Myocardial infarction

. 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 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. 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 "# and women over $#, smoking, excessive alcohol consumption, the abuse of certain illicit drugs, high triglyceride levels, high %&% ('%ow(density lipoprotein') and low )&% (')igh 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. *lassical symptoms of acute myocardial infarction include chest pain, shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety or a feeling of impending doom. +atients fre,uently feel suddenly ill. -omen often experience different symptoms than men. The most common symptoms of .I in women include shortness of breath, weakness, and fatigue. Approximately one third of all myocardial infarctions are silent, without chest pain or other symptoms.

&iagram of a myocardial infarction (5) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (6) of a branch of the left coronary artery (%*A, right coronary artery ; <*A).

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 (/*0, /10), a chest 2(ray and blood tests to detect elevated creatine kinase or troponin levels (these are chemical markers released by damaged tissues, especially the myocardium). 3urther 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. *oronary care unit admission allows rapid and safe treatment of complications such as abnormal heart rhythms.

Epidemiology:
.yocardial infarction is a common presentation of ischemic heart disease. The -)4 estimated that in 5##5, 65.78 of deaths worldwide were from ischemic heart disease. Ischemic heart disease is the leading cause of death in developed countries, but third to AI&9 and lower respiratory infections in developing countries. In the :nited 9tates, diseases of the heart are the leading cause of death, causing a higher mortality than cancer (malignant neoplasms). *oronary heart disease is responsible for 6 in $ deaths in the :.9... 9ome

=,5##,### men and 7,###,### women are living with some form of coronary heart disease. 6,5##,### people suffer a (new or recurrent) coronary attack every year, and about "#8 of them die as a result of the attack. This means that roughly every 7$ seconds, an American dies of a coronary event.

Risk factors:
<isk factors for atherosclerosis are generally risk factors for myocardial infarction>

4lder age .ale gender *igarette smoking )ypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density lipoprotein and low high density lipoprotein) &iabetes (with or without insulin resistance) )igh blood pressure 4besity (defined by a body mass index of more than ?# kg m5, or alternatively by waist circumference or waist(hip ratio).

.any of these risk factors are modifiable@ so many heart attacks can be prevented by maintaining a healthier lifestyle. +hysical activity, for example, is associated with a lower risk profile. Aon(modifiable risk factors include age, gender, and family history of an early heart attack (before the age of 7#), which is thought of as reflecting a genetic predisposition. 9ocioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of .I. To understand epidemiological study results, itBs important to note that many factors associated with .I mediate their risk via other factors. 3or example, the effect of education is partially based on its effect on income and marital status. -omen 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 pla,ue formation. *( reactive protein (*<+) is a sensitive but non(specific marker for inflammation. /levated *<+ blood levels, especially measured with high sensitivity assays, can predict the risk of .I, as well as stroke and development of diabetes. .oreover, some drugs for .I might also reduce *<+ levels. The use of high sensitivity *<+ assays as a means of screening the general population is advised against, but it may be used optionally at the physicianBs discretion, in patients who already present with other risk factors or known coronary artery disease. -hether *<+ 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 conse,uences for public health 9erological studies measuring antibody levels against typical periodontitis(causing bacteria found that such antibodies were more present in subCects with coronary heart disease +eriodontitis tends to increase blood levels of *<+, fibrinogen and cytokines@ thus, periodontitis may mediate its effect on .I risk via other risk factors. +reclinical 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.

Daldness, hair greying, a diagonal crease and possibly other skin features are independent risk factors for .I. Their role remains controversial@ a common denominator of these signs and the risk of .I are supposed, possibly genetic.

Pathophysiology:

A myocardial infarction occurs when an atherosclerotic pla,ue 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 is a type of acute coronary syndrome, which is most fre,uently (but not always) a manifestation of coronary artery disease. The most common triggering event is the disruption of an atherosclerotic pla,ue 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 pla,ues in the wall of arteries (in this case, the coronary arteries), typically over decades. Dlood stream column irregularities visible on angiographies reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. +la,ues can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery@ this can occur in minutes. -hen a severe enough pla,ue 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. <ecent studies indicate that another form a cell death called apoptosis also plays a role in the process of tissue damage subse,uent to myocardial infarction. As a result, the patientBs heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias. InCured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between inCured and uninCured 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 E3), 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 ET), which may or may not cause sudden cardiac death. )owever, ventricular tachycardia usually results in rapid heart rates

that prevent the heart from pumping blood effectively. *ardiac 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 depolariFe 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:
)eart 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 Guantitatively, the period of intense exercise and subse,uent recovery is associated with about a 7(fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are physically very fit 3or those in poor physical condition, the rate differential is over ?$(fold higher. 4ne 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 pla,ue rupture. Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis. -hile this intracellular organism has been demonstrated in atherosclerotic pla,ues, 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:

*lassification of acute coronary syndromes Acute myocardial infarction is a type of acute coronary syndrome, which is most fre,uently (but not always) a manifestation of coronary artery disease. The acute coronary syndromes include 9T segment elevation myocardial infarction (9T/.I), non(9T segment elevation myocardial infarction (A9T/.I), and unstable angina (:A). &epending on the location of the obstruction in the coronary circulation, different Fones of the heart can become inCured. :sing the anatomical terms of location, one can describe anterior, inferior, lateral, apical and septal infarctions (and combinations, such as anteroinferior, anterolateral, and so on). 3or example, an occlusion of the left anterior descending coronary artery will result in an anterior wall myocardial infarct. Another distinction is whether a .I 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 G(wave and non(G(wave myocardial infarction respectively, based on the presence or absence of G waves on the /*0. It has since been shown that there is no clear correlation between the presence of G waves with a transmural infarction and the absence of G waves with a subendocardial infarction, but G waves are associated with larger infarctions, while the lack of G waves is associated with smaller infarctions. The presence or absence of G(waves also has clinical importance, with improved outcomes associated with a lack of G waves. The phrase 'massive attack' is not an official medical term.

Symptoms:

<ough diagram of pain Fones in myocardial infarction (dark red ; most typical area, light red ; other possible areas, view of the chest). The onset of symptoms in myocardial infarction (.I) is usually gradual, over several minutes, and rarely instantaneous. *hest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or s,ueeFing. *hest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. +ain radiates most often to the left arm, but may also radiate to the lower Caw, 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 is called an acute coronary syndrome. 4ther conditions such as aortic dissection or pulmonary embolism may present with chest pain and must be considered in the differential diagnosis. 9hortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and conse,uent pulmonary edema. 4ther symptoms include diaphoresis (an excessive form of sweating), weakness, light(headedness, nausea, vomiting, and palpitations. %oss of consciousness and even sudden death can occur in myocardial infarctions. -omen often experience markedly different symptoms than men. The most common symptoms of .I in women include dyspnea, weakness, and fatigue. 3atigue, sleep disturbances, and dyspnea have been reported as fre,uently 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 .I 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 visualiFing 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. Aew regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction and are sometimes performed in e,uivocal cases. Technetium and thallium can be used in nuclear medicine to visualiFe areas of reduced blood flow and tissue viability, respectively. Technetium is used in a .:0A scan.

Diagnostic criteria:
-)4 criteria have classically been used to diagnose .I@ a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied> 6. *linical history of ischemic type chest pain lasting for more than 5# minutes 5. *hanges in serial /*0 tracings ?. <ise and fall of serum cardiac enFymes (biomarkers) such as creatine kinase, troponin I, and lactate dehydrogenase isoFymes specific for the heart.

The -)4 criteria were refined in 5### to give more prominence to cardiac biomarkers. According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological G waves, 9T elevation or depression or coronary intervention are diagnostic of .I.

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. 9ome patients have low(grade fever (?HI?J K*). Dlood pressure may be elevated or decreased, and the pulse can be become irregular. If heart failure ensues, elevated Cugular venous pressure and hepatoCugular reflux, or swelling of the legs due to peripheral edema may be found on inspection. <arely, a cardiac bulge with a pace different from the pulse rhythm can be felt on pericardial examination. Earious 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.

65(lead electrocardiogram (/*0) showing acute inferior 9T segment elevation .I (9T/.I). Aote the 9T segment elevation in leads II, III, and aE3 along with reciprocal 9T segment depression in leads I and aE%.

Electrocardiogram:
The primary purpose of the electrocardiogram is to detect ischemia or acute coronary inCury in broad, symptomatic emergency department populations. )owever, the standard 65 lead /*0 has several limitations. An /*0 represents a brief sample in time. Decause unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single /*0 may not accurately represent the entire picture. It is therefore desirable to obtain serial 65 lead /*0s, particularly if the first /*0 is obtained during a pain(free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous 9T segment monitoring. It should also be appreciated that the standard 65 lead /*0 does not directly examine the right ventricle, and does a relatively poor Cob 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 non diagnostic /*0. The use of non(standard /*0 leads like right(sided lead E"< and posterior leads E=, EH, and EJ may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 65 lead /*0 stands at the center of risk stratification for the patient with suspected acute myocardial infarction. .istakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the ,uality of patient care. The 65 lead /*0 is used to classify patients into one of three groups> 6. Those with 9T segment elevation or new bundle branch block (suspicious for acute inCury and a possible candidate for acute reperfusion therapy with Thrombolytic or primary +*I), 5. Those with 9T segment depression or T wave inversion (suspicious for ischemia), and ?. Those with a so(called non(diagnostic or normal /*0. A normal /*0 does not rule out acute myocardial infarction. 9ometimes the earliest presentation of acute myocardial infarction is the hyper acute T wave, which is treated the same as 9T segment elevation. In practice this is rarely seen, because it only exists for 5(?# minutes after the onset of infarction. )yper acute T waves need to be distinguished from the peaked T waves associated with hyperkalemia. The current guidelines for the /*0 diagnosis of acute myocardial infarction re,uire at least 6 mm (#.6 mE) of 9T segment elevation in 5 or more anatomically contiguous leads. This criterion is problematic, however, as acute myocardial infarction is not the most common cause of 9T segment elevation in chest pain patients. In addition, over J#8 of healthy men have at least 6 mm (#.6 mE) of 9T segment elevation in at least one precordial lead. The clinician must therefore be well versed in recogniFing the so(called /*0 mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, benign early repolariFation, +ericarditis, hyperkalemia, and ventricular aneurysm. %eft bundle branch block and pacing can interfere with the electrocardiography diagnosis of acute myocardial infarction. The 0:9T4 investigators 9garbossa 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 9T segment elevation L 6 mm (#.6 mE), discordant 9T segment elevation L $ mm (#.$ mE), and concordant 9T segment depression in the left precordial leads. The presence of reciprocal changes on the 65 lead /*0 may help distinguish true acute myocardial infarction from the mimics of acute myocardial infarction. The contour of the 9T segment may also be helpful, with a straight or upwardly convex (non(concave) 9T segment favoring the diagnosis of acute myocardial infarction. The presence of 9T segment elevation distinguishes between>

9T/.I ('9T(/levation .yocardial Infarction') A9T/.I ('Aon(9T(/levation .yocardial Infarction') (( diagnosed when cardiac enFymes are elevated.

The leads with 9T segment elevation help the clinician identify what area of the heart is infarcting. It also enables the clinician to predict the culprit artery>

Wall Affected

Leads Showing ST Segment Elevation E6, E5 E?, E" E6, E5, E?, E" E?, E", E$, E7, I, aE%

Leads Showing Reciprocal ST Segment Depression Aone Aone Aone

S spected ! lprit Artery %eft Anterior &escending (%A&) %eft Anterior &escending (%A&) %eft Anterior &escending (%A&) %eft Anterior &escending (%A&), *ircumflex (%*2), or 4btuse .arginal %eft main coronary artery (%*A) <ight *oronary Artery (<*A) or *ircumflex (%*2) *ircumflex (%*2) or 4btuse .arginal +osterior &escending (+&A) (branch of the <*A or *ircumflex (%*2)) <ight *oronary Artery (<*A)

9eptal Anterior Anteroseptal

Anterolateral /xtensive anterior (9ometimes called Anteroseptal with %ateral extension) Inferior %ateral +osterior (:sually associated with Inferior or %ateral but can be isolated) <ight ventricular (:sually associated with Inferior)

II, III, aE3

E6,E5,E?, E", E$, E7, I, aE%

II, III, aE3

II, III, aE3 I, aE%, E$, E7

I, aE% II, III, aE3

E=, EH, EJ II, III, aE3, E6, E"<

E6,E5,E?, E"

I, aE%

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

Cardiac markers:
*ardiac markers or cardiac enFymes 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. :ntil the 6JH#s, the enFymes 904T and %&) were used to assess cardiac inCury. Then it was found that disproportional elevation of the MB subtype of the enFyme creatine kinase (*1) was very

specific for myocardial inCury. *urrent 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 inCury develops. /levated 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 re,uires two out of three components (history, /*0, and enFymes). -hen damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 5" hour period. Decause these enFyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis.

Angiography:

Angiogram of the coronary arteries. 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. 4bstructed or narrowed arteries can be identified, and angioplasty applied as a therapeutic measure (see below). Angioplasty re,uires extensive skill, especially in emergency settings, and may not always be available out of hours. It is commonly performed by interventional cardiologists.

Histopathology:

.icroscopy image (magn. ca 6##x, )M/ stain) from autopsy specimen of myocardial infarct (= days post( infarction). )istopathological examination of the heart may reveal infarction at autopsy. :nder the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative necrosis (cell death). 4n gross examination, the infarct is not identifiable within the first 65 hours. Although earlier changes can be discerned using electron microscopy, one of the earliest changes under a normal microscope are so(called wavy fibers. 9ubse,uently, 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, which 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 recogniFed in cases where the perfusion was not restored@ reperfused infarcts can have other hallmarks, such as contraction band necrosis.

irst 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.

!mmediate care:
-hen symptoms of myocardial infarction occur, people wait on average of ? 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'). *ertain positions allow the patient to rest in a position which minimiFes 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 ,uickly (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. Aon(enteric coated or soluble

preparations are preferred. If chewed or dissolved, respectively, they can be absorbed by the body even ,uicker. If the patient cannot swallow, the aspirin can be used sublingually. :.9. guidelines recommend a dose of 675 I ?5$ mg. Australian guidelines recommend a dose of 6$# I ?## mg. 0lyceryl trinitrate (nitroglycerin) sublingually (under the tongue) can be given if it has been prescribed for the patient. If an A/& is available the rescuer should immediately bring the A/& to the patientBs 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 ,uestions once emergency medical technicians arrive (if the patient becomes unconscious). The victimBs 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 /.9 personnel. 4ther general first aid principles include monitoring pulse, breathing, and level of consciousness and, if possible, the blood pressure of the patient. In case of cardiac arrest, cardiopulmonary resuscitation (*+<) can be administered.

A"tomatic external defi#rillation $AED%:

9ince the publication of data showing that the availability of automated external defibrillators (A/&s) 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). A/&s analyFe the heartBs rhythm and determine whether the rhythm is amenable to defibrillation ('shockable'), as in ventricular tachycardia and ventricular fibrillation.

Emergency ser&ices:
/mergency .edical 9ervices (/.9) 9ystems vary considerably in their ability to evaluate and treat patients with suspected acute myocardial infarction. 9ome provide as little as first aid and early defibrillation. 4thers employ highly trained paramedics with sophisticated technology and advanced protocols. /arly access to /.9 is promoted by a J(6(6 system currently available to J#8 of the population in the :nited 9tates. .ost are capable of providing oxygen, IE access, sublingual nitroglycerine, morphine, and aspirin. 9ome are capable of providing Thrombolytic therapy in the prehospital setting. -ith primary +*I emerging as the preferred therapy for 9T segment elevation myocardial infarction, /.9 can play a key role in reducing door to balloon intervals (the time from presentation to a hospital /< to the restoration of coronary artery blood flow) by performing a 65 lead /*0 in the field and using this information to triage the patient to the most appropriate medical facility. In addition, the 65 lead /*0 can be transmitted to the receiving hospital, which enables time saving decisions to be made prior to the patientBs arrival. This may include a 'cardiac alert' or '9T/.I alert' that calls in off duty personnel in areas where the cardiac cath lab is not staffed 5" hours a day. /ven in the absence of a formal alerting

program, prehospital 65 lead /*0s are independently associated with reduced door to treatment intervals in the emergency department.

'ilderness first aid:

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

Air tra&el:
*ertified personnel traveling by commercial aircraft may be able to assist an .I 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. +ilots may divert the flight to land at a nearby airport. *ardiac 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 inCury instead of amelioration. 4ther treatment modalities may also cause complications@ the use of antithrombotics for example carries an increased risk of bleeding.

irst line:
4xygen, aspirin, glyceryl trinitrate (nitroglycerin) and analgesia (usually morphine, hence the popular mnemonic MON , morphine! o"y#en! 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. 4f the first line agents, only aspirin has been proven to decrease mortality. 4nce the diagnosis of myocardial infarction is confirmed, other pharmacologic agents are often given. These include beta blockers, anticoagulation (typically with heparin), and possibly additional antiplatelet agents such as clopidogrel. 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. -hile 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.

Reperf"sion:
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. +atients who present with suspected acute myocardial infarction and 9T segment elevation (9T/.I) or new bundle branch block on the 65 lead /*0 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 (+*I) or when these therapies are unsuccessful, bypass surgery. Individuals without 9T segment elevation are presumed to be experiencing either unstable angina (:A) or non(9T segment elevation myocardial infarction (A9T/.I). They receive many of the same initial therapies and are often stabiliFed with antiplatelet drugs and anticoagulant. If their condition remains (hemodynamically) stable, they can be offered either late coronary angiography with subse,uent restoration of blood flow (revasculariFation), or non(invasive stress testing to determine if there is significant ischemia that would benefit from revasculariFation. If hemodynamic instability develops in individuals with A9T/.Is, they may undergo urgent coronary angiography and subse,uent revasculariFation. The use of Thrombolytic agents is contraindicated in this patient subset, however. The basis for this distinction in treatment regimens is that 9T segment elevations on an /*0 are typically due to complete occlusion of a coronary artery. 4n the other hand, in A9T/.Is 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 6#8 of patients with 9T/.I donBt develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subse,uent , waves on /10 after reperfusion therapy. 9uch 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 5$8 of 9T/.Is can be aborted.

Throm#olytic therapy:
Thrombolytic therapy is indicated for the treatment of 9T/.I if the drug can be administered within 65 hours of the onset of symptoms, the patient is eligible based on exclusion criteria, and primary +*I is not immediately available. The effectiveness of Thrombolytic therapy is highest in the first 5 hours. After 65 hours, the risk associated with Thrombolytic therapy outweighs any benefit. Decause irreversible inCury occurs within 5I" 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 A9T/.I and for the treatment of individuals with evidence of cardiogenic shock. 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. *urrently available Thrombolytic agents include streptokinase, urokinase, and alteplase (recombinant tissue plasminogen activator, rt+A). .ore recently, Thrombolytic agents similar in structure to rt+A such as reteplase and tenecteplase have been used. These newer agents boast efficacy at least as good as rt+A with significantly

easier administration. The Thrombolytic agent used in a particular individual is based on institution preference and the age of the patient. &epending on the Thrombolytic agent being used, adCuvant anticoagulation with heparin or low molecular weight heparin may be of benefit. -ith t+A and related agents (reteplase and tenecteplase), heparin is needed to maintain coronary artery patency. Decause of the anticoagulant effect of fibrinogen depletion with streptokinase and urokinase treatment, it is less necessary there. Intracranial bleeding (I*D) and subse,uent cerebrovascular accident (*EA) is a serious side effect of Thrombolytic use. The risk of I*D is dependent on a number of factors, including a previous episode of intracranial bleed, age of the individual, and the Thrombolytic regimen that is being used. In general, the risk of I*D due to Thrombolytic use for the treatment of an acute myocardial infarction is between #.$ and 6 percent. Thrombolytic therapy to abort a myocardial infarction is not always effective. The degree of effectiveness of a Thrombolytic agent is dependent on the time since the myocardial infarction began, with the best results occurring if the Thrombolytic agent is used within an hour of the onset of symptoms.N If the individual presents more than 65 hours after symptoms commenced, the risk of intracranial bleed are considered higher than the benefits of the Thrombolytic agent. 3ailure rates of Thrombolytic can be as high as 5#8 or higher. In cases of failure of the Thrombolytic agent to open the infarct(related coronary artery, the patient is then either treated conservatively with anticoagulants or allowed to 'complete the infarction' or percutaneous coronary intervention (+*I, see below) is then performed. +ercutaneous coronary intervention in this setting is known as 'rescue +*I' or 'salvage +*I'. *omplications, particularly bleeding, are significantly higher with rescue +*I than with primary +*I due to the action of the Thrombolytic agent.

Perc"taneo"s coronary inter&ention:

Thrombus material (in a cup, upper left corner) removed from a coronary artery during a percutaneous coronary intervention to abort a myocardial infarction. 3ive pieces of thrombus are shown (arrow heads). 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 (+*I) via cardiac catheteriFation. The use of percutaneous coronary intervention as a therapy to abort a myocardial infarction is known as primary +*I. The goal of primary +*I is to open the artery as soon as possible and preferably within J# minutes of the patient presenting to the emergency room. This time is referred to as the door(to(balloon time. 3ew hospitals can provide +*I within the J# minute interval.

The current guidelines in the :nited 9tates restrict primary +*I to hospitals with available emergency bypass surgery as a backup, but this is not the case in other parts of the world. +rimary +*I involves performing a coronary angiogram to determine the anatomical location of the infarcting vessel, followed by balloon angioplasty (and fre,uently deployment of an intracoronary stent) of the thrombosis arterial segment. In some settings, an extraction catheter may be used to attempt to aspirate (remove) the thrombus prior to balloon angioplasty. -hile the uses of intracoronary stents do not improve the short term outcomes in primary +*I, the use of stents is widespread because of the decreased rates of procedures to treat restenosis compared to balloon angioplasty. AdCuvant therapy during primary +*I includes intravenous heparin, aspirin, and clopidogrel. The uses of glycoprotein IIb IIIa inhibitors are often used in the setting of primary +*I to reduce the risk of ischemic complications during the procedure. &ue to the number of antiplatelet agents and anticoagulants used during primary +*I, the risk of bleeding associated with the procedure are higher than during an elective +*I.

Coronary artery #ypass s"rgery:

!oronary artery "ypasses s rgery during mobiliFation (freeing) of the right coronary artery from its surrounding tissue, adipose tissue (yellow). The tube visible at the bottom is the aortic cannula (returns blood from the )%.). The tube above it (obscured by the surgeon on the right) is the venous cannula (receives blood from the body). The patientBs heart is stopped and the aorta is cross(clamped. The patientBs head (not seen) is at the bottom. &espite the guidelines, emergency bypass surgery for the treatment of an acute myocardial infarction (.I) is less common then +*I or medical management. In an analysis of patients in the :.9. Aational <egistry of .yocardial Infarction (A<.I) from Oanuary 6JJ$ to .ay 5##", the percentage of patients with *ardiogenic shock treated with primary +*I rose from 5=."8 to $"."8, while the increase in *AD0 treatment was only from 5.68 to ?.58. /mergency coronary artery bypass graft surgery (*AD0) is usually undertaken to simultaneously treat a mechanical complication, such as a ruptured papillary muscle, or a ventricular septal defect, with ensueing *ardiogenic shock. In uncomplicated .I, the mortality rate can be high when the surgery is performed immediately following the infarction. If this option is entertained, the patient should be stabiliFed prior to

surgery, with supportive interventions such as the use of an intra(aortic balloon pump. In patients developing *ardiogenic shock after a myocardial infarction, both +*I and *AD0 are satisfactory treatment options, with similar survival rates. *oronary artery bypass surgery involves an artery or vein from the patient being implanted to bypass narrowings or occlusions on the coronary arteries. 9everal 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. Dypass 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 obCectives are to prevent life(threatening arrhythmias or conduction disturbances. This re,uires monitoring in a coronary care unit and protocolised administration of antiarrhythmic agents. Antiarrhythmic agents are typically only given to individuals with life(threatening arrhythmias after a myocardial infarction and not to suppress the ventricular ectopy that is often seen after a myocardial infarction.

Reha#ilitation:
*ardiac rehabilitation aims to optimiFe function and ,uality 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. +hysical exercise is an important part of rehabilitation after a myocardial infarction, with beneficial effects on cholesterol levels, blood pressure, weight, stress and mood. 9ome patients become afraid of exercising because it might trigger another infarct. +atients are stimulated to exercise, and should only avoid certain exerting activities such as shoveling. %ocal authorities may place limitations on driving motoriFed vehicles. 9ome people are afraid to have sex after a heart attack. .ost people can resume sexual activities after ? to " weeks. The amount of activity needs to be dosed to the patients possibilities.

Secondary pre&ention:
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. +atients are usually commenced on several long(term medications post(.I, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (*EA). :nless contraindicated, such medications may include>

Antiplatelet drug therapy such as aspirin and or clopidogrel should be continued to reduce the risk of pla,ue 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. Deta 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 ischemia. P(Dlockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in A9T/.I. A*/ inhibitor therapy should be commenced 5"I"H hours post(.I in hemodynamically(stable patients, particularly in patients with a history of .I, diabetes mellitus, hypertension, anterior location of infarct (as assessed by /*0), and or evidence of left ventricular dysfunction. A*/ inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post(.I. 9tatin therapy has been shown to reduce mortality and morbidity post(.I. The effects of statins may be more than their %&% lowering effects. The general consensus is that statins have pla,ue stabiliFation 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(.I in patients with heart failure and left ventricular dysfunction, when used in conCunction with standard therapies above. 4mega(? fatty acids, commonly found in fish, have been shown to reduce mortality post(.I. -hile the mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that the survival benefit is due to electrical stabiliFation and the prevention of ventricular fibrillation.N6?$Q )owever, further studies in a high(risk subset have not shown a clear( cut decrease in potentially fatal arrhythmias due to omega(? fatty acids.

(e) therapies "nder in&estigation:

+atients who receive stem cell treatment by coronary artery inCections of stem cells derived from their own bone marrow after a myocardial infarction (.I) show improvements in left ventricular eCection fraction and end(diastolic volume not seen with placebo. The larger the initial infarct siFe, the greater the effect of the infusion. *linical trials of progenitor cell infusion as a treatment approach to 9T elevation .I are proceeding. There are currently ? biomaterial and tissue engineering approaches for the treatment of .I, but these are in an even earlier stage of medical research, so many ,uestions 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 utiliFes in vitro engineered cardiac tissue, which is subse,uently implanted in vivo. The final approach entails inCecting cells and or a scaffold into the myocardium to create in situ engineered cardiac tissue.

Complications:
*omplications 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 Fone if there are any live cells left in the infarct.

Congesti&e heart fail"re:

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 .I. The incidence of heart failure is particularly high in patients with diabetes and re,uires special management strategies.

Myocardial r"pt"re:
.yocardial 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 6#8 of all .Is. This may occur in the free walls of the ventricles, the septum between them, the papillary muscles, or less commonly the atria. <upture 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 localiFed dilation or ballooning of the heart chamber. <isk factors for myocardial rupture include completion of infarction (no revasculariFation 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. <upture 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. <upture 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. <upture of the papillary muscle may also lead to acute mitral regurgitation and subse,uent pulmonary edema and possibly even *ardiogenic shock.

*ife+threatening arrhythmia:

A 65 lead electrocardiogram showing ventricular tachycardia.

9ince the electrical characteristics of the infarcted tissue change (see +athophysiology section), arrhythmias are a fre,uent 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, doesnBt 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 +ericarditis. In &resslerBs 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. *ardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an ade,uate amount of oxygenated blood to the tissues of the body. -hile the data on performing interventions on individuals with *ardiogenic shock is sparse, trial data suggests a long(term mortality benefit in undergoing revasculariFation if the individual is less than =$ years old and if the onset of the acute myocardial infarction is less than ?7 hours and the onset of *ardiogenic shock is less than 6H hours. If the patient with cardiogenic shock is not going to be revasculariFed, aggressive hemodynamic support is warranted, with insertion of an intra(aortic balloon pump if not contraindicated. If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor.

Prognosis:
The prognosis for patients with myocardial infarction varies greatly, depending on the patient, the condition itself and the given treatment. :sing simple variables which are immediately available in the emergency room, patients with a higher risk of adverse outcome can be identified. 3or example, one study found that #."8 of patients with a low risk profile had died after J# days, whereas the mortality rate in high risk patients was 56.68. Although studies differ in the identified variables, some of the more reproduced risk stratifiers include age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or 1illip class of two or greater), 9T(segment deviation, diabetes, serum creatinine concentration, peripheral vascular disease and elevation of cardiac markers. Assessment of left ventricular eCection fraction may increase the predictive power of some risk stratification models. The prognostic importance of G(waves is debated. +rognosis is significantly worsened if a mechanical complication (papillary muscle rupture, myocardial free wall rupture, and so on) were to occur. There is evidence that case fatality of myocardial infarction has been improving over the years in all ethnicities.

*egal implications:
At common law, a myocardial infarction is generally a disease, but may sometimes be an inCury. This has implications for no(fault insurance schemes such as workersB compensation. A heart attack is generally not covered@ however, it may be a work(related inCury if it results, for example, from unusual emotional stress or unusual exertion. Additionally, in some Curisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line(of(duty inCuries 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 peopleBs lives at risk, for example driving a car, taxi or airplane.