Infark Miocard Bab II

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7urther 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.

B.Epidemiology

Myocardial infarction is a common presentation of ischemic heart disease. The *8 estimated

that in 3$$3, 43.9: of deaths worldwide were from ischemic heart disease. Ischemic heart disease is

the leading cause of death in deeloped countries, but third to AI'; and lower respiratory infections in

deeloping countries.

In the


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modifiable risk factors include age, gender, and family history of an early heart attack (before the age

of 9$), which is thought of as reflecting a genetic predisposition.

;ocioeconomic factors such as a shorter education and lower income (particularly in women),

and liing with a partner may also contribute to the risk of MI. To understand epidemiological study

results, itBs important to note that many factors associated with MI mediate their risk ia other factors.

7or example, the effect of education is partially based on its effect on income and marital status.

omen who use combined oral contraceptie pills hae 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.

+reactie protein (+6) is a sensitie but nonspecific marker for inflammation. /leated +6 blood

leels, especially measured with high sensitiity assays, can predict the risk of MI, as well as stroke

and deelopment of diabetes. Moreoer, some drugs for MI might also reduce +6 leels. The use of

high sensitiity +6 assays as a means of screening the general population is adised 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 +6 plays a direct role in atherosclerosis remains

uncertain.

Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis

is ery common, this could hae great conse-uences for public health ;erological studies measuring

antibody leels against typical periodontitiscausing bacteria found that such antibodies were more

present in subCects with coronary heart disease eriodontitis tends to increase blood leels of +6,

fibrinogen and cytokines@ thus, periodontitis may mediate its effect on MI risk ia 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 butremains to be established.

Daldness, hair greying, a diagonal crease and possibly other skin features are independent risk

factors for MI. Their role remains controersial@ a common denominator of these signs and the risk of

MI are supposed, possibly genetic.

http://en.wikipedia.org/wiki/Genetic_predispositionhttp://en.wikipedia.org/wiki/Socioeconomicshttp://en.wikipedia.org/wiki/Educationhttp://en.wikipedia.org/wiki/Incomehttp://en.wikipedia.org/wiki/Cohabitationhttp://en.wikipedia.org/wiki/Marital_statushttp://en.wikipedia.org/wiki/Combined_oral_contraceptive_pillhttp://en.wikipedia.org/wiki/Atheromahttp://en.wikipedia.org/wiki/C-reactive_proteinhttp://en.wikipedia.org/wiki/Biomarker_(medicine)http://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Strokehttp://en.wikipedia.org/wiki/Screening_(medicine)http://en.wikipedia.org/wiki/Coronary_artery_diseasehttp://en.wikipedia.org/wiki/Periodontiumhttp://en.wikipedia.org/wiki/Periodontitishttp://en.wikipedia.org/wiki/Public_healthhttp://en.wikipedia.org/wiki/Serologyhttp://en.wikipedia.org/wiki/Antibodyhttp://en.wikipedia.org/wiki/Bacteriahttp://en.wikipedia.org/wiki/Fibrinogenhttp://en.wikipedia.org/wiki/Cytokineshttp://en.wikipedia.org/wiki/Medical_researchhttp://en.wikipedia.org/wiki/Plateletshttp://en.wikipedia.org/wiki/Foam_cellhttp://en.wikipedia.org/wiki/Baldnesshttp://en.wikipedia.org/wiki/Grey_hairhttp://en.wikipedia.org/wiki/Skinhttp://en.wikipedia.org/wiki/Genetic_predispositionhttp://en.wikipedia.org/wiki/Socioeconomicshttp://en.wikipedia.org/wiki/Educationhttp://en.wikipedia.org/wiki/Incomehttp://en.wikipedia.org/wiki/Cohabitationhttp://en.wikipedia.org/wiki/Marital_statushttp://en.wikipedia.org/wiki/Combined_oral_contraceptive_pillhttp://en.wikipedia.org/wiki/Atheromahttp://en.wikipedia.org/wiki/C-reactive_proteinhttp://en.wikipedia.org/wiki/Biomarker_(medicine)http://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Strokehttp://en.wikipedia.org/wiki/Screening_(medicine)http://en.wikipedia.org/wiki/Coronary_artery_diseasehttp://en.wikipedia.org/wiki/Periodontiumhttp://en.wikipedia.org/wiki/Periodontitishttp://en.wikipedia.org/wiki/Public_healthhttp://en.wikipedia.org/wiki/Serologyhttp://en.wikipedia.org/wiki/Antibodyhttp://en.wikipedia.org/wiki/Bacteriahttp://en.wikipedia.org/wiki/Fibrinogenhttp://en.wikipedia.org/wiki/Cytokineshttp://en.wikipedia.org/wiki/Medical_researchhttp://en.wikipedia.org/wiki/Plateletshttp://en.wikipedia.org/wiki/Foam_cellhttp://en.wikipedia.org/wiki/Baldnesshttp://en.wikipedia.org/wiki/Grey_hairhttp://en.wikipedia.org/wiki/Skin


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D. Pat"op"ysiology

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 preenting

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 eent 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 oer decades. Dlood stream column irregularities isible on angiographies reflect artery lumen

narrowing as a result of decades of adancing 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 seere enough pla-ue rupture occurs in the coronary asculature, 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. 6ecent 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

http://en.wikipedia.org/wiki/Atherosclerosishttp://en.wikipedia.org/wiki/Atheromahttp://en.wikipedia.org/wiki/Coronary_arteryhttp://en.wikipedia.org/wiki/Acute_coronary_syndromehttp://en.wikipedia.org/wiki/Coronary_artery_diseasehttp://en.wikipedia.org/wiki/Atherosclerosishttp://en.wikipedia.org/wiki/Atheromahttp://en.wikipedia.org/wiki/Cholesterolhttp://en.wikipedia.org/wiki/Arteryhttp://en.wikipedia.org/wiki/Coronary_arteryhttp://en.wikipedia.org/wiki/Lumenhttp://en.wikipedia.org/wiki/Thrombushttp://en.wikipedia.org/wiki/Ischemic_cascadehttp://en.wikipedia.org/wiki/Ischemic_cascadehttp://en.wikipedia.org/wiki/Necrosishttp://en.wikipedia.org/wiki/Collagenhttp://en.wikipedia.org/wiki/Scarhttp://en.wikipedia.org/wiki/Apoptosishttp://en.wikipedia.org/wiki/Atherosclerosishttp://en.wikipedia.org/wiki/Atheromahttp://en.wikipedia.org/wiki/Coronary_arteryhttp://en.wikipedia.org/wiki/Acute_coronary_syndromehttp://en.wikipedia.org/wiki/Coronary_artery_diseasehttp://en.wikipedia.org/wiki/Atherosclerosishttp://en.wikipedia.org/wiki/Atheromahttp://en.wikipedia.org/wiki/Cholesterolhttp://en.wikipedia.org/wiki/Arteryhttp://en.wikipedia.org/wiki/Coronary_arteryhttp://en.wikipedia.org/wiki/Lumenhttp://en.wikipedia.org/wiki/Thrombushttp://en.wikipedia.org/wiki/Ischemic_cascadehttp://en.wikipedia.org/wiki/Ischemic_cascadehttp://en.wikipedia.org/wiki/Necrosishttp://en.wikipedia.org/wiki/Collagenhttp://en.wikipedia.org/wiki/Scarhttp://en.wikipedia.org/wiki/Apoptosis


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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 elocity between inCured and uninCured tissue can trigger reentry or a

feedback loop that is belieed to be the cause of many lethal arrhythmias. The most serious of these

arrhythmias is entricular fibrillation (E7ib!E7), an extremely fast and chaotic heart rhythm that is the

leading cause of sudden cardiac death. Another life threatening arrhythmia is entricular tachycardia

(ETach!ET), which may or may not cause sudden cardiac death. *oweer, entricular tachycardia

usually results in rapid heart rates that preent the heart from pumping blood effectiely. +ardiac

output and blood pressure may fall to dangerous leels, which is particularly bad for the patient

experiencing acute myocardial infarction.

The cardiac defibrillator is a deice that was specifically designed to terminate these potentially

fatal arrhythmias. The deice works by deliering 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.

E. T!igge!s

*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 indiidual usually performs

Guantitatiely, the period of intense exercise and subse-uent recoery is associated with about a 9fold

higher myocardial infarction rate (compared with other more relaxed time frames) for people who are

physically ery fit 7or those in poor physical condition, the rate differential is oer ?%fold higher. 8ne

obsered mechanism for this phenomenon is the increased arterial pulse pressure stretching andrelaxation of arteries with each heart beat which, as has been obsered with intraascular ultrasound,

increases mechanical shear stress on atheromas and the likelihood of pla-ue rupture.

Acute seere infection, such as pneumonia, can trigger myocardial infarction. A more

controersial link is that between +hlamydophila pneumoniae infection and atherosclerosis. hile this

intracellular organism has been demonstrated in atherosclerotic pla-ues, eidence is inconclusie as to

whether it can be considered a causatie factor. Treatment with antibiotics in patients with proen

http://en.wikipedia.org/wiki/Cardiac_arrhythmia#Re-entryhttp://en.wikipedia.org/wiki/Ventricular_fibrillationhttp://en.wikipedia.org/wiki/Ventricular_tachycardiahttp://en.wikipedia.org/wiki/Cardiac_outputhttp://en.wikipedia.org/wiki/Cardiac_outputhttp://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Defibrillatorhttp://en.wikipedia.org/wiki/Reboothttp://en.wikipedia.org/wiki/Stress_(psychology)http://en.wikipedia.org/wiki/Intravascular_ultrasoundhttp://en.wikipedia.org/wiki/Atheromahttp://en.wikipedia.org/wiki/Pneumoniahttp://en.wikipedia.org/wiki/Chlamydophila_pneumoniaehttp://en.wikipedia.org/wiki/Cardiac_arrhythmia#Re-entryhttp://en.wikipedia.org/wiki/Ventricular_fibrillationhttp://en.wikipedia.org/wiki/Ventricular_tachycardiahttp://en.wikipedia.org/wiki/Cardiac_outputhttp://en.wikipedia.org/wiki/Cardiac_outputhttp://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Defibrillatorhttp://en.wikipedia.org/wiki/Reboothttp://en.wikipedia.org/wiki/Stress_(psychology)http://en.wikipedia.org/wiki/Intravascular_ultrasoundhttp://en.wikipedia.org/wiki/Atheromahttp://en.wikipedia.org/wiki/Pneumoniahttp://en.wikipedia.org/wiki/Chlamydophila_pneumoniae


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atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary ascular

diseases.

#. Classifiation

+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 ;T

segment eleation myocardial infarction (;T/MI), non;T segment eleation myocardial infarction

(;T/MI), and unstable angina (


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heart muscle is more ulnerable 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

Gwae and nonGwae myocardial infarction respectiely, based on the presence or absence of G

waes on the /+0. It has since been shown that there is no clear correlation between the presence of G

waes with a transmural infarction and the absence of G waes with a subendocardial infarction, but G

waes are associated with larger infarctions, while the lack of G waes is associated with smaller

infarctions. The presence or absence of Gwaes also has clinical importance, with improed outcomes

associated with a lack of G waes.

$. Symptoms

6ough diagram of pain Fones in myocardial infarction (dark red 5 most typical area, light red 5

other possible areas, iew of the chest).

The onset of symptoms in myocardial infarction (MI) is usually gradual, oer seeral 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. 8ther conditions such as aortic dissection

or pulmonary embolism may present with chest pain and must be considered in the differential

diagnosis.

http://en.wikipedia.org/wiki/Epicardiumhttp://en.wikipedia.org/wiki/Endocardiumhttp://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Correlationhttp://en.wikipedia.org/wiki/Chest_painhttp://en.wikipedia.org/wiki/Ischemiahttp://en.wikipedia.org/wiki/Angina_pectorishttp://en.wikipedia.org/wiki/Armhttp://en.wikipedia.org/wiki/Jawhttp://en.wikipedia.org/wiki/Neckhttp://en.wikipedia.org/wiki/Human_backhttp://en.wikipedia.org/wiki/Epigastriumhttp://en.wikipedia.org/wiki/Heartburnhttp://en.wikipedia.org/wiki/Acute_coronary_syndromehttp://en.wikipedia.org/wiki/Aortic_dissectionhttp://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Differential_diagnosishttp://en.wikipedia.org/wiki/Differential_diagnosishttp://en.wikipedia.org/wiki/Epicardiumhttp://en.wikipedia.org/wiki/Endocardiumhttp://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Correlationhttp://en.wikipedia.org/wiki/Chest_painhttp://en.wikipedia.org/wiki/Ischemiahttp://en.wikipedia.org/wiki/Angina_pectorishttp://en.wikipedia.org/wiki/Armhttp://en.wikipedia.org/wiki/Jawhttp://en.wikipedia.org/wiki/Neckhttp://en.wikipedia.org/wiki/Human_backhttp://en.wikipedia.org/wiki/Epigastriumhttp://en.wikipedia.org/wiki/Heartburnhttp://en.wikipedia.org/wiki/Acute_coronary_syndromehttp://en.wikipedia.org/wiki/Aortic_dissectionhttp://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Differential_diagnosishttp://en.wikipedia.org/wiki/Differential_diagnosis


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;hortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left

entricle, causing left entricular failure and conse-uent pulmonary edema. 8ther symptoms include

diaphoresis (an excessie form of sweating), weakness, lightheadedness, nausea, omiting, and

palpitations. &oss of consciousness and een sudden death can occur in myocardial infarctions.

omen often experience markedly different symptoms than men. The most common symptoms

of MI in women include dyspnea, weakness, and fatigue. 7atigue, sleep disturbances, and dyspnea hae

been reported as fre-uently occurring symptoms which may manifest as long as one month before the

actual clinically manifested ischemic eent. In women, chest pain may be less predictie of coronary

ischemia than in men.

Approximately half of all MI patients hae 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 discoered 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 neres of

the host. In diabetics, differences in pain threshold, autonomic neuropathy, and psychological factors

hae been cited as possible explanations for the lack of symptoms.

H. 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 isualiFing narrowings or obstructions on the

heart essels, 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. ew regional wall motion

abnormalities on an echocardiogram are also suggestie of a myocardial infarction and are sometimes

performed in e-uiocal cases. Technetium and thallium can be used in nuclear medicine to isualiFe

areas of reduced blood flow and tissue iability, respectiely. Technetium is used in a M

http://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Cardiac_outputhttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_ventricular_failurehttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Diaphoresishttp://en.wikipedia.org/wiki/Sweatinghttp://en.wikipedia.org/wiki/Light-headednesshttp://en.wikipedia.org/wiki/Nauseahttp://en.wikipedia.org/wiki/Vomitinghttp://en.wikipedia.org/wiki/Palpitationhttp://en.wikipedia.org/wiki/Unconsciousnesshttp://en.wikipedia.org/wiki/Sudden_deathhttp://en.wikipedia.org/wiki/Fatigue_(physical)http://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Chest_painhttp://en.wikipedia.org/wiki/Ischemiahttp://en.wikipedia.org/wiki/Elderlyhttp://en.wikipedia.org/wiki/Diabetes_mellitushttp://en.wikipedia.org/wiki/Diabetes_mellitushttp://en.wikipedia.org/wiki/Heart_transplantationhttp://en.wikipedia.org/wiki/Organ_donationhttp://en.wikipedia.org/wiki/Pain_thresholdhttp://en.wikipedia.org/wiki/Autonomic_neuropathyhttp://en.wikipedia.org/wiki/Psychologyhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Cardiac_markerhttp://en.wikipedia.org/wiki/Blood_testhttp://en.wikipedia.org/wiki/Cardiac_musclehttp://en.wikipedia.org/wiki/Cell_(biology)http://en.wikipedia.org/wiki/Coronary_catheterizationhttp://en.wikipedia.org/wiki/Autopsyhttp://en.wikipedia.org/wiki/Pathologisthttp://en.wikipedia.org/wiki/Anatomical_pathologyhttp://en.wikipedia.org/wiki/Chest_radiographhttp://en.wikipedia.org/wiki/Emergency_departmenthttp://en.wikipedia.org/wiki/Medical_ultrasonographyhttp://en.wikipedia.org/wiki/Technetiumhttp://en.wikipedia.org/wiki/Thalliumhttp://en.wikipedia.org/wiki/Nuclear_medicinehttp://en.wikipedia.org/wiki/MUGA_scanhttp://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Cardiac_outputhttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_ventricular_failurehttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Diaphoresishttp://en.wikipedia.org/wiki/Sweatinghttp://en.wikipedia.org/wiki/Light-headednesshttp://en.wikipedia.org/wiki/Nauseahttp://en.wikipedia.org/wiki/Vomitinghttp://en.wikipedia.org/wiki/Palpitationhttp://en.wikipedia.org/wiki/Unconsciousnesshttp://en.wikipedia.org/wiki/Sudden_deathhttp://en.wikipedia.org/wiki/Fatigue_(physical)http://en.wikipedia.org/wiki/Dyspneahttp://en.wikipedia.org/wiki/Chest_painhttp://en.wikipedia.org/wiki/Ischemiahttp://en.wikipedia.org/wiki/Elderlyhttp://en.wikipedia.org/wiki/Diabetes_mellitushttp://en.wikipedia.org/wiki/Diabetes_mellitushttp://en.wikipedia.org/wiki/Heart_transplantationhttp://en.wikipedia.org/wiki/Organ_donationhttp://en.wikipedia.org/wiki/Pain_thresholdhttp://en.wikipedia.org/wiki/Autonomic_neuropathyhttp://en.wikipedia.org/wiki/Psychologyhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Cardiac_markerhttp://en.wikipedia.org/wiki/Blood_testhttp://en.wikipedia.org/wiki/Cardiac_musclehttp://en.wikipedia.org/wiki/Cell_(biology)http://en.wikipedia.org/wiki/Coronary_catheterizationhttp://en.wikipedia.org/wiki/Autopsyhttp://en.wikipedia.org/wiki/Pathologisthttp://en.wikipedia.org/wiki/Anatomical_pathologyhttp://en.wikipedia.org/wiki/Chest_radiographhttp://en.wikipedia.org/wiki/Emergency_departmenthttp://en.wikipedia.org/wiki/Medical_ultrasonographyhttp://en.wikipedia.org/wiki/Technetiumhttp://en.wikipedia.org/wiki/Thalliumhttp://en.wikipedia.org/wiki/Nuclear_medicinehttp://en.wikipedia.org/wiki/MUGA_scan


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*8 criteria hae classically been used to diagnose MI@ a patient is diagnosed with myocardial

infarction if two (probable) or three (definite) of the following criteria are satisfied>

4. +linical history of ischemic type chest pain lasting for more than 3$ minutes

3. +hanges in serial /+0 tracings

?. 6ise and fall of serum cardiac enFymes (biomarkers) such as creatine kinase, troponin I, and

lactate dehydrogenase isoFymes specific for the heart.

The *8 criteria were refined in 3$$$ to gie more prominence to cardiac biomarkers.

According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms,

pathological G waes, ;T eleation or depression or coronary interention are diagnostic of MI.

a. P"ysial e%amination>

The general appearance of patients may ary according to the experienced symptoms@ the

patient may be comfortable, or restless and in seere distress with an increased respiratory rate. A cool

and pale skin is common and points to asoconstriction. ;ome patients hae lowgrade feer (?H?J

K+). Dlood pressure may be eleated or decreased, and the pulse can be become irregular .

If heart failure ensues, eleated Cugular enous pressure and hepatoCugular reflux, or swelling of

the legs due to peripheral edema may be found on inspection. 6arely, 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 oer the lung.

http://en.wikipedia.org/wiki/Creatine_kinasehttp://en.wikipedia.org/wiki/Troponinhttp://en.wikipedia.org/wiki/Lactate_dehydrogenasehttp://en.wikipedia.org/wiki/Isozymehttp://en.wikipedia.org/wiki/Troponinhttp://en.wikipedia.org/wiki/Respiratory_ratehttp://en.wikipedia.org/wiki/Pallorhttp://en.wikipedia.org/wiki/Vasoconstrictionhttp://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Pulsehttp://en.wikipedia.org/wiki/Cardiac_arrhythmiahttp://en.wikipedia.org/wiki/Jugular_venous_pressurehttp://en.wikipedia.org/wiki/Hepatojugular_refluxhttp://en.wikipedia.org/wiki/Edemahttp://en.wikipedia.org/wiki/Precordial_examinationhttp://en.wikipedia.org/wiki/Auscultationhttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Heart_murmurhttp://en.wikipedia.org/wiki/Pericardiumhttp://en.wikipedia.org/wiki/Raleshttp://en.wikipedia.org/wiki/Creatine_kinasehttp://en.wikipedia.org/wiki/Troponinhttp://en.wikipedia.org/wiki/Lactate_dehydrogenasehttp://en.wikipedia.org/wiki/Isozymehttp://en.wikipedia.org/wiki/Troponinhttp://en.wikipedia.org/wiki/Respiratory_ratehttp://en.wikipedia.org/wiki/Pallorhttp://en.wikipedia.org/wiki/Vasoconstrictionhttp://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Pulsehttp://en.wikipedia.org/wiki/Cardiac_arrhythmiahttp://en.wikipedia.org/wiki/Jugular_venous_pressurehttp://en.wikipedia.org/wiki/Hepatojugular_refluxhttp://en.wikipedia.org/wiki/Edemahttp://en.wikipedia.org/wiki/Precordial_examinationhttp://en.wikipedia.org/wiki/Auscultationhttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Heart_murmurhttp://en.wikipedia.org/wiki/Pericardiumhttp://en.wikipedia.org/wiki/Rales


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43lead electrocardiogram (/+0) showing acute inferior ;T segment eleation MI (;T/MI). ote the

;T segment eleation in leads II, III, and aE7 along with reciprocal ;T segment depression in leads I

and aE&.

&. Elet!oa!diog!am'

The primary purpose of the electrocardiogram is to detect ischemia or acute coronary inCury in

broad, symptomatic emergency department populations. *oweer, the standard 43 lead /+0 has

seeral limitations. An /+0 represents a brief sample in time. Decause unstable ischemic syndromes

hae rapidly changing supply ersus demand characteristics, a single /+0 may not accurately

represent the entire picture. It is therefore desirable to obtain serial 43 lead /+0s, particularly if the

first /+0 is obtained during a painfree episode. Alternatiely, many emergency departments and chest

pain centers use computers capable of continuous ;T segment monitoring. It should also be appreciated

that the standard 43 lead /+0 does not directly examine the right entricle, and does a relatiely poor

Cob of examining the posterior basal and lateral walls of the left entricle. In particular, acute

myocardial infarction in the distribution of the circumflex artery is likely to produce a non diagnostic

/+0. The use of nonstandard /+0 leads like rightsided lead E#6 and posterior leads E=, EH, and

EJ may improe sensitiity for right entricular and posterior myocardial infarction. In spite of these

limitations, the 43 lead /+0 stands at the center of risk stratification for the patient with suspected

acute myocardial infarction. Mistakes in interpretation are relatiely common, and the failure to

identify high risk features has a negatie effect on the -uality of patient care. The 43 lead /+0 is used

to classify patients into one of three groups>

http://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Ischemiahttp://en.wikipedia.org/wiki/Emergency_departmenthttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/ECGhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Emergency_departmenthttp://en.wikipedia.org/w/index.php?title=Chest_pain_center&action=edithttp://en.wikipedia.org/w/index.php?title=Chest_pain_center&action=edithttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Ischemiahttp://en.wikipedia.org/wiki/Emergency_departmenthttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/ECGhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Emergency_departmenthttp://en.wikipedia.org/w/index.php?title=Chest_pain_center&action=edithttp://en.wikipedia.org/w/index.php?title=Chest_pain_center&action=edithttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Electrocardiogram


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4. Those with ;T segment eleation or new bundle branch block (suspicious for acute inCury and a

possible candidate for acute reperfusion therapy with Thrombolytic or primary +I),

3. Those with ;T segment depression or T wae inersion (suspicious for ischemia), and

?. Those with a socalled nondiagnostic or normal /+0.

A normal /+0 does not rule out acute myocardial infarction. ;ometimes the earliest presentation

of acute myocardial infarction is the hyper acute T wae, which is treated the same as ;T segment

eleation. In practice this is rarely seen, because it only exists for 3?$ minutes after the onset of

infarction. *yper acute T waes need to be distinguished from the peaked T waes associated with

hyperkalemia. The current guidelines for the /+0 diagnosis of acute myocardial infarction re-uire at

least 4 mm ($.4 mE) of ;T segment eleation in 3 or more anatomically contiguous leads. This

criterion is problematic, howeer, as acute myocardial infarction is not the most common cause of ;T

segment eleation in chest pain patients. In addition, oer J$: of healthy men hae at least 4 mm ($.4

mE) of ;T segment eleation in at least one precordial lead. The clinician must therefore be well

ersed in recogniFing the socalled /+0 mimics of acute myocardial infarction, which include left

entricular hypertrophy, left bundle branch block , paced rhythm, benign early repolariFation,

ericarditis, hyperkalemia, and entricular aneurysm.

&eft bundle branch block and pacing can interfere with the electrocardiography diagnosis of acute

myocardial infarction. The 0

• ;T/MI (;T/leation Myocardial Infarction)

• ;T/MI (on;T/leation Myocardial Infarction) diagnosed when cardiac enFymes are

eleated.

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The leads with ;T segment eleation help the clinician identify what area of the heart is infarcting. It

also enables the clinician to predict the culprit artery>

all Affected

&eads ;howing

;T ;egment

/leation

&eads ;howing

6eciprocal ;T

;egment 'epression

;uspected +ulprit Artery

;eptal E4, E3 one&eft Anterior 'escending

(&A')

Anterior E?, E# one&eft Anterior 'escending

(&A')

Anteroseptal E4, E3, E?, E# one&eft Anterior 'escending

(&A')

AnterolateralE?, E#, E%, E9, I,

aE&II, III, aE7

&eft Anterior 'escending

(&A'), +ircumflex (&+2),

or 8btuse Marginal

/xtensie anterior (;ometimes

called Anteroseptal with

&ateral extension)

E4,E3,E?, E#, E%,

E9, I, aE&II, III, aE7

&eft main coronary artery

(&+A)

Inferior II, III, aE7 I, aE&6ight +oronary Artery

(6+A) or +ircumflex (&+2)

&ateral I, aE&, E%, E9 II, III, aE7+ircumflex (&+2) or 8btuse

Marginal

osterior (


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. Ca!dia ma!ke!s'

+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.


14/27

especially in emergency settings, and may not always be aailable out of hours. It is commonly

performed by interentional cardiologists.

e. Histopat"ology'

Microscopy image (magn. ca 4$$x, */ stain) from autopsy specimen of myocardial infarct (=

days postinfarction).

*istopathological examination of the heart may reeal infarction at autopsy.


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The interstitial space (the space between cells outside of blood essels) may be infiltrated with red

blood cells

These features can be recogniFed in cases where the perfusion was not restored@ reperfused

infarcts can hae other hallmarks, such as contraction band necrosis.

I. (anagement

Immediate a!e'

hen symptoms of myocardial infarction occur, people wait on aerage of ? hours, instead of

doing what is recommended> calling for help immediately. Acting immediately by calling the

emergency serices can preent sustained damage to the heart (time is muscle).

+ertain positions allow the patient to rest in a position which minimiFes breathing difficulties. A

halfsitting position with knees bent is often recommended. Access to more oxygen can be gien by

opening the window and widening the collar for easier breathing.

Aspirin can be gien -uickly (if the patient is not allergic to aspirin)@ but taking aspirin before

calling the emergency medical serices may be associated with unwanted delay. Aspirin has an

antiplatelet effect which inhibits formation of further thrombi (blood clots) that clog arteries. on

enteric coated or soluble preparations are preferred. If chewed or dissoled, respectiely, they can be

absorbed by the body een -uicker. If the patient cannot swallow, the aspirin can be used sublingually.


16/27


17/27

I. T!eatment

A heart attack is a medical emergency which demands both immediate attention and actiation of

the emergency medical serices. The ultimate goal of the management in the acute phase of the disease

is to salage as much myocardium as possible and preent 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 hae 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. 8ther

treatment modalities may also cause complications@ the use of antithrombotics for example carries an

increased risk of bleeding.

a. #i!st line

8xygen, aspirin, glyceryl trinitrate (nitroglycerin) and analgesia (usually morphine, hence the

popular mnemonic M8A, morphine, oxygen, nitro, aspirin) are administered as soon as possible. In

many areas, first responders can be trained to administer these prior to arrial at the hospital.

8f the first line agents, only aspirin has been proen to decrease mortality.

8nce the diagnosis of myocardial infarction is confirmed, other pharmacologic agents are often

gien. 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 ealuated

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.

&. Repe!f)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 ;T segment eleation (;T/MI) or new bundle branch block on the 43 lead

/+0 are presumed to hae an occlusie thrombosis in an epicardial coronary artery. They are therefore

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candidates for immediate reperfusion, either with Thrombolytic therapy, percutaneous coronary

interention (+I) or when these therapies are unsuccessful, bypass surgery.

Indiiduals without ;T segment eleation are presumed to be experiencing either unstable angina

(


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Although no perfect Thrombolytic agent exists, an ideal Thrombolytic drug would lead to rapid

reperfusion, hae a high sustained patency rate, be specific for recent thrombi, be easily and rapidly

administered, create a low risk for intracerebral and systemic bleeding, hae no antigenicity, aderse

hemodynamic effects, or clinically significant drug interactions, and be cost effectie. +urrently

aailable Thrombolytic agents include streptokinase, urokinase, and alteplase (recombinant tissue

plasminogen actiator , rtA). More recently, Thrombolytic agents similar in structure to rtA such as

reteplase and tenecteplase hae been used. These newer agents boast efficacy at least as good as rtA

with significantly easier administration. The Thrombolytic agent used in a particular indiidual is based

on institution preference and the age of the patient.

'epending on the Thrombolytic agent being used, adCuant anticoagulation with heparin or low

molecular weight heparin may be of benefit. ith tA 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 cerebroascular accident (+EA) is a serious side effect

of Thrombolytic use. The risk of I+D is dependent on a number of factors, including a preious episode

of intracranial bleed, age of the indiidual, 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 4 percent.

Thrombolytic therapy to abort a myocardial infarction is not always effectie. The degree of

effectieness 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 indiidual presents more than 43 hours after symptoms commenced, the risk of

intracranial bleed are considered higher than the benefits of the Thrombolytic agent. 7ailure rates of

Thrombolytic can be as high as 3$: or higher. In cases of failure of the Thrombolytic agent to open the

infarctrelated coronary artery, the patient is then either treated conseratiely with anticoagulants or

allowed to complete the infarction or percutaneous coronary interention (+I, see below) is then

performed. ercutaneous coronary interention in this setting is known as rescue +I or salage +I.

+omplications, particularly bleeding, are significantly higher with rescue +I than with primary +I due

to the action of the Thrombolytic agent.

Pe!)taneo)s o!ona!y inte!,ention>

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20/27

Thrombus material (in a cup, upper left corner) remoed from a coronary artery during a

percutaneous coronary interention to abort a myocardial infarction. 7ie 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 interention

(+I) ia cardiac catheteriFation. The use of percutaneous coronary interention 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 doortoballoon time. 7ew hospitals can proide +I within the J$ minute interal.

The current guidelines in the


21/27

d. Co!ona!y a!te!y &ypass s)!ge!y

+oronary artery bypasses surgery during mobiliFation (freeing) of the right coronary artery from its

surrounding tissue, adipose tissue (yellow). The tube isible at the bottom is the aortic cannula (returns

blood from the *&M). The tube aboe it (obscured by the surgeon on the right) is the enous cannula

(receies blood from the body). The patientBs heart is stopped and the aorta is crossclamped. The

patientBs head (not seen) is at the bottom.

'espite the guidelines, emergency bypass surgery for the treatment of an acute myocardial

infarction (MI) is less common then +I or medical management. In an analysis of patients in the


22/27

is associated with higher longterm surial rates compared to percutaneous interentions In patients

with single essel disease, surgery is comparably safe and effectie, and may be a treatment option in

selected cases. Dypass surgery has higher costs initially, but becomes costeffectie in the long term. A

surgical bypass graft is more inasie initially but bears less risk of recurrent procedures (but these may

be again minimally inasie).

". (onito!ing fo! a!!"yt"mias

Additional obCecties are to preent lifethreatening arrhythmias or conduction disturbances. This

re-uires monitoring in a coronary care unit and protocolised administration of antiarrhythmic agents.

Antiarrhythmic agents are typically only gien to indiiduals with lifethreatening arrhythmias after a

myocardial infarction and not to suppress the entricular ectopy that is often seen after a myocardialinfarction.

i. Re"a&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 leels, blood pressure, weight, stress and mood. ;ome patients become afraid of

exercising because it might trigger another infarct. atients are stimulated to exercise, and should only

aoid certain exerting actiities such as shoeling. &ocal authorities may place limitations on driing

motoriFed ehicles. ;ome people are afraid to hae sex after a heart attack. Most people can resume

sexual actiities after ? to # weeks. The amount of actiity needs to be dosed to the patients possibilities.

-. Seonda!y p!e,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 seeral longterm medications postMI, with the aim of

preenting secondary cardioascular eents such as further myocardial infarctions, congestie heart

failure or cerebroascular accident (+EA).

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• 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 firstline, owing to its low cost

and comparable efficacy, with clopidogrel resered for patients intolerant of aspirin. The

combination of clopidogrel and aspirin may further reduce risk of cardioascular eents@ howeer

the risk of hemorrhage is increased.

• Deta blocker therapy such as metoprolol or caredilol should be commenced. These hae been

particularly beneficial in highrisk patients such as those with left entricular dysfunction and!or

continuing cardiac ischemia. PDlockers decrease mortality and morbidity. They also improe

symptoms of cardiac ischemia in ;T/MI.

• A+/ inhibitor therapy should be commenced 3##H hours postMI in hemodynamicallystable

patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior

location of infarct (as assessed by /+0), and!or eidence of left entricular dysfunction. A+/

inhibitors reduce mortality, the deelopment of heart failure, and decrease entricular remodelling

postMI.

• ;tatin therapy has been shown to reduce mortality and morbidity postMI. The effects of statins

may be more than their &'& lowering effects. The general consensus is that statins hae pla-ue

stabiliFation and multiple other (pleiotropic) effects that may preent myocardial infarction inaddition to their effects on blood lipids.

• The aldosterone antagonist agent eplerenone has been shown to further reduce risk of

cardioascular death postMI in patients with heart failure and left entricular dysfunction, when

used in conCunction with standard therapies aboe.

• 8mega? fatty acids, commonly found in fish, hae been shown to reduce mortality postMI.

hile the mechanism by which these fatty acids decrease mortality is unknown, it has been

postulated that the surial benefit is due to electrical stabiliFation and the preention of

entricular fibrillation.N4?%Q *oweer, further studies in a highrisk subset hae not shown a clear

cut decrease in potentially fatal arrhythmias due to omega? fatty acids.

Ne t"e!apies )nde! in,estigation>

atients who receie stem cell treatment by coronary artery inCections of stem cells deried from

their own bone marrow after a myocardial infarction (MI) show improements in left entricular eCection

fraction and enddiastolic olume not seen with placebo. The larger the initial infarct siFe, the greater the

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effect of the infusion. +linical trials of progenitor cell infusion as a treatment approach to ;T eleation

MI are proceeding.

There are currently ? biomaterial and tissue engineering approaches for the treatment of MI, but

these are in an een earlier stage of medical research, so many -uestions and issues need to be addressed

before they can be applied to patients. The first inoles polymeric left entricular restraints in the

preention of heart failure. The second utiliFes in itro engineered cardiac tissue, which is subse-uently

implanted in io. The final approach entails inCecting cells and!or a scaffold into the myocardium to

create in situ engineered cardiac tissue.

/. Compliations

+omplications may occur immediately following the heart attack (in the acute phase), or may

need time to deelop (a chronic problem). After an infarction, an obious 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 lie cells left in the infarct.

a. Congesti,e "ea!t fail)!e>

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 rightsided (or bilateral)

heart failure may occur depending on the affected part of the heart, and it is a lowoutput type of

failure. If one of the heart ales is affected, this may cause dysfunction, such as mitral regurgitation

in the case of leftsided MI. The incidence of heart failure is particularly high in patients with

diabetes and re-uires special management strategies.

&. (yoa!dial !)pt)!e>

Myocardial rupture is most common three to fie days after myocardial infarction, commonly of

small degree, but may occur one day to three weeks later, in as many as 4$: of all MIs. This may

occur in the free walls of the entricles, the septum between them, the papillary muscles, or less

commonly the atria. 6upture occurs because of increased pressure against the weakened walls of the

heart chambers due to heart muscle that cannot pump blood out effectiely. The weakness may also

lead to entricular aneurysm, a localiFed dilation or ballooning of the heart chamber.

http://en.wikipedia.org/wiki/Clinical_trialhttp://en.wikipedia.org/wiki/Progenitor_cellhttp://en.wikipedia.org/wiki/Biomaterialhttp://en.wikipedia.org/wiki/Tissue_engineeringhttp://en.wikipedia.org/wiki/Medical_researchhttp://en.wikipedia.org/wiki/Polymerhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/In_vitrohttp://en.wikipedia.org/wiki/In_vivohttp://en.wikipedia.org/wiki/In_situhttp://en.wikipedia.org/wiki/Acute_(medical)http://en.wikipedia.org/wiki/Chronic_(medicine)http://en.wikipedia.org/wiki/Circulatory_systemhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Myocardial_rupturehttp://en.wikipedia.org/wiki/Septumhttp://en.wikipedia.org/wiki/Papillary_muscleshttp://en.wikipedia.org/wiki/Atriahttp://en.wikipedia.org/wiki/Aneurysmhttp://en.wikipedia.org/wiki/Clinical_trialhttp://en.wikipedia.org/wiki/Progenitor_cellhttp://en.wikipedia.org/wiki/Biomaterialhttp://en.wikipedia.org/wiki/Tissue_engineeringhttp://en.wikipedia.org/wiki/Medical_researchhttp://en.wikipedia.org/wiki/Polymerhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/In_vitrohttp://en.wikipedia.org/wiki/In_vivohttp://en.wikipedia.org/wiki/In_situhttp://en.wikipedia.org/wiki/Acute_(medical)http://en.wikipedia.org/wiki/Chronic_(medicine)http://en.wikipedia.org/wiki/Circulatory_systemhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Myocardial_rupturehttp://en.wikipedia.org/wiki/Septumhttp://en.wikipedia.org/wiki/Papillary_muscleshttp://en.wikipedia.org/wiki/Atriahttp://en.wikipedia.org/wiki/Aneurysm


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6isk factors for myocardial rupture include completion of infarction (no reasculariFation

performed), female sex, adanced age, and a lack of a preious history of myocardial infarction. The

shear stress between the infarcted segment and the surrounding normal myocardium (which may be

hypercontractile in the postinfarction period) makes it a nidus for rupture.

6upture is usually a catastrophic eent that may result a lifethreatening 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 effectiely. 6upture of the intraentricular septum (the

muscle separating the left and right entricles) causes a entricular septal defect with shunting of

blood through the defect from the left side of the heart to the right side of the heart. 6upture of the

papillary muscle may also lead to acute mitral regurgitation and subse-uent pulmonary edema and

possibly een +ardiogenic shock .

0ife1t"!eatening a!!"yt"mia>

A 43 lead electrocardiogram showing entricular tachycardia.

;ince the electrical characteristics of the infarcted tissue change (see athophysiology section),

arrhythmias are a fre-uent complication. The reentry phenomenon may cause too fast heart rates

(entricular tachycardia and een entricular 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).

. Pe!ia!ditis>

http://en.wikipedia.org/wiki/Cardiac_tamponadehttp://en.wikipedia.org/wiki/Cardiac_tamponadehttp://en.wikipedia.org/wiki/Pericardiumhttp://en.wikipedia.org/wiki/Ventricular_septal_defecthttp://en.wikipedia.org/wiki/Shunt_(medical)http://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Cardiogenic_shockhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Myocardial_infarction#Pathophysiologyhttp://en.wikipedia.org/wiki/Arrhythmiashttp://en.wikipedia.org/wiki/Ventricular_tachycardiahttp://en.wikipedia.org/wiki/Ventricular_fibrillationhttp://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttp://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttp://en.wikipedia.org/wiki/Third_degree_heart_blockhttp://en.wikipedia.org/wiki/Sinoatrial_nodehttp://en.wikipedia.org/wiki/Cardiac_tamponadehttp://en.wikipedia.org/wiki/Cardiac_tamponadehttp://en.wikipedia.org/wiki/Pericardiumhttp://en.wikipedia.org/wiki/Ventricular_septal_defecthttp://en.wikipedia.org/wiki/Shunt_(medical)http://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Cardiogenic_shockhttp://en.wikipedia.org/wiki/Electrocardiogramhttp://en.wikipedia.org/wiki/Myocardial_infarction#Pathophysiologyhttp://en.wikipedia.org/wiki/Arrhythmiashttp://en.wikipedia.org/wiki/Ventricular_tachycardiahttp://en.wikipedia.org/wiki/Ventricular_fibrillationhttp://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttp://en.wikipedia.org/wiki/Electrical_conduction_system_of_the_hearthttp://en.wikipedia.org/wiki/Third_degree_heart_blockhttp://en.wikipedia.org/wiki/Sinoatrial_node


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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

seeral weeks after the initial eent.

d. Ca!diogeni s"ok >

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 interentions on indiiduals with +ardiogenic shock is sparse, trial data

suggests a longterm mortality benefit in undergoing reasculariFation if the indiidual is less than =%

years old and if the onset of the acute myocardial infarction is less than ?9 hours and the onset of

+ardiogenic shock is less than 4H hours. If the patient with cardiogenic shock is not going to be

reasculariFed, aggressie hemodynamic support is warranted, with insertion of an intraaortic balloon

pump if not contraindicated. If diagnostic coronary angiography does not reeal a culprit blockage that

is the cause of the cardiogenic shock, the prognosis is poor.

2. P!ognosis

The prognosis for patients with myocardial infarction aries greatly, depending on the patient, the

condition itself and the gien treatment.


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on) were to occur. There is eidence that case fatality of myocardial infarction has been improing oer

the years in all ethnicities.

Documents

Infark Miocard Bab II