 90 minutes of the patient presenting to
   the emergency room. This time is referred to as the door-to-balloon
   time. Few hospitals can provide PCI within the 90 minute interval.

   The current guidelines in the United States restrict primary PCI to
   hospitals with available emergency bypass surgery as a backup, but this
   is not the case in other parts of the world.

Coronary artery bypass surgery

   Emergency coronary surgery, in the form of coronary artery bypass
   surgery is another option, if cardiothoracic surgery services are
   available. In these heart bypass operations, an artery or vein from the
   patient is implanted on the aorta to bypass narrowings or occlusions on
   the coronary arteries. Several arteries and veins can be used, however
   internal mammary artery grafts have demonstrated significantly better
   long-term patency rates than great saphenous vein grafts. In patients
   with two or more coronary arteries affected, bypass surgery is
   associated with higher long-term survival rates compared to
   percutaneous interventions. In patients with single vessel disease,
   surgery is comparably safe and effective, and may be a treatment option
   in selected cases. Bypass surgery has higher costs initially, but
   becomes cost-effective in the long term. A surgical bypass graft is
   more invasive initially but bears less risk of recurrent procedures
   (but these may be again minimally invasive).

Monitoring for arrhythmias

   Additional objectives are to prevent life-threatening arrhythmias or
   conduction disturbances. This requires monitoring in a coronary care
   unit and protocolised administration of antiarrhythmic agents.
   Antiarrhythmic agents are typically only given to individuals with
   life-threatening arrhythmias after a myocardial infarction and not to
   suppress the ventricular ectopy that is often seen after a myocardial
   infarction.

Rehabilitation

   Cardiac rehabilitation aims to optimize function and quality of life in
   those afflicted with a heart disease. This can be with the help of a
   physician, or in the form of a cardiac rehabilitation program.

   Physical exercise is an important part of rehabilitation after a
   myocardial infarction, with beneficial effects on cholesterol levels,
   blood pressure, weight, stress and mood. Some patients become afraid of
   exercising because it might trigger another infarct. Patients are
   stimulated to exercise, and should only avoid certain exerting
   activities such as shovelling. Local authorities may place limitations
   on driving motorised vehicles. Some people are afraid to have sex after
   a heart attack. Most people can resume sexual activities after 3 to 4
   weeks. The amount of activity needs to be dosed to the patients
   possibilities.

Secondary prevention

   The risk of a recurrent myocardial infarction decreases with strict
   blood pressure management and lifestyle changes, chiefly smoking
   cessation, regular exercise, a sensible diet for patients with heart
   disease, and limitation of alcohol intake.

   Patients are usually commenced on several long-term medications
   post-MI, with the aim of preventing secondary cardiovascular events
   such as further myocardial infarctions, congestive heart failure or
   cerebrovascular accident (CVA). Unless contraindicated, such
   medications may include:
     * Antiplatelet drug therapy such as aspirin and/or clopidogrel should
       be continued to reduce the risk of thrombus formation. Aspirin is
       first-line, owing to its low cost and comparable efficacy, with
       clopidogrel reserved for patients intolerant of aspirin. The
       combination of clopidogrel and aspirin may further reduce risk of
       cardiovascular events, however the risk of hemorrhage is increased.
     * Beta blocker therapy such as metoprolol or carvedilol should be
       commenced. These have been particularly beneficial in high-risk
       patients such as those with left ventricular dysfunction and/or
       continuing cardiac ischaemia. β-Blockers decrease mortality and
       morbidity. They also improve symptoms of cardiac ischemia in
       NSTEMI.

     * ACE inhibitor therapy should be commenced 24–48 hours post-MI in
       hemodynamically-stable patients, particularly in patients with a
       history of MI, diabetes mellitus, hypertension, anterior location
       of infarct (as assessed by ECG), and/or evidence of left
       ventricular dysfunction. ACE inhibitors reduce mortality, the
       development of heart failure, and decrease ventricular remodelling
       post-MI.

     * Statin therapy has been shown to reduce mortality and morbidity
       post-MI. The effects of statins may be more than their LDL lowering
       effects. The general consensus is that statins have plaque
       stabilization and multiple other ("pleiotropic") effects that may
       prevent myocardial infarction in addition to their effects on blood
       lipids.

     * The aldosterone antagonist agent eplerenone has been shown to
       further reduce risk of cardiovascular death post-MI in patients
       with heart failure and left ventricular dysfunction, when used in
       conjunction with standard therapies above.
     * Omega-3 fatty acids, commonly found in fish, have been shown to
       reduce mortality post-MI. While the mechanism by which these fatty
       acids decrease mortality is unknown, it has been postulated that
       the survival benefit is due to electrical stabilization and the
       prevention of ventricular fibrillation. However, further studies in
       a high-risk subset have not shown a clear-cut decrease in
       potentially fatal arrhythmias due to omega-3 fatty acids.

New therapies under investigation

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

   There are currently 3 biomaterial and tissue engineering approaches for
   the treatment of MI, but these are in an even earlier stage of medical
   research, so many questions and issues need to 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.

Complications

   Complications may occur immediately following the heart attack (in the
   acute phase), or may need time to develop (a chronic problem). After an
   infarction, an obvious complication is a second infarction, which may
   occur in the domain of another atherosclerotic coronary artery, or in
   the same zone if there are any live cells left in the infarct.

   A myocardial infarction may compromise the function of the heart as a
   pump for the circulation, a state called heart failure. There are
   different types of heart failure; left- or right-sided (or bilateral)
   heart failure may occur depending on the affected part of the heart,
   and it is a low-output type of failure. If one of the heart valves is
   affected, this may cause dysfunction, such as mitral regurgitation in
   the case of left-sided MI.

   Myocardial rupture is most common three to five days after myocardial
   infarction, commonly of small degree, but may occur one day to three
   weeks later, in as many as 10% of all MIs. This may occur in the free
   walls of the ventricles, the septum between them, the papillary
   muscles, or less commonly the atria. Rupture occurs because of
   increased pressure against the weakened walls of the heart chambers due
   to heart muscle that cannot pump blood out effectively. The weakness
   may also lead to ventricular aneurysm, a localized dilation or
   ballooning of the heart chamber.

   Rupture is usually a catastrophic event that may result a
   life-threatening process known as cardiac tamponade, in which blood
   accumulates within the pericardium or heart sac, and compresses the
   heart to the point where it cannot pump effectively. Rupture of the
   intraventricular septum (the muscle separating the left and right
   ventricles) causes a ventricular septal defect with shunting of blood
   through the defect from the left side of the heart to the right side of
   the heart. Rupture of the papillary muscle may also lead to acute
   mitral regurgitation and subsequent pulmonary edema and possibly even
   cardiogenic shock.

   Since the electrical characteristics of the infarcted tissue change
   (see pathophysiology section), arrhythmias are a frequent complication.
   The re-entry phenomenon may cause too fast heart rates ( ventricular
   tachycardia and even ventricular fibrillation), and lesions at the site
   of the sinoatrial node may cause a complete heart block (when the
   impulse from the atrioventricular node, the normal cardiac pacemaker,
   doesn't reach the heart chambers any more). Both cause the blood flow
   to decrease, and stagnating blood starts to clot. These blood clots may
   enter the circulation and get trapped when the vessel diameter
   decreases (for example in the lung, causing pulmonary embolism).

   As a reaction to the damage of the heart muscle, inflammatory cells are
   attracted. The inflammation may reach out and affect the heart sac.
   This is called pericarditis. In Dressler's syndrome, this occurs
   several weeks after the initial event.

   The final state can be cardiogenic shock (inadequate circulation of
   blood and oxygen delivery due to primary failure of the ventricles of
   the heart to function effectively) and death.

Prognosis

   The prognosis for patients after a myocardial infarction depends
   largely on infarct size, left ventricular function and the presence or
   absence of ventricular arrhythmias. Prognosis is significantly worsened
   if a mechanical complication ( papillary muscle rupture, myocardial
   free wall rupture, and so on) were to occur.

Legal implications

   At common law, a myocardial infarction is generally a disease, but may
   sometimes be an injury. This has implications for no-fault insurance
   schemes such as workers' compensation. A heart attack is generally not
   covered; however, it may be a work-related injury if it results, for
   example, from unusual emotional stress or unusual exertion.
   Additionally, 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 who has 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, taxi or airplane.

   Retrieved from " http://en.wikipedia.org/wiki/Myocardial_infarction"
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