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Acute myocardial infarction (AMI or MI), commonly known as a heart attack, is a disease that occurs when the blood supply to a part of the heart is interrupted, causing death of heart tissue. It is the leading cause of death for both men and women all over the world.
The term myocardial infarction is derived from myocardium (the heart muscle) and infarction (tissue death due to oxygen starvation or ischemia). The phrase "heart attack" sometimes refers to heart problems other than MI, such as unstable angina pectoris and sudden cardiac death.
Acute myocardial infarction is usually characterized by varying degrees of chest pain, discomfort, sweating, weakness, nausea, vomiting, and arrhythmia, sometimes causing loss of consciousness and even sudden death. Chest pain is the most common symptom of acute myocardial infarction (MI) and is often described as a sensation of tightness, pressure, or squeezing. Pain radiates most often to the left arm, but may also radiate to the jaw, neck, right arm, back, and epigastrium. The patient may complain of shortness of breath (dyspnea) especially if the decrease in myocardial contractility due to the infarct is sufficient to cause left ventricular failure with pulmonary congestion or even pulmonary edema. Approximately half of all MI patients have experienced warning symptoms like angina pectoris prior to the infarction.
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 prodromal 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
Myocardial infarctions vary greatly in severity. Many cases of myocardial infarction are identified by ambulance staff, emergency room doctors and cardiac specialist nurse practitioners quickly. Other, often smaller myocardial infarctions sometimes are not recognized by victims, never receive medical attention, and can result in heart weakness and other complications. Adequate diagnosis requires a medical history, an electrocardiogram, and blood tests for heart muscle cell damage. Other information, including results of myocardial perfusion tests (see stress tests) and echocardiograms can also help establish the diagnosis of MI.
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. 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:
|Wall affected||Leads||Artery involved||Reciprocal changes|
|Anterior||V2-V4||Left coronary artery, Left Anterior descending (LAD)||II, III, aVF|
|Anterolateral||I, aVL, V3-V6||LAD and diagonal branches, circumflex and marginal branches||II, III, aVF|
|Inferior||II, III, aVF||right coronary artery (RCA)||I, aVL|
|Lateral||I, aVL, V5, V6||circumflex branch or left coronary artery||II, III, aVF|
|Posterior||V8, V9||RCA or circumflex artery||V1-V4 (R greater than S in V1 & V2, ST-segment depression, elevated T wave)|
Cardiac markers or 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 sub-units I or T, which are very specific for the myocardium and 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 requires two out of three components (history, ECG, and enzymes) to be positive for MI. Currently the cardiac markers, namely the troponins 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 very small risk of plaque and vessel rupture on balloon inflation; should this occur, then emergency open-chest cardiac surgery may be required. Patients commonly experience bruising at the catheter insertion point in the groin and occasionally a hematoma. Dissection (tearing) of the blood vessel is rare but usually managed with a local thrombotic injection.
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:
- Clinical history of ischaemic type chest pain lasting for more than 20 minutes
- Changes in serial ECG tracings
- 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.
Ischemia and infarctionThe 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:
- Heart muscle which has lost blood flow long enough, e.g. 10-15 minutes, undergoes the ischemic cascade, dies (necrosis) and does not grow back. A collagen scar, which does not have the ability to contract, forms in its place. Thus the heart ends up permanently weaker as a pump for the remainder of the individual's life.
- Injured, but still living, heart muscle conducts the electrical impulses which initiate each heart beat much more slowly. The speed can become so slow that the spreading impulse is preserved long enough for the uninjured muscle to complete contraction; now the slowed electrical signal, still 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 stops and resets the electrical impulses in all heart cells--in effect "rebooting" the heart--thereby stimulating the entire heart muscle to contract together in synchrony, hopefully stopping continuation of the re-entry process. If used within one minute of onset of V-Tach or V-Fib, the defibrillator has a high success rate in stopping these often fatal arrhythmias allowing a functional heart rhythm to return.
- 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 because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out as effectively. Rupture is usually a catastrophic event that results in pericardial tamponade (compression of the heart by blood pooling in the pericardium, the heart sac) and/or sudden death unless (or despite being) immediately treated.
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 they lose their transversal striations and the nucleus. The interstitial space (the space between cells outside of blood vessels) may be infiltrated with red blood cells.
When the healing has commenced (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 ("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.
Atherosclerosis / other predisposing factors
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, typically over decades. However 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).
Risk factors for atherosclerosis may also be risk factors for ischemic heart disease: older age, smoking, hypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density lipoprotein (LDL) and low high density lipoprotein (HDL)), diabetes (with or without insulin resistance), high blood pressure, and obesity. Many of these factors are modifiable. Other cardiac risk factors include elevated C-reactive protein, or a waist measurement of more than 35 inches for women or more than 40 for men. Age, smoking, and family history of early heart disease can increase the risks. Having increased blood pressure above 120 systolic may increase the risk of cardiovascular disease. Elevated triglycerides levels and small LDL particle size may also increase the risk of cardiovascular disease.
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 rates are higher in association with intense exertion, be it stress or physical exertion, especially if the exertion is unusually 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 IVUS, 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 infecton, 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 atherosclerosic 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.
As myocardial infarction is a common medical emergency, the signs are often part of first aid courses. General management in the acute setting is:
- Seek emergency medical assistance immediately.
- Help the patient to rest in a position which minimises breathing difficulties. A half-sitting position with knees bent is often recommended.
- Give access to more oxygen, e.g. by opening the window and widening the collar for easier breathing; but keep the patient warm, e.g. by a blanket or a jacket
- Give aspirin, if the patient is not allergic to aspirin. Aspirin has an antiplatelet effect which inhibits formation of further thrombi (blood clots).
- Non-enteric coated or soluble preparations are preferred. These should be chewed or dissolved, respectively, to facilitate quicker absorption. If the patient cannot swallow, the aspirin can be used sublingually.
- U.S. guidelines recommend a dose of 160 – 325 mg.
- Australian guidelines recommend a dose of 150 – 300 mg.
- Give glyceryl trinitrate (nitroglycerin) sublingually (under the tongue) if it has been prescribed for the patient.
- Monitor pulse, breathing, level of consciousness and, if possible, the blood pressure of the patient continually.
- Administer cardiopulmonary resuscitation (CPR) if cardiac arrest occurs due to ventricular arrhythmia
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 are also becoming popular for use in the home, where most attacks occur. 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 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.
Recent attempts to reduce the damage to the heart from an acute myocardial infarction have resulted in studies of prehospital use of thrombolytics or clot busters. In rural areas or congested urban areas trained paramedics are giving thrombolytics to patients who meet specific rigid criteria. Determining the effectiveness of this treatment is done through various studies. Studies, like the TIMI-19, evaluate time of the onset of symptoms and time of administration of thrombolytics and the patients outcome. Studies have also been done comparing prehospital thrombolytics and inhospital administration of thrombolytics and interventional angioplasty. The specific medication utilized and the criteria the patient must meet are factors for each of several different studies.
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. A sublingual aspirin tablet may help.
Doctors traveling by commercial aircraft may be able to assist an MI patient by using the on-board first aid kit, which contains some cardiac drugs used in advanced cardiac life support, and oxygen. Flight attendants are generally aware of the location of these materials. Pilots may divert the flight to land at a nearby airport.
A heart attack, especially because of cardiac arrhythmias, is often a life-threatening medical emergency which demands both immediate attention and activation of the emergency medical services. Immediate termination of arrhythmias and transport by ambulance to a hospital where advanced cardiac life support (ACLS) is available can greatly improve both chances for survival and recovery. The more time that passes, even 1 – 2 minutes, before medical attention is available/sought, the more likely the occurrence of both (a) life threatening arrhythmias/death and (b) more severe and permanent heart damage.
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.
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 ineffective. Aspirin is a standard therapy that is part of all reperfusion regimens. Because irreversible ischemic injury occurs within 2-4 hours of the infarction, there is a limited window of time available for reperfusion to work.
Although clinical trials suggest better outcomes, angioplasty via cardiac catheterization 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. The goal of primary angioplasty is to open the artery within 90 minutes of the patient presenting to the emergency room. This time is referred to as the door-to-balloon time. If this door-to-balloon time exceeds the time required to administer a thrombolytic agent by > 60 minutes, then the administration of a thrombolytic agents is preferred.
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.
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, or increasingly before discharge from hospital, further investigations are performed to objectivate coronary artery disease. If rescue angioplasty has not already been performed, a coronary angiogram (or alternatively a thallium scintigram or treadmill test) may be done to identify treatable causes, as this will decrease the risk of future myocardial infarction.
Patients are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:
- Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of thrombus formation. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased.
- Beta blocker therapy such as bisoprolol or metoprolol should be commenced. These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction (LVD) 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), tachycardia, 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, irrespective of the patient's cholesterol level.
- 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.
Patients' blood pressure is also treated to target, and lifestyle changes are suggested, chiefly smoking cessation, regular aerobic exercise, a sensible diet, and limitation of alcohol intake.
- Congestive heart failure +
- Recurrent infarction
- Mitral regurgitation - especially right-sided MI
- Papillary muscle rupture +
- Arrhythmias (ventricular tachycardia, ventricular fibrillation, complete heart block)
- Cardiac tamponade
- Cardiogenic shock
(Points labelled '+' can all lead to cardiogenic shock)
A person who has suffered from a myocardial infarction may be prevented from participating in activity that puts other people's lives at risk, eg driving a car or airplane.
- Angina pectoris
- Dressler's syndrome
- Coronary heart disease
- Coronary thromboses
- Hibernating myocardium
- Stunned myocardium
- Ventricular remodeling
- Cardiac arrest
- Diet and heart disease
- ↑ World Health Organization. Annex Table 2: Deaths by cause, sex and mortality stratum in WHO regions, estimates for 2002 The world health report 2004.
- ↑ McSweeney JC, Cody M, O'Sullivan P, Elberson K, Moser DK, Garvin BJ (2003). Women's early warning symptoms of acute myocardial infarction. Circulation 108 (21): 2619-23. PMID 14597589.
- ↑ Spodick DH (2004). Decreased recognition of the post-myocardial infarction (Dressler) syndrome in the postinfarct setting: does it masquerade as "idiopathic pericarditis" following silent infarcts?. Chest 126 (5): 1410-1. PMID 15539705.
- ↑ Davis TM, Fortun P, Mulder J, Davis WA, Bruce DG (2004). Silent myocardial infarction and its prognosis in a community-based cohort of Type 2 diabetic patients: the Fremantle Diabetes Study. Diabetologia 47 (3): 395-9. PMID 14963648.
- ↑ Springhouse,. ECG Facts Made Incredibly Quick! (Incredibly Easy! Series), Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 1-58255-672-5.
- ↑ Gillum RF, Fortmann SP, Prineas RJ, Kottke TE. International diagnostic criteria for acute myocardial infarction and acute stroke. Am Heart J 1984;108:150-8. PMID 6731265
- ↑ Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000;36:959-69. PMID 10987628.
- ↑ Beers MH, Berkow R, editors. The Merck Manual, 17th edition. Whitehouse Station (NJ): Merck Research Laboratories; 1999. ISBN 0-911910-10-7.
- ↑ 9.0 9.1 Rossi S, editor. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006. ISBN 0-9757919-2-3.
- ↑ Smith A, Aylward P, Campbell T, et al. Therapeutic Guidelines: Cardiovascular, 4th edition. North Melbourne: Therapeutic Guidelines; 2003. ISSN 1327-9513
- ↑ Yusuf S, Peto R, Lewis J, Collins R, Sleight P. Beta blockade during and after myocardial infarction: an overview of the randomized trials. Prog Cardiovasc Dis 1985;27:335-71. PMID 2858114
- ↑ Pitt B, Remme W, Zannad F, Neaton J, Martinez F, Roniker B, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 2003;348(14):1309-21. PMID 12668699.
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