myocardial infarction

Myocardial infarction
Classification & external resources

Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA, right coronary artery = RCA).
ICD-10	I21.-I22.
ICD-9	410
DiseasesDB	8664
MedlinePlus	000195
eMedicine	med/1567  emerg/327 ped/2520

Acute myocardial infarction (AMI or MI), more commonly known as a heart attack, is a medical condition that occurs when the blood supply to a part of the heart is interrupted, most commonly due to rupture of a vulnerable plaque. The resulting ischemia or 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.^[1] Important risk factors are a previous history of vascular disease such as atherosclerotic coronary heart disease and/or angina, a previous heart attack or stroke, any previous episodes of abnormal heart rhythms or syncope, older age—especially men over 40 and women over 50, smoking, excessive alcohol consumption, the abuse of certain illicit drugs, high triglyceride levels, high LDL ("Low-density lipoprotein") and low HDL ("High density lipoprotein"), diabetes, high blood pressure, obesity, and chronically high levels of stress in certain persons.

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 (typically radiating to the left arm), 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 from men. The most common symptoms of MI in women include shortness of breath, 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, usually morphine sulfate. The patient will receive a number of diagnostic tests, such as an electrocardiogram (ECG, EKG), a chest X-ray and blood tests to detect elevated creatine kinase or troponin levels (these are chemical markers released by damaged tissues, especially the myocardium). 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 percent of deaths worldwide were from ischemic heart disease.^[1] Ischemic heart disease is the leading cause of death in developed countries, but third to AIDS and lower respiratory infections in developing countries.^[2]

In the United States, diseases of the heart are the leading cause of death, causing a higher mortality than cancer (malignant neoplasms).^[3] 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.^[4] This means that roughly 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 sex^[5]
• Tobacco smoking
• Hypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density lipoprotein and low high density lipoprotein)
• Hyperhomocysteinemia (high homocysteine, a toxic blood amino acid that is elevated when intakes of vitamins B2, B6, B12 and folic acid are insufficient)
• Diabetes (with or without insulin resistance)
• High blood pressure
• Obesity^[6] (defined by a body mass index of more than 30 kg/m², 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.^[7] Non-modifiable risk factors include age, sex, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition.^[5]

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.^[8] 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.^[8]

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.^[9]

Inflammation is known to be an important step in the process of atherosclerotic plaque formation.^[10] 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.^[10] Moreover, some drugs for MI might also reduce CRP levels.^[10] 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.^[11] Whether CRP plays a direct role in atherosclerosis remains uncertain.^[10]

Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis is very common, this could have great consequences for public health.^[12] Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease.^[13] Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines;^[14] thus, periodontitis may mediate its effect on MI risk via other risk factors.^[15] Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells.^[16][17] A role for specific periodontal bacteria has been suggested but remains to be established.^[18]

Baldness, hair greying, a diagonal earlobe crease^[19] 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.^[20]

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.

Main article: Acute coronary syndrome

Acute myocardial infarction is a type of acute coronary syndrome, which is most frequently (but not always) a manifestation of coronary artery disease. The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades. 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).

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 of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.^[21] 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/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life threatening arrhythmia is ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which is particularly bad for the patient experiencing acute myocardial infarction.

The cardiac defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.

Triggers

Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if the exertion is more intense than the individual usually performs.^[5] 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 time frames) for people who are physically very fit.^[5] For those in poor physical condition, the rate differential is over 35-fold higher.^[5] 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.^[5]

Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.^[22] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.^[22] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.^[23]

Classification

Classification of acute coronary syndromes.^[24]

Acute myocardial infarction is a type of acute coronary syndrome, which is most frequently (but not always) a manifestation of coronary artery disease. The acute coronary syndromes include ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

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).^[25] For example, an occlusion of the left anterior descending coronary artery will result in an anterior wall myocardial infarct.^[26]

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.^[27] 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.^[26]

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,^[28] 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,^[29] with improved outcomes associated with a lack of Q waves.^[30]

The phrase "massive attack" is not a recognized medical term.

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.

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.^[31] 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.^[32] Other conditions such as aortic dissection or pulmonary embolism may present with chest pain and must be considered in the differential diagnosis.

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.

Women often experience markedly 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.^[33]

Approximately half of all MI patients have experienced warning symptoms such as chest pain prior to the infarction.^[34]

Approximately one fourth of all myocardial infarctions are silent, without chest pain or other symptoms.^[35] 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^[36] and after heart transplantation, probably because the donor heart is not connected to nerves of the host.^[37] In diabetics, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.^[36]

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).^[38] 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.^[39] Technetium and thallium can be used in nuclear medicine to visualize areas of reduced blood flow and tissue viability, respectively.^[39][40] Technetium is used in a MUGA scan.

Diagnostic criteria

WHO criteria^[41] have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers such as creatine kinase, troponin I, and lactate dehydrogenase isozymes specific for the heart.

The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.^[24] 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.^[42][43]

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.^[42][44]

12-lead electrocardiogram (ECG) showing acute inferior ST segment elevation MI (STEMI). Note the ST segment elevation in leads II, III, and aVF along with reciprocal ST segment depression in leads I and aVL.

Electrocardiogram

Main article: Electrocardiogram

The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. However, the standard 12 lead ECG has several limitations. An ECG represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture.^[45] It is therefore desirable to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring.^[46] It should also be appreciated that the standard 12 lead ECG does not directly examine the right ventricle, and does a relatively poor job of examining the posterior basal and lateral walls of the left ventricle. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG.^[45] The use of non-standard ECG leads like right-sided lead V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care.^[47] The 12 lead ECG is used to classify patients into one of three groups:

1. those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI),

2. those with ST segment depression or T wave inversion (suspicious for ischemia), and

3. those with a so-called non-diagnostic or normal ECG.^[48]

A normal ECG does not rule out acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is the hyperacute T wave, which is treated the same as ST segment elevation.^[49] In practice this is rarely seen, because it only exists for 2-30 minutes after the onset of infarction.^[50] Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia.^[51] The current guidelines for the ECG diagnosis of acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in 2 or more anatomically contiguous leads.^[48] This criterion is problematic, however, as acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients.^[52] In addition, over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead.^[53] The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, benign early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.^[54][55][53]

Left bundle branch block and pacing can interfere with the electrocardiographic diagnosis of acute myocadial 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 > 1 mm (0.1 mV), discordant ST segment elevation > 5 mm (0.5 mV), and concordant ST segment depression in the left precordial leads.^[56] The presence of reciprocal changes on the 12 lead ECG may help distinguish true acute myocardial infarction from the mimics of acute myocardial infarction. The contour of the ST segment may also be helpful, with a straight or upwardly convex (non-concave) ST segment favoring the diagnosis of acute myocardial infarction.^[57]

The constellation of leads with ST segment elevation enables the clinician to identify what area of the heart is injured, which in turn helps predict the so-called culprit artery.

As the myocardial infarction evolves, there may be loss of R wave height and development of pathological Q waves. T wave inversion may persist for months or even permanently following acute myocardial infarction.^[58] Typically, however, the T wave recovers, leaving a pathological Q wave as the only remaining evidence that an acute myocardial infarction has occurred.

Cardiac markers

Main article: Cardiac marker

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.^[59] Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future.^[60]

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.^[61]

Angiography

Angiogram of the coronary arteries.

Main article: Coronary catheterization

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 post-infarction).

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.^[62]

Although earlier changes can be discerned using electron microscopy, one of the earliest changes under a normal microscope are so-called wavy fibers.^[63] 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.^[64] 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.^[62]

These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis.^[65]

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 an average of three hours, instead of doing what is recommended: calling for help immediately.^[66][67] Acting immediately by calling the emergency services can prevent sustained damage to the heart ("time is muscle").^[68]

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.^[69] 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.^[70] Australian guidelines recommend a dose of 150 – 300 mg.^[71]

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

If an Automated External Defibrillator (AED) is available the rescuer should immediately bring the AED to the patient's side and be prepared to follow its instructions should the victim lose consciousness.

If possible the rescuer should obtain basic information from the victim, in case the patient is unable to answer questions once emergency medical technicians arrive (if the patient becomes unconscious). The victim's name and any information regarding the nature of the victims pain will useful to health care providers. Also the exact time that these symptoms started, what the patient was doing at the onset of symptoms, and anything else that might give clues to the pathology of the chest pain. It is also very important to relay any actions that have been taken, such as the number or dose of aspirin or nitroglycerin given, to the EMS personnel.

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 Medical Services (EMS) Systems vary considerably in their ability to evaluate and treat patients with suspected acute myocardial infarction. Some provide as little as first aid and early defibrillation. Others employ highly trained paramedics with sophisticated technology and advanced protocols.^[72] Early access to EMS is promoted by a 9-1-1 system currently available to 90% of the population in the United States.^[72] Most are capable of providing oxygen, IV access, sublingual nitroglycerine, morphine, and aspirin. Some are capable of providing thrombolytic therapy in the prehospital setting.^[73][74]

With primary PCI emerging as the preferred therapy for ST segment elevation myocardial infarction, EMS can play a key role in reducing door to balloon intervals (the time from presentation to a hospital ER to the restoration of coronary artery blood flow) by performing a 12 lead ECG in the field and using this information to triage the patient to the most appropriate medical facility.^{[75][76][77][78]} In addition, the 12 lead ECG can be transmitted to the receiving hospital, which enables time saving decisions to be made prior to the patient's arrival. This may include a "cardiac alert" or "STEMI alert" that calls in off duty personnel in areas where the cardiac cath lab is not staffed 24 hours a day.^[79] Even in the absence of a formal alerting program, prehospital 12 lead ECGs are independently associated with reduced door to treatment intervals in the emergency department.^[80]

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.^[81]

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.^[68]

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.^[82] Other treatment modalities may also cause complications; the use of antithrombotics for example carries an increased risk of bleeding.

First line

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. Morphine is the preferred pain relief drug due to its ability to dilate blood vessels, which aids in blood flow to the heart as well as its pain relief properties.

Of the first line agents, only aspirin has been proven to decrease mortality.^[83]

Once the diagnosis of myocardial infarction is confirmed, other pharmacologic agents are often given. These include beta blockers,^[84][85] anticoagulation (typically with heparin),^[70] and possibly additional antiplatelet agents such as clopidogrel.^[70] These agents are typically not started until the patient is evaluated by an emergency room physician or under the direction of a cardiologist. These agents can be used regardless of the reperfusion strategy that is to be employed. While these agents can decrease mortality in the setting of an acute myocardial infarction, they can lead to complications and potentially death if used in the wrong setting.

Reperfusion

The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era.^[86][87] Patients who present with suspected acute myocardial infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead ECG are presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates for immediate reperfusion, either with thrombolytic therapy, percutaneous coronary intervention (PCI) or when these therapies are unsuccessful, bypass surgery.

Individuals without ST segment elevation are presumed to be experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial therapies and 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.^[88]

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.^[89]

Thrombolytic therapy

Main article: Thrombolysis

Thrombolytic therapy is indicated for the treatment of STEMI if the drug can be administered within 12 hours of the onset of symptoms, the patient is eligible based on exclusion criteria, and primary PCI is not immediately available.^[70] The effectiveness of thrombolytic therapy is highest in the first 2 hours. After 12 hours, the risk associated with thrombolytic therapy outweighs any benefit.^[88][90] Because irreversible injury occurs within 2–4 hours of the infarction, there is a limited window of time available for reperfusion to work.

Thrombolytic drugs are contraindicated for the treatment of unstable angina and NSTEMI^[88][91] and for the treatment of individuals with evidence of cardiogenic shock.^[92]

Although no perfect thrombolytic agent exists, an ideal thrombolytic drug would lead to rapid reperfusion, have a high sustained patency rate, be specific for recent thrombi, be easily and rapidly administered, create a low risk for intra-cerebral and systemic bleeding, have no antigenicity, adverse hemodynamic effects, or clinically significant drug interactions, and be cost effective.^[93] Currently available 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.^[94][95] 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^[96] and urokinase^[97][98][99] treatment, it is less necessary there.^[94]

Intracranial bleeding (ICB) and subsequent cerebrovascular accident (CVA) is a serious side effect of thrombolytic use. The risk of ICB is dependent on a number of factors, including a previous episode of intracranial bleed, age of the individual,