Myocardial infarction

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

Acute myocardial infarction (AMI or MI), commonly known as a heart attack, is a serious, sudden heart condition usually characterized by varying degrees of chest pain or discomfort, weakness, sweating, nausea, and vomiting, sometimes causing loss of consciousness. It occurs when a part of the heart muscle dies because of sudden total interruption of blood flow to that area. The medical term myocardial infarction comes from "myo" referring to muscle, "cardium" referring to the heart (myocardium is the heart muscle) and "infarction" meaning tissue death, in this case caused by an obstruction of blood flow. (The phrase "heart attack" is occasionally used to refer to heart problems other than a myocardial infarction, such as unstable angina pectoris.)

A heart attack is a life-threatening medical emergency which demands immediate activation of the emergency medical services. Immediate transport by ambulance to a hospital where advanced cardiac life support (ACLS) is available needs to be arranged. The more time that passes before medical attention is sought, the more severe the permanent heart damage is likely to be, and the less likely survival will be.


Signs and symptoms

The main symptom of myocardial infarction is most commonly central chest discomfort, which is present in about 2/3 of all cases. It is often described as "intense pressure" ("like an elephant sitting on your chest") however the pressure may be mild, or felt as either a sharp or stabbing pain. The discomfort may radiate to the shoulders and/or arms (usually the left side), neck (carotid area usually) or the back and can be slight, moderate, or severe. Associated symptoms include nausea, vomiting, shortness of breath, diaphoresis (excessive sweating), palpitations and dizziness. The more of these symptoms present, the more likely the diagnosis. Women's symptoms often have atypical features.

Some patients present with acute arrhythmia, mainly ventricular fibrillation or ventricular tachycardia, but occasionally pulseless electrical activity (PEA, formerly known as "electro-mechanical dissociation" or EMD) which can rapidly lead to death if untreated. These complications require cardiopulmonary resuscitation (CPR).

Myocardial infarctions vary widely in severity. Not all heart attacks are recognized by either the people having them nor, necessarily, by well-trained medical personnel on clinical grounds alone.

In women and patients with diabetes mellitus, the symptoms of myocardial infarction can be vague and non-specific. Women often simply report decreased exercise tolerance and breathlessness.

Diabetics less commonly experience chest discomfort; they may have only cold sweats, nausea, pain in the arm, back, jaw, or stomach (so called "anginal equivalents"), or abdominal pain. The mechanism behind this phenomenon is thought to be polyneuropathy (peripheral nerve damage), which commonly develops in longstanding diabetics and may blunt or alter the symptoms associated with a heart attack. This results in a high incidence of "silent" myocardial infarctions in patients with diabetes.


Classical cases of myocardial infarction are often identified by ambulance staff or emergency room doctors without further investigations. Nevertheless, for a complete diagnosis, the medical history, combined with electrocardiogram results and blood tests, is vital.

Missing image
12 Lead Electrocardiogram (ECG) with ST segment elevation in Leads II, III and aVF for an inferior Acute Miocardial Infarction (AMI).


Electrocardiogram (ECG/EKG) findings suggestive of MI are elevations of the ST segment and changes in the T wave. After a myocardial infarction, changes can often be seen on the ECG called Q waves, representing scarred heart tissue.

Myocardial markers

Cardiac enzymes are proteins from cardiac tissue found in the blood. 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 phosphokinase (CPK) was very specific for myocardial injury. Current guidelines are generally in favor of troponin isoenzymes I or T, which are thought to rise before permanent injury develops. A positive troponin 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 used to require that all three components (history, ECG, and enzymes) were positive for MI. Currently the cardiac enzymes have become so reliable that enzyme elevations alone are considered reliable measures of cardiac injury, with ECG serving to determine where in the heart the damage has occurred, and history serving to screen patients for further enzyme and ECG testing.

In difficult cases or in situations where intervention to restore blood flow is appropriate, an angiogram can be done (see below for an image). Using a catheter inserted into an artery (usually the femoral artery), obstructed or narrowed vessels can be identified, and angioplasty applied as a therapeutic measure (see below). Angiography requires extensive skill, especially in emergency settings, and may not always be available out of hours. It is commonly performed by cardiologists. There is a small risk of dissection (tearing) of the blood vessels and of hemorrhage at the insertion site of the catheter: when this occurs open chest cardiac surgery is used as a last-ditch fallback therapy.


Ischemia and infarction

The underlying mechanism of a heart attack is the 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.

The decrease in blood supply has the following consequences:

  1. Heart muscle which has lost blood flow long enough, e.g. 10-15 minutes, ends up dying (necrosis) and does not grow back. Thus the heart ends up permanently weaker as a pump for the remainder of the individual's life;
  2. Injured, but still living, heart muscle conducts the electrical impulses which initiate each heart beat much more slowly. The speed can end up so slow that the spreading impulse is preserved long enough for the uninjured muscle to complete contraction; now the slowed electrical signal, still traveling 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 called ventricular tachycardia (V-Tach) or ventricular fibrillation (V-Fib), then the rapid heart rate effectively stops heart pumping. 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 stimulates the entire heart muscle to contract all at once, 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.

Histopathological examination of the heart shows that there is a circumscribed area of ischemic necrosis (coagulative necrosis). In the first 12-48 hours, myocardial fibers are still well delineated, with intense eosinophilic (pink) cytoplasm, but lose their transversal striations and the nucleus. The interstitial space may be infiltrated with red blood cells.

When the healing has commenced (e.g. after 5 -10 days) the area of coagulative ischemic necrosis shows myocardial fibers with preservation of their contour, but the cytoplasm is intensely eosinophilic and transversal striations and nuclei are completely lost. The interstitium of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages, in order to phagocytose the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the infarct with a fibrous (collagenous) scar.


The most common cause of heart attack by far is atherosclerosis, a gradual buildup of cholesterol and fibrous tissue in plaques in the arterial wall. Plaques can become unstable, rupture, and form a thrombus (blood clot) that occludes the artery. When this process happens in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium). All risk factors for atherosclerosis are also (modifiable) risk factors for ischemic heart disease: older age, smoking, hypercholesterolemia, diabetes (or insulin resistance) and obesity.


The blood flow problem is nearly always a result of exposure of atheroma tissue within the wall of the artery to the blood flow inside the artery, atheroma being the primary lesion of the atherosclerotic process. The many blood stream column irregularities, visible in the single frame angiogram image to the right, reflects artery lumen changes as a result of decades of advancing atherosclerosis.

Heart attacks can also infrequently occur if the workload of the heart suddenly rises and the necessary oxygen cannot be supplied quickly enough. This is why extreme stress or physical exertion can result in heart attacks. Sudden contraction of coronary arteries in cocaine abuse can also precipitate myocardial infarction.

First aid

Immediate care

As myocardial infarction is a common medical emergency, the signs are often part of first aid courses. General management in the acute setting is:

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 rhythm and determine whether the arrhythmia is amenable to defibrillation ("shockable").

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 medical 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

Doctors traveling by commercial aircraft may be able to assist an MI patient by using the on-board first aid kit, which contains basic cardiac drugs used in advanced cardiac life support, and oxygen. Flight attendants are generally aware of the location of these materials. Pilots are required to divert the flight to the nearest airport.


First line

In the hospital, oxygen, aspirin, nitroglycerin and analgesia (usually morphine, hence the popular mnemonic MONA) are administered as soon as possible, if this has not already happened during transport.


The ultimate goal of the management in the acute phase of the disease is to salvage as much myocardium as possible and restore contractile function of heart chambers. This is achieved primarily with thrombolytic drugs, such as streptokinase, urokinase, alteplase (recombinant tissue plasminogen activator, rtPA) or reteplase. Heparin alone as an anticoagulant is substandard.

Although clinical trials suggest better outcomes, angioplasty as a first-line measure is probably still underused. This is largely dependent on the availability of an experienced interventional cardiologist on-site, or the availability of rapid transport to a referral centre.

Emergency coronary surgery, in the form of coronary artery bypass surgery is another option, although this option is in decline since the development of primary angioplasty. The same limitations apply here: cardiothoracic surgery services are not available in many hospitals.

Monitoring and follow-up

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.

Long-term beta-blocker medication is routinely commenced. Patients are also initiated on aspirin and/or clopidogrel (Plavix®); other anticoagulant drugs have not shown additional benefit. ACE inhibitors are commenced in the course of follow-up to assist in ventricular remodeling. Recent studies have shown benefit of the initiation of a statin (e.g. simvastatin 40 mg daily), even in patients without known hypercholesterolemia.

Patients are discouraged from working and sexual activity for about two months, while they undergo cardiac rehabilitation training. Local authorities may place limitations on driving motorised vehicles.

During a follow-up outpatient visit, it will be determined if the patient suffers from angina pectoris. If this is the case, treadmill testing or angiography are often performed to identify treatable causes, as this will decrease the risk of future myocardial infarction.


Before the discovery of the electrocardiogram, it was impossible to diagnose myocardial infarction. The term angina pectoris had already been extant for 150 years (William Heberden coined the term in 1772), but little was known about the disease mechanism.

As a disease entity, myocardial infarction was described in full by Dr James Herrick in an 1912 article in JAMA. He is credited as the originator of the "thrombogenic theory", i.e. the theory that myocardial infarction is due to thrombosis in the coronary artery.

A major breakthrough in the identification of risk factors was the 1956 British doctors study, which showed an increased risk of myocardial infarction in heavy smokers.


  • Herrick JB. Clinical features of sudden obstruction of the coronary arteries. JAMA 1912;59:2015-2019.
  • Atlas of Pathology (

See also

de:Myokardinfarkt es:Ataque cardiaco fr:Infarctus du myocarde ko:심근경색 it:Infarto del miocardio he:התקף לב nl:Hartaanval ja:心筋梗塞 no:Hjerinfarkt sv:Hjrtinfarkt pl:Zawał mięśnia sercowego


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