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 is chemia 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 ageespecially men
over 40and women over 50,smoking, excessive alcohol consumption, the abuse of certain
illicit drugs, high triglyceride levels, high LDL("Low-density lipoprotein") and low
HDL("High density lipoprotein"),diabetes, high blood pressure, obesity, and chronically
high levels of stress incertain persons. The term myocardial infarctionis derived
from myocardium (the heart muscle) and infarction (tissue death due to oxygen starvation).
The phrase "heart attack" is sometimes used incorrectly to describe sudden cardiac death,
which may or may not be the result of acute myocardial infarction. Classical symptoms of
acute myocardial infarction includechest pain,shortness of
breath, nausea,vomiting, palpitations,sweating, and anxietyor a feeling of impending
doom.Patients frequently feel suddenly ill. Women often experiencedifferent symptoms
than men. The most common symptomsof MI in women include shortness of breath,
weakness, andfatigue. Approximately one third of all myocardial infarctionsare silent,
without chest pain or other symptoms.Immediate treatment for suspected acute
myocardial infarction includesoxygen, aspirin, glyceryl trinitrate and pain relief . The
patient will receive a number of diagnostic tests, such as anelectrocardiogram(ECG,EKG), a
chestX-rayand blood teststo detect elevated creatine kinase or troponinlevels (these
arechemical markers released by damaged tissues, especially the myocardium). Further
treatment mayinclude either medicationsto break down blood clots that block the blood
flow to the heart, or mechanically restoring the flow bydilatationor bypass surgeryof the
blocked coronary artery. Coronarycare unitadmission allows rapid and safe treatment of
complications such as abnormal heart rhythms.
Epimology:
Myocardial infarction is a common presentation of ischemic heart disease. The WHO
estimated that in2002, 12.6% of deaths worldwide were from ischemic heart disease.
Ischemic heart disease is the leadingcause of death in developed countries, but third
to AIDSandlower respiratory infectionsin developingcountries.In theUnited States,diseases
of the heartare theleading cause of death, causing a
higher mortalitythancancer (malignant neoplasms).Coronary heart diseaseis responsible
for 1 in 5 deaths in the U.S... Some 7,200,000 men and 6,000,000 women are living with
some form of coronary heart disease. 1,200,000 people suffer a (new or recurrent)
coronary attack every year, and about 40% of them die as a result of theattack. This means
that roughly every 65 seconds, an American dies of a coronary event.

Risk factors :
Risk factors for atherosclerosisare generally risk factors for myocardial infarction:
Older age
Malegender
Cigarette smoking
Hypercholesterolemia(more accuratelyhyperlipoproteinemia,especially high low
densitylipoproteinand lowhigh density lipoprotein)
Diabetes(with or withoutinsulin resistance)
High blood pressure
Obesity(defined by a body mass index of more than 30 kg/m2, or alternatively by
waistcircumference or waist-hip ratio).Many of these risk factors are modifiable; so many
heart attacks can be prevented by maintaining ahealthier lifestyle. Physical activity, for
example, is associated with a lower risk profile. Non-modifiablerisk factors include age,
gender, and family history of an early heart attack (before the age of 60), which isthought
of as reflecting agenetic predisposition.Socioeconomicfactors such as a shorter
educationand lower income(particularly in women), andlivingwith a partner may also
contribute to the risk of MI. To understand epidemiological study results, it'simportant to
note that many factors associated with MI mediate their risk via other factors. For
example,the effect of education is partially based on its effect on income andmarital
status.Women who usecombined oral contraceptive pillshave a modestly increased risk of
myocardialinfarction, especially in the presence of other risk factors, such as
smoking.Inflammation is known to be an important step in the process of atherosclerotic
plaqueformation.C-reactive protein(CRP) is a sensitive but non-specific marker for
inflammation.Elevated CRP blood levels,especially measured with high sensitivity assays,
can predict the risk of MI, as well as strokeanddevelopment of diabetes. Moreover, some
drugs for MI might also reduce CRP levels. The use of highsensitivity CRP assays as a means
of screening the general population is advised against, but it may beused optionally at the
physician's discretion, in patients who already present with other risk factors or
knowncoronary artery disease. Whether CRP plays a direct role in atherosclerosis remains
uncertain.Inflammation in periodontal disease may be linked coronary heart disease, and
since periodontitisis verycommon, this could have great consequences for public health
Serologicalstudies measuringantibody levels against typical periodontitis-causing
bacteriafound that such antibodies were more present insubjects with coronary heart
disease Periodontitis tends to increase blood levels of CRP,fibrinogen andcytokines; thus,
periodontitis may mediate its effect on MI risk via other risk factors.Preclinical research
suggests that periodontal bacteria can promote aggregation of plateletsand promote the
formation of foamcells. A role for specific periodontal bacteria has been suggested but
remains to be established.

Baldness, hair greying, a diagonal crease and possibly other skin features are independent
risk factors for MI. Their role remains controversial; a common denominator of these signs
and the risk of MI aresupposed, possibly genetic.
A myocardial infarction occurs when anatherosclerotic plaqueslowly builds up in the
inner lining of acoronary arteryand then suddenly ruptures, totally occluding the artery
and preventing blood flowdownstream.Acute myocardial infarction is a type of acute
coronary syndrome, which is most frequently (but notalways) a manifestation of coronary
artery disease.The most common triggering event is the disruption
of an atherosclerotic plaquein an epicardial coronary artery, which leads to a clotting
cascade, sometimesresulting in total occlusion of the artery. Atherosclerosis is the
gradual buildup of cholesteroland fibroustissue in plaques in the wall of arteries (in this
case, thecoronary arteries), typically over decades. Bloodstream column irregularities
visible on angiographies reflect arterylumen narrowing as a result of decadesof advancing
atherosclerosis. Plaques can become unstable, rupture, and additionally promote
a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe
enough plaque ruptureoccurs in the coronary vasculature, it leads to myocardial infarction
(necrosis of downstreammyocardium).If impaired blood flow to the heart lasts long
enough, it triggers a process called theischemic cascade; theheart cells die (chiefly
throughnecrosis) and do not grow back. Acollagen scar forms in its place. Recentstudies
indicate that another form a cell death calledapoptosis also plays a role in the process of
tissuedamage subsequent to myocardial infarction. As a result, the patient's heart can be
permanently damaged.This scar tissue also puts the patient at risk for potentially life
threatening arrhythmias.Injured heart tissue conducts electrical impulses more slowly
than normal heart tissue. The difference inconduction velocity between injured and
uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of
many lethal arrhythmias. The most serious of these arrhythmias isventricular fibrillation(
V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of
suddencardiac death. Another life threatening arrhythmia isventricular tachycardia(VTach/VT), which may or may not cause sudden cardiac death. However, ventricular
tachycardia usually results in rapid heart rates that prevent the heart from pumping blood
effectively.Cardiac output and blood pressuremay fall todangerous levels, which is
particularly bad for the patient experiencing acute myocardial infarction.Thecardiac
defibrillator is a device that was specifically designed to terminate these potentially
fatalarrhythmias. The device works by delivering an electrical shock to the patient in order
to depolarize acritical mass of the heart muscle, in effect "rebooting" the heart. This
therapy is time dependent, and theodds of successful defibrillation decline rapidly after the
onset of cardiopulmonary arrest.
Triggers:
Heart attack rates are higher in association with intense exertion, be it psychological
stressor physicalexertion, especially if the exertion is more intense than the individual
usually performs Quantitatively, the period of intense exercise and subsequent recovery is

associated with about a 6-fold higher myocardialinfarction rate (compared with other
more relaxed time 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 eachheart beat which, as has been observed with intravascular ultrasound,increases
mechanical "shear stress"onatheromas and the likelihood of plaque rupture.Acute severe
infection, such as pneumonia,can trigger myocardial infarction. A more controversial link
isthat between
Chlamydophila pneumoniae
infection and atherosclerosis. While this intracellular organismhas been demonstrated in
atherosclerotic plaques, evidence is inconclusive as to whether it can beconsidered a
causative factor. Treatment with antibiotics in patients with proven atherosclerosis has
notdemonstrated a decreased risk of heart attacks or other coronary vascular diseases.

Classification of acute coronary syndromesAcute myocardial infarction is a type of acute

coronary syndrome, which is most frequently (but notalways) a manifestation of coronary
artery disease.The acute coronary syndromes include ST segmentelevation myocardial
infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI),and unstable
angina (UA).Depending on the location of the obstruction in the coronary circulation, different
zones of the heart can become injured. Using theanatomical terms of location, one can describe
anterior, inferior, lateral, apicaland septal infarctions (and combinations, such as anteroinferior,
anterolateral, and so on). For example, anocclusion of theleft anterior descending coronary
arterywill result in an anterior wall myocardial infarct.Another distinction is whether a MI is
subendocardial, affecting only the inner third to one half of theheart muscle, or transmural,
damaging (almost) the entire wall of the heart. The inner part of the heartmuscle is more
vulnerable to oxygen shortage, because the coronary arteries run inward from theepicardiumto
theendocardium, and because the blood flow through the heart muscle is hindered by theheart
contraction.The phrases transmural and subendocardial infarction used to be
considered synonymous with Q-waveand non-Q-wave myocardial infarction respectively, based
on the presence or absence of Q waves on theECG. It has since been shown that there is no
clear correlation between the presence of Q waves with atransmural infarction and the
absence of Q waves with a subendocardial infarction, but Q waves areassociated with larger
infarctions, while the lack of Q waves is associated with smaller infarctions. The presence or
absence of Q-waves also has clinical importance, with improved outcomes associated with
alack of Q waves.The phrase "massive attack" is not an official medical term
Classification of acute coronary syndromesAcute myocardial infarction is a type of acute
coronary syndrome, which is most frequently (but notalways) a manifestation of coronary artery

disease.The acute coronary syndromes include ST segmentelevation myocardial infarction

(STEMI), non-ST segment elevation myocardial infarction (NSTEMI),and unstable angina
(UA).Depending on the location of the obstruction in the coronary circulation, different zones of
the heart can become injured. Using theanatomical terms of location, one can describe anterior,
inferior, lateral, apicaland septal infarctions (and combinations, such as anteroinferior,
anterolateral, and so on). For example, anocclusion of theleft anterior descending coronary
arterywill result in an anterior wall myocardial infarct.Another distinction is whether a MI is
subendocardial, affecting only the inner third to one half of theheart muscle, or transmural,
damaging (almost) the entire wall of the heart. The inner part of the heartmuscle is more
vulnerable to oxygen shortage, because the coronary arteries run inward from theepicardiumto
theendocardium, and because the blood flow through the heart muscle is hindered by theheart
contraction.The phrases transmural and subendocardial infarction used to be
considered synonymous with Q-waveand non-Q-wave myocardial infarction respectively, based
on the presence or absence of Q waves on theECG. It has since been shown that there is no
clear correlation between the presence of Q waves with atransmural infarction and the absence
of Q waves with a subendocardial infarction, but Q waves areassociated with larger infarctions,
while the lack of Q waves is associated with smaller infarctions. The presence or absence of Qwaves also has clinical importance, with improved outcomes associated with alack of Q
waves.The phrase "massive attack" is not an official medical term.
Rough diagram of pain zones in myocardial infarction (dark red = most typical area, light red =
other possible areas, view of the chest).The onset of symptoms in myocardial infarction (MI) is
usually gradual, over several minutes, and rarelyinstantaneous.Chest pain is the most common
symptom of acute myocardial infarction and is oftendescribed as a sensation of tightness,
pressure, or squeezing. Chest pain due toischemia(a lack of bloodand hence oxygen supply) of
the heart muscle is termed angina pectoris. Pain radiates most often to theleftarm, but may also
radiate to the lower jaw, neck , right arm, back , andepigastrium, where it may
mimicheartburn. Any group of symptoms compatible with a sudden interruption of the blood
flow to theheart is called anacute coronary syndrome.Other conditions such as aortic
dissectionor pulmonaryembolismmay present with chest pain and must be considered in
thedifferential diagnosis.Shortness of breath (dyspnea) occurs when the damage to the heart
limits theoutputof the left ventricle,causingleft ventricular failureand consequent pulmonary
edema. Other symptoms include diaphoresis (anexcessive form of sweating), weakness,lightheadedness, nausea, vomiting, and palpitations.Loss of consciousnessand evensudden deathcan
occur in myocardial infarctions.Women often experience markedly different symptoms than
men. The most common symptoms of MI inwomen include dyspnea, weakness, andfatigue.
Fatigue, sleep disturbances, and dyspneahave beenreported as frequently occurring symptoms
which may manifest as long as one month before the actualclinically manifested ischemic event.
In women,chest painmay be less predictive of coronaryischemia than in men.Approximately half
of all MI patients have experienced warning symptoms such as chest pain prior to
theinfarction.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 relatedcomplaints. A silent course is more common in theelderly,in
patients withdiabetes 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 psychologicalfactors have been cited as possibleexplanations for the lack of
symptoms.
Diagnosis:
The diagnosis of myocardial infarction is made by integrating the history of the presenting
illness and physical examination withelectrocardiogramfindings and cardiac markers( blood
testsfor heart muscle cell damage). Acoronary angiogramallows visualizing narrowings or
obstructions on the heart vessels,and therapeutic measures can follow immediately. Atautopsy,
a pathologistcan diagnose a myocardialinfarction based onanatomopathologicalfindings.Achest
radiographand routine blood tests may indicate complications or precipitating causes and
areoften performed on admittance to anemergency department. New regional wall motion
abnormalities onan echocardiogramare also suggestive of a myocardial infarction and are
sometimes performed inequivocal cases.Technetiumandthalliumcan be used innuclear
medicineto visualize areas of reduced blood flow and tissue viability, respectively. Technetium
is used in aMUGA scan.
Diagnostic Criteria:
WHO criteria have classically been used to diagnose MI; a patient is diagnosed with myocardial
infarctionif two (probable) or three (definite) of the following criteria are satisfied:1.Clinical
history of ischemic type chest pain lasting for more than 20 minutes2 . C h a n g e s i n
s e r i a l E C G t r a c i n g s 3.Rise and fall of serum cardiac enzymes (biomarkers) such
as creatine kinase, troponinI, andlactate dehydrogenase isozymesspecific for the heart.
The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.
According to thenew guidelines, a cardiactroponinrise accompanied by either typical symptoms,
pathological Q waves,ST elevation or depression or coronary intervention are diagnostic of MI.
Physical Examination:
The general appearance of patients may vary according to the experienced symptoms; the
patient may becomfortable, or restless and in severe distress with an increased respiratory rate. A
cool and pale skiniscommon and points tovasoconstriction. Some patients have low-grade fever
(3839 C).Blood pressure may be elevated or decreased, and the pulsecan be
becomeirregular . If heart failure ensues, elevated jugular venous pressure and hepatojugular
reflux,or swelling of the legsdue to peripheraledemamay be found on inspection. Rarely, a
cardiac bulge with a pace different fromthe pulse rhythm can be felt on pericardial
examination.Various abnormalities can be found onauscultation, such as a third and fourthheart
sound, systolic murmurs,paradoxical splitting of the secondheart sound, a pericardial friction rub
andralesover the lung.12-leadelectrocardiogram (ECG) showing acute inferior ST segment

elevation MI (STEMI). Note the STsegment elevation in leads II, III, and aVF along with
reciprocal ST segment depression in leads I andaVL.
Electrocardiogram:
The primary purpose of theelectrocardiogramis to detect ischemia or acute coronary injury in
broad,symptomaticemergency departmentpopulations. However, the standard 12 leadECG has
severallimitations. AnECGrepresents a brief sample in time. Because unstable ischemic
syndromes have rapidlychanging supply versus demand characteristics, a singleECG may not
accurately represent the entire picture. It is therefore desirable to obtain serial 12
lead ECGs,particularly if the firstECGis obtainedduring a pain-free episode. Alternatively,
manyemergency departments and chest pain centersusecomputers capable of continuous ST
segment monitoring. It should also be appreciated that the standard12 leadECGdoes not directly
examine theright ventricle, and does a relatively poor job of examining the posterior basal and
lateral walls of the left ventricle. In particular, acute myocardial infarction in the distribution of
the circumflex artery is likely to produce a non diagnosticECG. The use of nonstandardECGleads like right-sided lead V4R and posterior leads V7, V8, and V9 may improve
sensitivity for rightventricular and posterior myocardial infarction. In spite of these limitations,
the 12 leadECGstands at thecenter of risk stratification for the patient with suspected acute
myocardial infarction. Mistakes ininterpretation are relatively common, and the failure to
identify high risk features has a negative effect onthe quality of patient care. The 12 lead ECG is
used to classify patients into one of three groups:1. Those with ST segment elevation or
new bundle branch block (suspicious for acute injury and a possible candidate for acute
reperfusion therapy with Thrombolyticor primary PCI),2. Those with ST segment depression or
T wave inversion (suspicious for ischemia), and3. Those with a so-called non-diagnostic
or normal ECG.A normal ECG does not rule out acute myocardial infarction. Sometimes the
earliest presentation of acutemyocardial infarction is the hyper acute T wave, which is treated the
same as ST segment elevation. In practice this is rarely seen, because it only exists for 2-30
minutes after the onset of infarction. Hyper acute T waves need to be distinguished from the
peaked T waves associated withhyperkalemia.Thecurrent guidelines for the ECG diagnosis of
acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in 2 or more
anatomically contiguous leads. This criterion is problematic, however,as acute myocardial
infarction is not the most common cause of ST segment elevation inchest pain patients. In
addition, over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in
atleast one precordial lead. The clinician must therefore be well versed in recognizing the socalled ECGmimics of acute myocardial infarction, which includeleft ventricular hypertrophy, left
bundle branch block , paced rhythm,benign early repolarization, Pericarditis, hyperkalemia, and
ventricular aneurysm.Left bundle branch block and pacing can interfere with the
electrocardiography diagnosis of acutemyocardial infarction. The GUSTO investigators
Sgarbossa et al. developed a set of criteria for identifyingacute myocardial infarction in the
presence of left bundle branch block and paced rhythm. They includeconcordant ST segment
elevation > 1 mm (0.1 mV), discordant ST segment elevation > 5 mm (0.5 mV),and concordant

ST segment depression in the left precordial leads. The presence of reciprocal changes onthe 12
lead ECG may help distinguish true acute myocardial infarction from the mimics of
acutemyocardial infarction. The contour of the ST segment may also be helpful, with a straight
or upwardlyconvex (non-concave) ST segment favoring the diagnosis of acute myocardial
infarction.The presence of ST segment elevation distinguishes between:

STEMI ("ST-Elevation Myocardial Infarction")

NSTEMI ("Non-ST-Elevation Myocardial Infarction") -- diagnosed when cardiac enzymes

areelevated.The leads with ST segment elevation help the clinician identify what area of the
heart is infarcting. It alsoenables the clinician to predict the culprit artery As the myocardial
infarction evolves, there may be loss of R wave height and development of pathologicalQ waves.
T wave inversion may persist for months or even permanently following acute
myocardialinfarction. Typically, however, the T wave recovers, leaving a pathological Q wave
as the only remainingevidence that an acute myocardial infarction has occurred.
Cardiacmarkers:
Cardiac markers or cardiac enzymes are proteins from cardiac tissue found in the blood. These
proteinsare released into the bloodstream when damage to the heart occurs, as in the case of a
myocardialinfarction. Until the1980s, the enzymesSGOTandLDHwere used to assess cardiac
injury. Then it wasfound that disproportional elevation of the
MB
subtype of the enzyme creatine kinase (CK) was very specific for myocardial injury. Current
guidelines are generally in favor of troponinsub-units I or T, whichare very specific for the heart
muscle and are thought to rise before permanent injury develops. Elevatedtroponins in the
setting of chest pain may accurately predict a high likelihood of a myocardial infarction inthe
near future.The diagnosis of myocardial infarction requires two out of three components
(history, ECG, andenzymes). When damage to the heart occurs, levels of cardiac markers rise
over time, which is why bloodtestsfor them are taken over a 24 hour period. Because these
enzyme levels are not elevated immediatelyfollowing a heart attack, patients presenting with
chest pain are generally treated with the assumption thata myocardial infarction has occurred
and then evaluated for a more precise diagnosis.

specific for myocardial injury. Current guidelines are generally in favor of troponinsub-units I or T,
whichare very specific for the heart muscle and are thought to rise before permanent injury
develops. Elevatedtroponins in the setting of chest pain may accurately predict a high likelihood
of a myocardial infarction inthe near future.The diagnosis of myocardial infarction requires two
out of three components (history, ECG, andenzymes). When damage to the heart occurs, levels
of cardiac markers rise over time, which is why bloodtestsfor them are taken over a 24 hour
period. Because these enzyme levels are not elevated immediatelyfollowing a heart attack,
patients presenting with chest pain are generally treated with the assumption thata myocardial
infarction has occurred and then evaluated for a more precise diagnosis.

Angiography:
Angiogramof the coronary arteries.In difficult cases or in situations where intervention to restore
blood flow is appropriate, coronaryangiographycan be performed. Acatheter is inserted into an
artery (usually the femoral artery) and pushedto the vessels supplying the heart. Obstructed or
narrowed arteries can be identified, and angioplasty applied as a therapeutic measure (see
below). Angioplasty requires extensive skill, especially inemergency settings, and may not
always be available out of hours. It is commonly performed byinterventional cardiologists.

Microscopy image (magn. ca 100x,H&E stain) from autopsy specimen of myocardial infarct (7
days post-infarction).Histopathological examination of the heart may reveal infarction at
autopsy. Under the microscope,myocardial infarction presents as a circumscribed area of
ischemic, coagulativenecrosis(cell death). Ongross examination, the infarct is not identifiable
within the first 12 hours.Although earlier changes can be discerned using electron
microscopy,one of the earliest changes under anormal microscope are so-called
wavy fibers
. Subsequently, the myocytecytoplasmbecomes moreeosinophilic(pink) and the cells lose their
transversal striations, with typical changes and eventually lossof thecell nucleus. The interstitium
at the margin of the infarcted area is initially infiltrated withneutrophils, then
withlymphocytes andmacrophages, which phagocytose ("eat") the myocyte debris. Thenecrotic
area is surrounded and progressively invaded bygranulation tissue, which will replace the
infarctwith a fibrous (collagenous)scar (which are typical steps inwound healing). The
interstitial space (thespace between cells outside of blood vessels) may be infiltrated withred
blood cellsThese features can be recognized in cases where the perfusion was not restored;
reperfused infarcts canhave other hallmarks, such as contraction band necrosis.
Firsta
d:
As myocardial infarction is a common medical emergency, the signs are often part of first
aid courses. Theemergency action principlesalso apply in the case of myocardial infarction.
Immediatecare:
When symptoms of myocardial infarction occur, people wait on average of 3 hours, instead of
doing whatis recommended:calling for helpimmediately. Acting immediately by calling
the emergency services can prevent sustained damage to the heart ("time is muscle").Certain
positions allow the patient to rest in a position which minimizes breathing difficulties. A halfsitting position with knees bent is often recommended. Access to more oxygen can be given
by openingthe window and widening the collar for easier breathing.Aspirincan be given quickly
(if the patient is not allergicto aspirin); but taking aspirin before calling theemergency medical
servicesmay be associated with unwanted delay. Aspirin has anantiplateleteffectwhich inhibits
formation of further thrombi (blood clots) that clog arteries. Non-enteric coatedor soluble
preparations are preferred. If chewed or dissolved, respectively, they can beabsorbedby the body
evenquicker. If the patient cannot swallow, the aspirin can be used sublingually. U.S. guidelines
recommend adose of 162 325 mg. Australian guidelines recommend a dose of 150 300
mg.Glyceryl trinitrate (nitroglycerin)sublingually(under the tongue) can be given if it has been
prescribed for the patient.If an AED is available the rescuer should immediately bring the AED

to the patient's side and be preparedto 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 toanswer questions onceemergency medical technicians arrive (if the patient
becomes unconscious). Thevictim's name and any information regarding the nature of the
victims pain will useful to health care providers. Also the exact time that these symptoms started,
what the patient was doing at the onset of symptoms, and anything else that might give clues to
the pathology of the chest pain. It is also veryimportant to relay any actions that have been taken,
such as the number or dose of aspirin or nitroglyceringiven, to the EMS personnel.Other 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 (CPR)can be administered.
Automatic external defibrillation (AED) :
Since the publication of data showing that the availability of automated external
defibrillators (AEDs) in public places may significantly increase chances of survival, many of
these have been installed in public buildings, public transport facilities, and in non-ambulance
emergency vehicles (e.g. police carsandfireengines). AEDs analyze the heart's rhythm and
determine whether the rhythm is amenable todefibrillation ("shockable"), as inventricular
tachycardiaandventricular fibrillation.
Emergencyservices:
Emergency Medical Services(EMS) Systems vary considerably in their ability to evaluate and
treat patients with suspected acute myocardial infarction. Some provide as little as first aid and
earlydefibrillation. Others employ highly trained paramedics with sophisticated technology and
advanced protocols. Early access to EMS is promoted by a 9-1-1 system currently available to
90% of the population in the United States. Most are capable of providingoxygen, IV access,
sublingualnitroglycerine, morphine,andaspirin.Some are capable of providing Thrombolytic
therapyin the prehospital setting.With primary PCIemerging as the preferred therapy for ST
segment elevation myocardial infarction,EMS can play a key role in reducingdoor to
balloon intervals (the time from presentation to a hospitalER to therestoration of coronary artery
blood flow) by performing a 12 lead ECGin the field and using thisinformation to triage the
patient to the most appropriate medical facility. In addition, the 12 lead ECG can be transmitted
to the receiving hospital, which enables time saving decisions to be made prior to the patient's
arrival. This may include a "cardiac alert" or "STEMI alert" that calls in off duty personnel
inareas where the cardiac cath labis not staffed 24 hours a day. Even in the absence of a
formal alerting program, prehospital 12 lead ECGs are independently associated with reduced
door to treatment intervalsin the emergency department.
Wildernessfirstaid:
Inwilderness first aid,a possible heart attack justifies evacuationby the fastest available means,
includingMEDEVAC, even in the earliest or precursor stages. The patient will rapidly be incapable
of further exertion and have to be carried out.
Air travel :

Certified personnel traveling by commercial aircraft may be able to assist an MI patient by using
the on- board first aid kit, which may contain some cardiac drugs (such asglyceryl
trinitratespray,aspirin, or opioidpainkillers) andoxygen. Pilots may divert the flight to land at a
nearby airport.Cardiac monitorsare being introduced by some airlines, and they can be used by
both on-board and ground-based physicians.
Trea
tmen
t:
A heart attack is amedical emergencywhich demands both immediate attention and activation of
theemergency medical services. The ultimate goal of the management in the acute phase of the
disease is tosalvage 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", andtime wasted is muscle lost.The treatments itself may have
complications. If attempts to restore the blood flow are initiated after acritical period of only a
few hours, the result is reperfusion injuryinstead of amelioration. Other treatmentmodalities may
also cause complications; the use of antithrombotics for example carries an increased
risk of bleeding.
Firstline:
Oxygen,aspirin,glyceryl trinitrate (nitroglycerin) and analgesia (usuallymorphine, hence the
popular mnemonic
MONA
,
morphine, oxygen, nitro, aspirin
) are administered as soon as possible. In many areas,first responders can be trained to administer
these prior to arrival at the hospital.Of the first line agents, only aspirin has been proven to
decreasemortality.Once the diagnosis of myocardial infarction is confirmed, other pharmacologic
agents are often given.These include beta blockers, anticoagulation (typically withheparin), and
possibly additional antiplateletagents such asclopidogrel.These agents are typically not started
until the patient is evaluated by anemergency room physician or under the direction of a
cardiologist. These agents can be used regardless of the reperfusion strategy that is to be
employed. While these agents can decrease mortality in the setting of an acute myocardial
infarction, they can lead to complications and potentially death if used in the wrong setting
Reperfusion:
The concept of reperfusion has become so central to the modern treatment of acute myocardial
infarction,that we are said to be in the reperfusion era. Patients who present with suspected acute
myocardialinfarction and ST segment elevation (STEMI) or new bundle branch block on the 12
leadECG are presumed to have an occlusive thrombosis in an epicardial coronary artery. They
are therefore candidatesfor immediate reperfusion, either withThrombolytic
therapy, percutaneous coronary intervention(PCI) or when these therapies are
unsuccessful, bypass surgery.Individuals without ST segment elevation are presumed to be
experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction
(NSTEMI). They receive many of the same initialtherapies and are often stabilized
withantiplatelet drugs and anticoagulant.If their condition remains(hemodynamically) stable,
they can be offered either latecoronary angiography with subsequentrestoration of blood flow
(revascularization), or non-invasive stress testing to determine if there issignificant ischemia that
would benefit from revascularization. If hemodynamic instability develops inindividuals with
NSTEMIs, they may undergo urgent coronary angiography and subsequentrevascularization. The

use of Thrombolytic agents is contraindicated in this patient subset, however.The basis for this
distinction in treatment regimens is that ST segment elevations on an ECG are typicallydue to
complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a
suddennarrowing of a coronary artery with preserved (but diminished) flow to the distal
myocardium.Anticoagulation and antiplatelet agents are given to prevent the narrowed artery
from occluding.At least 10% of patients with STEMI don't develop myocardial necrosis (as
evidenced by a rise in cardiacmarkers) and subsequent q waves on EKG after reperfusion
therapy. Such a successful restoration of flowto the infarct-related artery during an acute
myocardial infarction is known as "aborting" the myocardialinfarction. If treated within the hour,
about 25% of STEMIs can be aborted.
Thrombolytictherapy:
Thrombolytic therapy is indicated for the treatment of STEMI if the drug can be administered
within 12hours of the onset of symptoms, the patient is eligible based on exclusion criteria, and
primary PCI is notimmediately available. The effectiveness of Thrombolytic therapyis highest in
the first 2 hours. After 12hours, the risk associated with Thrombolytic therapy outweighs any
benefit. Because irreversible injuryoccurs within 24 hours of the infarction, there is a limited
window of time available for reperfusion towork.Thrombolytic drugs are contraindicated for the
treatment of unstable angina and NSTEMI and for thetreatment of individuals with evidence
of cardiogenic shock .Although no perfect Thrombolytic agent exists, an ideal Thrombolytic
drug would lead to rapidreperfusion, have a high sustained patency rate, be specific for recent
thrombi, be easily and rapidlyadministered, create a low risk for intra-cerebral and systemic
bleeding, have no antigenicity, adversehemodynamic effects, or clinically significant drug
interactions, and be cost effective. Currently availableThrombolytic agents
includestreptokinase, urokinase, andalteplase (recombinanttissue plasminogenactivator , rtPA).
More recently, Thrombolytic agents similar in structure to rtPA such
asreteplaseandtenecteplasehave been used. These newer agents boast efficacy at least as good as
rtPA with significantly easier administration. The Thrombolytic agent used in a particular
individual is based on institution preference and the age of the patient.Depending on the
Thrombolytic agent being used,adjuvantanticoagulation with heparinor low molecular weight
heparinmay be of benefit. With tPA and related agents (reteplase and tenecteplase), heparin
isneeded to maintain coronary artery patency. Because of the anticoagulant effect of fibrinogen
depletionwith streptokinase and urokinase treatment, it is less necessary there.Intracranial
bleeding (ICB) and subsequentcerebrovascular accident (CVA) is a serious side effect
of Thrombolytic use. The risk of ICB is dependent on a number of factors, including a previous
episode of intracranial bleed, age of the individual, and the Thrombolytic regimen that is being
used. In general, therisk of ICB due to Thrombolytic use for the treatment of an acute myocardial
infarction is between 0.5 and1 percent.Thrombolytic therapy to abort a myocardial infarction is
not always effective. The degree of effectivenessof a Thrombolytic agent is dependent on the
time since the myocardial infarction began, with the bestresults occurring if the Thrombolytic
agent is used within an hour of the onset of symptoms.
[

If theindividual presents more than 12 hours after symptoms commenced, the risk of intracranial
bleed areconsidered higher than the benefits of the Thrombolytic agent. Failure rates of
Thrombolytic can be ashigh as 20% or higher. In cases of failure of the Thrombolytic agent to
open the infarct-related coronaryartery, the patient is then either treated conservatively with
anticoagulants or allowed to "complete theinfarction" or percutaneous coronary
intervention(PCI, see below) is then performed. Percutaneouscoronary intervention in this setting
is known as "rescue PCI" or "salvage PCI". Complications, particularly bleeding, are
significantly higher with rescue PCI than with primary PCI due to the action of the Thrombolytic
agent.
The current guidelines in the United States restrict primary PCI to hospitals with available
emergency bypass surgery as a backup, but this is not the case in other parts of the
world.Primary PCI involves performing a coronaryangiogram to determine the anatomical
location of theinfarcting vessel, followed by balloon angioplasty(and frequently deployment of
an intracoronary stent)of the thrombosis arterial segment. In some settings, an extraction
catheter may be used to attempt toaspirate (remove) the thrombus prior to balloon
angioplasty. While the uses of intracoronary stentsdo notimprove the short term outcomes in
primary PCI, the use of stents is widespread because of the decreasedrates of procedures
to treat restenosis compared to balloon angioplasty.Adjuvant therapy during primary PCI
includes intravenous heparin, aspirin,and clopidogrel.The uses of glycoprotein IIb/IIIa
inhibitors are often used in the setting of primary PCI to reduce the risk of
ischemiccomplications during the procedure. Due to the number of antiplatelet agents and
anticoagulants usedduring primary PCI, the risk of bleeding associated with the procedure are
higher than during an electivePCI.
Coronary artery bypasses surgery
during mobilization (freeing) of the right coronary arteryfrom itssurrounding tissue, adipose
tissue(yellow). The tube visible at the bottom is the aortic cannula (returns blood from
the HLM). The tube above it (obscured by the surgeon on the right) is the venous
cannula(receives blood from the body). The patient's heartis stopped and theaortais crossclamped. The patient'shead (not seen) is at the bottom.Despite the guidelines, emergency bypass
surgery for the treatment of an acute myocardial infarction (MI)is less common then PCI or
medical management. In an analysis of patients in the U.S. National Registryof Myocardial
Infarction(NRMI) from January 1995 to May 2004, the percentage of patients withCardiogenic
shock treated with primary PCI rose from 27.4% to 54.4%, while the increase in CABGtreatment
was only from 2.1% to 3.2%.Emergency coronary artery bypass graft surgery (CABG) is usually
undertaken to simultaneously treat amechanical complication, such as a ruptured papillary
muscle, or a ventricular septal defect, with ensueingCardiogenic shock. In uncomplicated MI,
the mortality ratecan be high when the surgery is performedimmediately following the infarction.
If this option is entertained, the patient should be stabilized prior to surgery, with supportive
interventions such as the use of an intra-aortic balloon pump.In patientsdeveloping Cardiogenic
shock after a myocardial infarction, both PCI and CABG are satisfactorytreatment options, with
similar survival rates.Coronary artery bypass surgery involves an artery or vein from the patient

being implanted to bypassnarrowingsor occlusions on the coronary arteries. Several arteries and
veins can be used; however internal mammary arterygrafts have demonstrated significantly
better long-term patency rates than greatsaphenous veingrafts. In patients with two or more
coronary arteries affected, bypass surgery is associatedwith higher long-termsurvival
ratescompared to percutaneous interventions In patients with single vesseldisease, surgery is
comparably safe and effective, and may be a treatment option in selected cases. Bypasssurgery
has higher costs initially, but becomescost-effectivein the long term. A surgical bypass
graft ismoreinvasiveinitially but bears less risk of recurrent procedures (but these may be
again minimallyinvasive).
Monitoringforarrhythmias:
Additional objectives are to prevent life-threatening arrhythmias or conduction disturbances.
This requiresmonitoring in acoronary care unit and protocolised administration of antiarrhythmic
agents.Antiarrhythmic agents are typically only given to individuals with life-threatening
arrhythmias after amyocardial infarction and not to suppress the ventricular ectopythat is often
seen after a myocardialinfarction.
Rehabiltation:
Cardiac rehabilitation aims to optimize function and quality of lifein those afflicted with a heart
disease.This can be with the help of a physician, or in the form of a cardiac rehabilitation
program.Physical exerciseis an important part of rehabilitationafter a myocardial infarction, with
beneficial effectson cholesterol levels, blood pressure, weight, stress and mood. Some patients
become afraid of exercising because it might trigger another infarct. Patients are stimulated to
exercise, and should only avoid certainexerting activities such as shoveling. Local authorities
may place limitations on driving motorizedvehicles.Some people are afraid to havesex after a
heart attack. Most people can resume sexual activitiesafter 3 to 4 weeks. The amount of activity
needs to be dosed to the patients possibilities.
Secondaryprevention:
The risk of a recurrent myocardial infarction decreases with strict blood pressure management
andlifestyle changes, chiefly smoking cessation, regular exercise,a sensiblediet for patients with
heartdisease, andlimitation of alcohol intake.Patients are usually commenced on several longterm medications post-MI, with the aim of preventingsecondary cardiovascular events such as
further myocardial infarctions,congestive heart failureor cerebrovascular accident(CVA). Unless
contraindicated, such medications may include:

Antiplatelet drugtherapy such as aspirin and/or clopidogrelshould be continued to reduce the

risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low
costand 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 hemorrhageis increased.

Beta blocker therapy such asmetoprololor carvedilolshould be commenced. These have

been particularly beneficial in high-risk patients such as those withleft ventricular dysfunction

and/or continuing cardiacischemia. -Blockers decrease mortality and morbidity. They also
improvesymptoms of cardiac ischemia in NSTEMI.

ACE inhibitor therapy should be commenced 2448 hours post-MI in hemodynamicallystable patients, particularly in patients with a history of MI,diabetes
mellitus,hypertension,anterior location of infarct (as assessed by ECG), and/or evidence of left
ventricular dysfunction. ACEinhibitors reduce mortality, the development of heart failure, and
decrease ventricular remodelling post-MI.

Statintherapy has been shown to reduce mortality and morbidity post-MI. The effects of
statinsmay be more than their LDL lowering effects. The general consensus is that statins
have plaquestabilization and multiple other ("pleiotropic") effects that may prevent myocardial
infarction inaddition to their effects on blood lipids.

Thealdosterone antagonist agenteplerenonehas been shown to further reduce risk

of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction,
whenused in conjunction with standard therapies above.

Omega-3 fatty acids,commonly found in fish, have been shown to reduce mortality postMI.While the mechanism by which these fatty acids decrease mortality is unknown, it has
been postulated that the survival benefit is due to electrical stabilization and the prevention
of ventricular fibrillation.
[135]
However, further studies in a high-risk subset have not shown a clear-cut decrease in potentially
fatal arrhythmias due to omega-3 fatty acids.
New therapies under investigation :
Patients who receivestem cell treatmentby coronary artery injections of stem cellsderived from
their own bone marrowafter a myocardial infarction (MI) show improvements in left
ventricular ejection fraction and end-diastolic volume not seen with placebo. The larger the
initial infarct size, the greater the effect of the infusion.Clinical trialsof progenitor cell infusion
as a treatment approach to ST elevation MI are proceeding.There are currently
3 biomaterialandtissue engineeringapproaches for the treatment of MI, but these arein an even
earlier stage of medical research, so many questions and issues need to be addressed beforethey
can be applied to patients. The first involves polymericleft ventricular restraints in the prevention
of heart failure.The second utilizes
in vitro
engineered cardiac tissue, which is subsequently implanted
invivo
. The final approach entails injecting cells and/or a scaffold into the myocardium to create
in situ
engineered cardiac tissue.
Complications:
Complications may occur immediately following the heart attack (in theacutephase), or may
need time todevelop (achronic problem). After an infarction, an obvious complication is a
second infarction, whichmay occur in the domain of another atherosclerotic coronary artery or in
the same zone if there are anylive cells left in the infarct.

Congestiveheartfailure:
A myocardial infarction may compromise the function of the heart as a pump for thecirculation,
a statecalledheart failure. There are different types of heart failure; left- or right-sided (or
bilateral) heart failuremay occur depending on the affected part of the heart, and it is a lowoutput type of failure. If one of theheart valves is affected, this may cause dysfunction, such
asmitral regurgitationin the case of left-sidedMI. The incidence of heart failure is particularly
high in patients with diabetes and requires specialmanagement strategies.
Myocardialrupture:
Myocardial ruptureis most common three to five days after myocardial infarction, commonly of
smalldegree, but may occur one day to three weeks later, in as many as 10% of all MIs. This may
occur in thefree walls of the ventricles, theseptumbetween them, the papillary muscles, or less
commonly the atria.Rupture occurs because of increased pressure against the weakened walls of
the heart chambers due toheart muscle that cannot pump blood out effectively. The weakness
may also lead to ventricular aneurysm,a localized dilation or ballooning of the heart
chamber.Risk factors for myocardial rupture include completion of infarction (no
revascularization performed),female sex, advanced age, and a lack of a previous history of
myocardial infarction. The shear stress between the infarcted segment and the surrounding
normal myocardium (which may be hypercontractilein the post-infarction period) makes it a
nidus for rupture.Rupture is usually a catastrophic event that may result a life-threatening process
known ascardiactamponade, in which blood accumulates within the pericardium or heart sac, and
compresses the heart tothe point where it cannot pump effectively. Rupture of the
intraventricular septum (the muscle separatingthe left and right ventricles) causes aventricular
septal defectwith shuntingof blood through the defectfrom the left side of the heart to the right
side of the heart. Rupture of the papillary muscle may also leadto acutemitral regurgitationand
subsequent pulmonary edemaand possibly evenCardiogenic shock .
Life-threateningarrhythmia:
A 12 leadelectrocardiogram showing ventricular tachycardia.
Congestiveheartfailure:
A myocardial infarction may compromise the function of the heart as a pump for thecirculation,
a statecalledheart failure. There are different types of heart failure; left- or right-sided (or
bilateral) heart failuremay occur depending on the affected part of the heart, and it is a lowoutput type of failure. If one of theheart valves is affected, this may cause dysfunction, such
asmitral regurgitationin the case of left-sidedMI. The incidence of heart failure is particularly
high in patients with diabetes and requires specialmanagement strategies.
Myocardialrupture:
Myocardial ruptureis most common three to five days after myocardial infarction, commonly of
smalldegree, but may occur one day to three weeks later, in as many as 10% of all MIs. This may
occur in thefree walls of the ventricles, theseptumbetween them, the papillary muscles, or less
commonly the atria.Rupture occurs because of increased pressure against the weakened walls of
the heart chambers due toheart muscle that cannot pump blood out effectively. The weakness
may also lead to ventricular aneurysm,a localized dilation or ballooning of the heart
chamber.Risk factors for myocardial rupture include completion of infarction (no
revascularization performed),female sex, advanced age, and a lack of a previous history of
myocardial infarction. The shear stress between the infarcted segment and the surrounding

normal myocardium (which may be hypercontractilein the post-infarction period) makes it a

nidus for rupture.Rupture is usually a catastrophic event that may result a life-threatening process
known ascardiactamponade, in which blood accumulates within the pericardium or heart sac, and
compresses the heart tothe point where it cannot pump effectively. Rupture of the
intraventricular septum (the muscle separatingthe left and right ventricles) causes aventricular
septal defectwith shuntingof blood through the defectfrom the left side of the heart to the right
side of the heart. Rupture of the papillary muscle may also leadto acutemitral regurgitationand
subsequent pulmonary edemaand possibly evenCardiogenic shock .
Life-threateningarrhythmia:
A 12 leadelectrocardiogram showing ventricular tachycardia.
ince the electrical characteristics of the infarcted tissue change (seePathophysiology
section),arrhythmias are a frequent complication. The re-entry phenomenon may cause too fast
heart rates(ventricular tachycardia and evenventricular fibrillation), and ischemia in the electrical
conduction systemof the heartmay cause acomplete heart block (when the impulse from
the sinoatrial node, the normalcardiac pacemaker, doesn't reach the heart chambers any more).
Pericarditis:
As a reaction to the damage of the heart muscle,inflammatorycells are attracted. The
inflammation mayreach out and affect the heart sac. This is called Pericarditis. InDressler's
syndrome,this occurs severalweeks after the initial event.
Cardiogenicshock:
A complication that may occur in the acute setting soon after a myocardial infarction or in the
weeksfollowing it iscardiogenic shock .Cardiogenic shock is defined as a hemodynamic state in
which the heartcannot produce enough of acardiac outputto supply an adequate amount
of oxygenated blood to thetissues of the body.While the data on performing interventions on
individuals with Cardiogenic shock is sparse, trial datasuggests a long-term mortality benefit in
undergoing revascularization if the individual is less than 75years old and if the onset of the
acute myocardial infarction is less than 36 hours and the onset of Cardiogenic shock is less than
18 hours. If the patient with cardiogenic shock is not going to berevascularized, aggressive
hemodynamic support is warranted, with insertion of an intra-aortic balloon pumpif not
contraindicated. If diagnostic coronary angiography does not reveal a culprit blockage that isthe
cause of the cardiogenic shock, the prognosis is poor.
P
rog
nsi:
The prognosis for patients with myocardial infarction varies greatly, depending on the
patient, thecondition itself and the given treatment. Using simplevariables which are immediately
available in theemergency room, patients with a higher risk of adverse outcome can be identified.
For example, one studyfound that 0.4% of patients with a low risk profile had died after 90 days,
whereas themortality rateinhigh risk patients was 21.1%.Although studies differ in the identified
variables, some of the morereproducedrisk stratifiers includeage,hemodynamicparameters (such
asheart failure, cardiac arreston admission, systolic blood pressure,or Killip class of two
or greater), ST-segment deviation,diabetes, serum creatinineconcentration, peripheral vascular
disease and elevation of cardiac markers.Assessment of left ventricular ejection fractionmay
increase the predictive power of some risk stratification models. The prognostic importance of
Q-waves is debated. Prognosis is significantlyworsened if a mechanical complication ( papillary
musclerupture, myocardial free wall rupture, and so on)were to occur. There is evidence that
case fatality of myocardial infarction has been improving over theyears in all ethnicities.

Legalimplications:
Atcommon law,a myocardial infarction is generally adisease, but may sometimes be aninjury.
This hasimplications for no-fault insurance schemes such asworkers' compensation. A heart
attack is generally notcovered; however, it may be awork-related injuryif it results, for example,
from unusual emotional stressor unusual exertion. Additionally, in some jurisdictions,
heart attacks suffered by persons in particular occupations such as police officersmay be
classified as line-of-duty injuries by statute or policy. In somecountries or states, a person who
has suffered from a myocardial infarction may be prevented from participating in activity that
puts other people's lives at risk, for example driving a car, taxi or airplane.