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Myocardial infarction
Specialty	Cardiology

Acute myocardial infarction (AMI or MI), commonly known as a heart attack, is a disease state 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" is sometimes used incorrectly to describe sudden cardiac death, which may or may not be the result of acute myocardial infarction.

Classical symptoms of acute myocardial infarction include chest pain, shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety or a feeling of impending doom. Patients frequently feel suddenly ill. Women often experience different symptoms than men. The most common symptoms of MI in women include dyspnea, weakness, and fatigue. Approximately one third of all myocardial infarctions are silent, without chest pain or other symptoms.

Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, glyceryl trinitrate and pain relief. The patient will receive a number of diagnostic tests, such as an electrocardiogram (ECG, EKG), a chest X-ray 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 developed countries, but third to AIDS and lower respiratory infections in developing countries.

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 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 are generally risk factors for myocardial infarction:

• 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, or alternatively by waist circumference or waist-hip ratio).

Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile. Non-modifiable risk factors include age, gender, and 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), and living with a partner may also contribute 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 its effect on income and marital status.

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.

Inflammation is known to be an important step in the process of atherosclerotic plaque formation. 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. 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.

Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis is very common, this could have great consequences for public health. Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease. Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines; thus, periodontitis may mediate its effect on MI risk via other risk factors. Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells. A role for specific periodontal bacteria has been suggested but remains to be established.

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

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If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form a cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction. As a result, the patient's heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias.

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), 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), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. Heart output and blood pressure may fall to dangerous levels, which is particularly bad for the patient experiencing acute myocardial infarction.

The cardiac defibrillator device was specifically designed for stopping these potentially fatal arrhythmias. If used properly, defibrillation stops and resets the electrical impulses in all heart cells —in effect "rebooting" the heart. If used quickly after the onset of V-Tach or V-Fib, the defibrillator has a high success rate in reverting the heart back to a normal heart rhythm.

Causes

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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 Sohbet 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 absence of Q-waves also has clinical importance, with improved outcomes associated with a lack of Q waves.

Symptoms

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.

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 ST segment elevation and changes in the T wave. ST segment elevation is usually evident within minutes 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 may also be 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:

Left bundle branch block and pacing can interfere with the electrocardiographic diagnosis of coronary ischemia. They are known as QRS confounders, or mimics of acute myocardial infarction. The GUSTO investigators Sgarbossa et al. developed a set of criteria for identifying acute myocardial infarction in the presence of left bundle branch block and paced rhythm. They include concordant ST segment elevation, discordant ST segment elevation > 5 mm, and concordant ST segment depression in the left precordial leads.

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 favor 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

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

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, the signs are often part of first aid courses. The emergency action principles also apply in the case of myocardial infarction.

Immediate care

When symptoms of myocardial infarction occur, people wait on average 3 hours, instead of doing what is recommended: calling for help immediately. Acting immediately by calling the emergency services can prevent sustained damage to the heart ("time is muscle").

Certain positions allow the patient to rest in a position which minimizes breathing difficulties. A half-sitting position with knees bent is often recommended. Access to more oxygen can be given by opening the window and widening the collar for easier breathing.

Aspirin can be given quickly (if the patient is not allergic to aspirin); but taking aspirin before calling the emergency medical services may be associated with unwanted delay. Aspirin has an antiplatelet effect which inhibits formation of further thrombi (blood clots) that clog arteries. Non-enteric coated or soluble preparations are preferred. If chewed or dissolved, respectively, they can be absorbed by the body even quicker. If the patient cannot swallow, the aspirin can be used sublingually. U.S. guidelines recommend a dose of 162 – 325 mg. Australian guidelines recommend a dose of 150 – 300 mg.

Glyceryl trinitrate (nitroglycerin) sublingually (under the tongue) can be given if it has been prescribed for the patient.

Other general first aid principles include monitoring pulse, breathing, level of consciousness and, if possible, the blood pressure of the patient. In case of cardiac arrest, cardiopulmonary resuscitation (CPR) can be administered.

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 personnel 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, only aspirin has been proven to decrease mortality.

Reperfusion

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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 their 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. If hemodynamic instability develops in individuals with NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of thrombolytic agents is contraindicated in this patient subset, however.

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) and subsequent q waves on EKG after reperfusion therapy. Such a successful 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 are contraindicated for the treatment of NSTEMIs and for the treatment of individuals with evidence of cardiogenic shock.

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.

Primary PCI involves performing a coronary angiogram to determine the anatomical location of the infarcting vessel, followed by balloon angioplasty (and frequently deployment of an intracoronary stent) of the thrombosed arterial segment. In some settings, an extraction catheter may be used to attempt to aspirate (remove) the thrombus prior to balloon angioplasty. While the use of intracoronary stents do not improve the short term outcomes in primary PCI, the use of stents is widespread because of the decreased rates of procedures to treat restenosis compared to balloon angioplasty.

Adjuvent therapy during primary PCI include intravenous heparin, aspirin, and clopidogrel. The use of glycoprotein IIb/IIIa inhibitors are often used in the setting of primary PCI to reduce the risk of ischemic complications during the procedure. Due to the number of antiplatelet agents and anticoagulants used during primary PCI, the risk of bleeding associated with the procedure are higher than during an elective PCI.

Coronary artery bypass surgery

The current data for emergency bypass surgery for the treatment of an acute myocardial infarction is sparse. Current surgical literature suggests waiting a number of weeks to allow the infarction to "cool down" prior to undergoing coronary artery bypass graft surgery (CABG). The mortality is significantly higher if the bypass surgery is performed during the acute ischemic period.

Due to the safety afforded by percutaneous coronary intervention during the acute ischemic period of a myocardial infarction, the number of patients that are sent for emergency bypass surgery for treatment of the myocardial infarction has decreased in the last decade. Emergency CABG for treatment of an acute myocardial infarction is reserved for individuals with extremely high risk features in the cardiac catheterization lab, including thrombosis of the left main or ostial left anterior descending arteries, or for features of cardiogenic shock with viable myocardium that appears to be in jeopardy due to the infarction. However, even these extremely high risk patients may undergo successful PCI when performed by experienced operators, and the decision on which patients would benefit from urgent CABG requires a collaborative approach between the interventional cardiologist and the cardiothoracic surgeon.

Coronary artery bypass surgery involves an artery or vein from the patient being 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 *Canlı Tv 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 plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased.
• 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

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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.

Congestive heart failure

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

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.

Risk factors for myocardial rupture include completion of infarction (no revascularization performed), female sex, advanced age, and a lack of a previous history of myocardial infarction. The shear stress between the infarcted segment and the surrounding normal myocardium (which may be hypercontractile in the post-infarction period) makes it a nidus for rupture.

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.

Life-threatening arrhythmia

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 ischemia in the electrical conduction system of the heart may cause a complete heart block (when the impulse from the sinoatrial node, the normal cardiac pacemaker, doesn't reach the heart chambers any more).

Pericarditis

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.

Cardiogenic shock

A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following it is cardiogenic shock. Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amout of oxygenated blood to the tissues of the body.

While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated.

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.

See also

• Cardiac arrest
• Hibernating myocardium
• Stunned myocardium
• Ventricular remodeling

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External links

• Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study, from the United States National Heart, Lung and Blood Institute
• Heart Attack - overview of resources from MedlinePlus.
• Regional PCI for STEM Resource Center - Evidence based online resource center for the development of regional PCI networks for acute STEMI

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• Articles lacking sources from November 2006
• Cardiovascular diseases
• Ischemic heart disease
• Medical emergencies
• Causes of death