Вы находитесь на странице: 1из 25

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart

attack, is the interruption of blood supplyto a part of the heart, causing heart cells to die. This is
most commonly due to occlusion (blockage) of a coronary artery following the rupture of
a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and white
blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in
blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause
damage or death (infarction) of heart muscle tissue (myocardium).

Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating
to the left arm or left side of the neck),shortness of
breath, nausea, vomiting, palpitations, sweating, and anxiety (often described as a sense of
impending doom).[1] Women may experience fewer typical symptoms than men, most commonly
shortness of breath, weakness, a feeling of indigestion, and fatigue.[2]Approximately one quarter
of all myocardial infarctions are "silent", without chest pain or other symptoms.

Among the diagnostic tests available to detect heart muscle damage are
an electrocardiogram (ECG), echocardiography, and various blood tests. The most often used
markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels. Immediate
treatment for suspected acute myocardial infarction includes oxygen, aspirin, and
[3]
sublingual nitroglycerin.

Most cases of STEMI (ST elevation MI) are treated with thrombolysis or percutaneous coronary
intervention (PCI). NSTEMI (non-ST elevation MI) should be managed with medication, although
PCI is often performed during hospital admission. In people who have multiple blockages and
who are relatively stable, or in a few emergency cases, bypass surgery may be an option.

Heart attacks are the leading cause of death for both men and women worldwide.[4] Important risk
factors are previous cardiovascular disease, older age, tobacco smoking, high blood levels of
certain lipids (triglycerides, low-density lipoprotein) and low levels of high density
lipoprotein (HDL), diabetes, high blood pressure, obesity, chronic kidney disease, heart
failure, excessive alcohol consumption, the abuse of certain drugs (such
[5][6]
as cocaine and methamphetamine), and chronic high stress levels.

There are two basic types of acute myocardial infarction:

 Transmural: associated with atherosclerosis involving major coronary artery. It can be


subclassified into anterior, posterior, or inferior. Transmural infarcts extend through the whole
thickness of the heart muscle and are usually a result of complete occlusion of the area's
blood supply.[7]
 Subendocardial: involving a small area in the subendocardial wall of the left ventricle,
ventricular septum, or papillary muscles. Subendocardial infarcts are thought to be a result of
locally decreased blood supply, possibly from a narrowing of the coronary arteries. The
subendocardial area is farthest from the heart's blood supply and is more susceptible to this
type of pathology.[7]

Clinically, a myocardial infarction can be further subclassified into a ST elevation MI (STEMI)


versus a non-ST elevation MI (non-STEMI) based on ECG changes.[8]

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. A heart attack is different from, but
can be the cause of cardiac arrest, which is the stopping of the heartbeat, and cardiac arrhythmia,
an abnormal heartbeat. It is also distinct from heart failure, in which the pumping action of the
heart is impaired; severe myocardial infarction may lead to heart failure, but not necessarily. [citation
needed]

A 2007 consensus document classifies myocardial infarction into five main types:[9]

 Type 1 – Spontaneous myocardial infarction related to ischaemia due to a primary


coronary event such as plaque erosion and/or rupture, fissuring, or dissection
 Type 2 – Myocardial infarction secondary to ischaemia due to either increased oxygen
demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia,
arrhythmias, hypertension, or hypotension
 Type 3 – Sudden unexpected cardiac death, including cardiac arrest, often with
symptoms suggestive of myocardial ischaemia, accompanied by presumably new ST
elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography
and/or at autopsy, but death occurring before blood samples could be obtained, or at a time
before the appearance of cardiac biomarkers in the blood
 Type 4 – Associated with coronary angioplasty or stents:
 Type 4a – Myocardial infarction associated with PCI
 Type 4b – Myocardial infarction associated with stent thrombosis as documented
by angiography or at autopsy
 Type 5 – Myocardial infarction associated with CABG
Risk factors
Risk factors for atherosclerosis are generally risk factors for myocardial infarction:[citation needed]

 Diabetes (with or without insulin resistance) – the single most important risk factor
for ischaemic heart disease (IHD)
 Tobacco smoking
 Hypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density
lipoprotein and low high density lipoprotein)
 Low HDL
 High Triglycerides
 High blood pressure
 Family history of ischaemic heart disease (IHD)
 Obesity[27] (defined by a body mass index of more than 30 kg/m², or alternatively by waist
circumference or waist-hip ratio).
 Age: Men acquire an independent risk factor at age 45, Women acquire an independent
risk factor at age 55; in addition individuals acquire another independent risk factor if they
have a first-degree male relative (brother, father) who suffered a coronary vascular event at
or before age 55. Another independent risk factor is acquired if one has a first-degree female
relative (mother, sister) who suffered a coronary vascular event at age 65 or younger.
 Hyperhomocysteinemia (high homocysteine, a toxic blood amino acid that is elevated
when intakes of vitamins B2, B6, B12 and folic acid are insufficient)
 Stress (occupations with high stress index are known to have susceptibility
for atherosclerosis)
 Alcohol Studies show that prolonged exposure to high quantities of alcohol can increase
the risk of heart attack
 Males are more at risk than females.[20]

Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged
ischemia. This usually results from an imbalance of oxygen supply and demand. The appearance
of cardiac enzymes in the circulation generally indicates myocardial necrosis. Myocardial
infarction is considered, more appropriately, part of a spectrum referred to as acute coronary
syndromes (ACSs), which also includes unstable angina and non–ST-elevation MI (NSTEMI).
Patients with ischemic discomfort may or may not have ST-segment elevation. Most of those with
ST-segment elevation will develop Q waves. Those without ST elevations will ultimately be
diagnosed with unstable angina or NSTEMI based on the presence of cardiac enzymes.

Myocardial infarction may lead to impairment of systolic function or diastolic function and to
increased predisposition to arrhythmias and other long-term complications.

Frequency
United States

Approximately 1.5 million cases of myocardial infarction occur each year.

International

Cardiovascular diseases cause 12 million deaths throughout the world each year, according to
the third monitoring report of the World Health Organization, 1991-93. They cause half of all
deaths in several developed countries and are one of the main causes of death in many
developing countries; they are the major cause of death in adults everywhere.

Mortality/Morbidity

• Cardiovascular disease is the leading cause of death in the United States; approximately
500,000-700,000 deaths related to the coronary artery occur each year.
• Ischemic heart disease is the leading cause of death worldwide.
• Approximately 6.3 million deaths due to heart disease occurred in 1990 worldwide, which
represents 29% of all deaths. The prevalence of coronary artery disease (CAD) is
increasing rapidly in nonindustrialized countries.
• Beck et al found that elevated blood glucose level on admission is associated with
increased short-term mortality in nondiabetic patients presenting with a first acute
myocardial infarction. Analysis of data from a German myocardial infarction registry
database showed that among 1,631 nondiabetic acute myocardial infarction patients with
admission glucose level more than 152 mg/dL (top quartile), the risk of death within 28
days was higher than among those in the bottom quartile (odds ratio, 2.82; 95%
confidence interval, 1.30-6.12). However, in 659 registry patients with type 2 diabetes,
admission glucose levels did not correlate significantly with short-term mortality. Beck et
al conclude that nondiabetic acute myocardial infarction patients with elevated glucose
levels constitute a high-risk group that requires aggressive intervention.1

Race
Cardiovascular disease is the leading cause of morbidity and mortality among African American,
Hispanic, and white populations in the United States.

Sex

• A male predominance in incidence exists up to approximately age 70 years, when the


sexes converge to equal incidence.
• Premenopausal women appear to be somewhat protected from atherosclerosis, possibly
owing to the effects of estrogen.
Age

• Incidence increases with age.


• Most patients who develop an acute myocardial infarction are older than 60 years. Elderly
people also tend to have higher rates of morbidity and mortality from their infarcts.

Physical
Physical examination findings for myocardial infarction can vary; one patient may be comfortable
in bed, with normal examination results, while another may be in severe pain with significant
respiratory distress requiring ventilatory support.

• Low-grade fever may be present.


• Hypotension or hypertension can be observed depending on the extent of the myocardial
infarction.
• Fourth heart sound (S 4 ) may be heard in patients with ischemia. With ischemia, diastolic
dysfunction is the first physiologically measurable effect and this can then cause a stiff
ventricle and an audible S 4 .
• Dyskinetic cardiac bulge (in anterior wall myocardial infarction) can occasionally be
palpated.
• Systolic murmur can be heard if mitral regurgitation (MR) or ventricular septal defect
(VSD) develops.
• Other findings include cool, clammy skin and diaphoresis.
• Signs of congestive heart failure (CHF) may be found, including the following:
o Third heart sound (S 3 ) gallop
o Pulmonary rales
o Lower extremity edema
o Elevated jugular venous pressure

Causes

• Atherosclerosis with occlusive or partially occlusive thrombus formation


• Nonmodifiable risk factors for atherosclerosis
o Age
o Sex
o Family history of premature coronary heart disease
• Modifiable risk factors for atherosclerosis
o Smoking or other tobacco use
o Diabetes mellitus
o Hypertension
o Dyslipidemia
o Obesity
• New and other risk factors for atherosclerosis
o Elevated homocysteine levels
o Male pattern baldness
o Sedentary lifestyle and/or lack of exercise
o Psychosocial stress
o Presence of peripheral vascular disease
o Poor oral hygiene
• Nonatherosclerotic causes
o Vasculitis
o Coronary emboli
o Congenital coronary anomalies
o Coronary trauma
o Coronary spasm
o Drug use (cocaine)
o Factors that increase oxygen requirement, such as heavy exertion, fever, or
hyperthyroidism
o Factors that decrease oxygen delivery, such as hypoxemia of severe anemia

Laboratory Studies
Lab studies for patients with myocardial infarction include the following:

• Cardiac enzymes: In patients with suspected myocardial infarction, obtain cardiac


enzymes at regular intervals, starting upon admission and serially for as long as 24
hours.
• Troponin levels
o Troponin levels are now considered the criterion standard in defining and
diagnosing myocardial infarction, according to the American College of
Cardiology (ACC)/American Heart Association (AHA) consensus statement on
myocardial infarction.2,3
o Cardiac troponin levels (troponin-T and troponin-I) have a greater sensitivity and
specificity than CK-MB levels in detecting myocardial infarction. They have
important diagnostic and prognostic roles. Positive troponin levels are considered
virtually diagnostic of myocardial infarction in the most recent ACC/AHA
revisions, as they are without equal in combined specificity and sensitivity in this
diagnosis.
o Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-
48 hours, and return to baseline over 5-14 days.
o According to a 2009 study published in the New England Journal new sensitive
cardiac troponin assays have greater diagnostic accuracy than the standard
assays, especially for early diagnosis. These assays can substantially improve
the early diagnosis of acute myocardial infarction, particularly in patients with a
recent onset of chest pain.4
• Creatine kinase level
o Creatine kinase comprises 3 isoenzymes, including creatine kinase with muscle
subunits (CK-MM), which is found mainly in skeletal muscle; creatine kinase with
brain subunits (CK-BB), predominantly found in the brain; and myocardial muscle
creatine kinase (CK-MB), which is found mainly in the heart.
o Serial measurements of CK-MB isoenzyme levels were previously the standard
criterion for diagnosis of myocardial infarction. CK-MB levels increase within 3-12
hours of onset of chest pain, reach peak values within 24 hours, and return to
baseline after 48-72 hours. Levels peak earlier (wash out) if reperfusion occurs.
Sensitivity is approximately 95%, with high specificity. However, sensitivity and
specificity are not as high as for troponin levels, and the trend has favored using
troponins for the diagnosis of myocardial infarction.
o Myoglobin levels
 Urine myoglobin levels rise within 1-4 hours from the onset of chest pain.
 Myoglobin levels are highly sensitive but not specific, and they may be
useful within the context of other studies and in early detection of
myocardial infarction in the emergency department.
o Complete blood cell count
 Obtain a CBC count if myocardial infarction is suspected to rule out
anemia as a cause of decreased oxygen supply and prior to giving
thrombolytics.
 Leukocytosis is also common, but not universal, in the setting of acute
myocardial infarction.
 A platelet count is necessary if a IIb/IIIa agent is considered; furthermore,
the patient's WBC count may be elevated modestly in the setting of
myocardial infarction, signifying an acute inflammatory state.
o Chemistry profile
 In the setting of myocardial infarction, closely monitor potassium and
magnesium levels.
 Creatinine level is also needed prior to initiating treatment with an
angiotensin-converting enzyme (ACE) inhibitor.
o Lipid level profile: This may be helpful if obtained upon presentation because
levels can change after 12-24 hours of an acute illness.
o C-reactive protein (CRP) levels: Consider measuring CRP levels and other
markers of inflammation upon presentation if an acute coronary syndrome is
suspected.

Imaging Studies

• Chest radiography
o Upon presentation, obtain a chest radiograph to assess the patient's heart size
and the presence or absence of decompensated congestive heart failure with or
without pulmonary edema.
o A chest radiograph may also assist in diagnosing concomitant disease, such as
pneumonia in an elderly patient, as a precipitating cause for myocardial
infarction.
o A chest radiograph may be helpful in evaluation for aortic dissection.
• Echocardiography
o An echocardiogram may play an important role in the setting of myocardial
infarction.
o Regional wall motion abnormalities can be identified, which are especially helpful
if the diagnosis is questionable.
o An echocardiogram can also define the extent of the infarction and assess
overall left ventricle (LV) and right ventricle (RV) function. In addition, an
echocardiogram can identify complications, such as acute mitral regurgitation, LV
rupture, or pericardial effusion.
• Myocardial perfusion imaging
o Prior to discharge, obtain myocardial perfusion imaging to assess the extent of
residual ischemia if the patient has not undergone cardiac catheterization. The
extent of ischemia can guide further therapy as to whether to proceed with
catheterization or to continue conservative therapy.
o Myocardial perfusion has been shown to be a valuable method for triage of
patients with chest pain in the emergency department. Significant variability
exists among centers, and the results of the trials can be applied only to those
centers with proven reliability and experience.
• Cardiac angiography
o Cardiac catheterization defines the patient's coronary anatomy and the extent of
the disease. Most investigators recommend that all patients with myocardial
infarction should undergo cardiac catheterization, if it is available.
o Patients with cardiogenic shock, intractable angina despite medications, or
severe pulmonary congestion should undergo cardiac catheterization
immediately.
• SPECT and MCE
o Dwivedi et al compared the accuracy of single-photon emission computed
tomography (SPECT) and myocardial contrast echocardiography (MCE) for
assessing myocardial viability after acute myocardial infarction. In 95 patients
who had undergone simultaneous rest low-power MCE and nitrate-enhanced
SPECT 7 days after an acute myocardial infarction, the only independent
predictors of cardiac death or acute myocardial infarction were age (P =0.01) and
myocardial viability as determined by MCE (P =0.002).5

Other Tests
The electrocardiogram (ECG) is the most important tool in the initial evaluation and triage of
patients in whom an ACS is suspected (see images below). It is confirmatory of the diagnosis in
approximately 80% of cases.

• Obtain an ECG immediately if myocardial infarction is considered or suspected.


• In patients with inferior myocardial infarction, record a right-sided ECG to rule out RV
infarct.
• Qualified personnel should review the ECG as soon as possible.
• Perform ECGs serially upon presentation to evaluate progression and assess changes
with and without pain.
• Obtain daily serial ECGs for the first 2-3 days and additionally as needed.
• Convex ST-segment elevation with upright or inverted T waves is generally indicative of
myocardial infarction in the appropriate clinical setting.
• ST depression and T-wave changes may also indicate evolution of NSTEMI.
Acute anterior myocardial infarction.

Acute inferior myocardial infarction.

Posterolateral myocardial infarction.

Treatment

Medical Care
Initial therapy for acute myocardial infarction is directed toward restoration of perfusion as soon
as possible to salvage as much of the jeopardized myocardium as possible. This may be
accomplished through medical or mechanical means, such as percutaneous coronary
intervention (PCI) or coronary artery bypass grafting.

A study published in 2010 determined that treatment strategies for myocardial infarction are more
effective if done as the guidelines recommend (<90 min for PCI and <30 min for lytics).
Reperfusion delivered outside these recommendations was associated with significantly
increased 30-day mortality, a statistically nonsignificant increase in 1-year mortality, and
significantly increased risk of the composite of mortality or readmission for acute myocardial
infarction or heart failure at 1 year.6

Treatment is based on (1) restoration of the balance between the oxygen supply and demand to
prevent further ischemia, (2) pain relief, and (3) prevention and treatment of any complications
that may arise.

• Thrombolytic therapy has been shown to improve survival rates in patients with acute
myocardial infarction if administered in a timely fashion in the appropriate group of
patients. If PCI capability is not available or will cause a delay greater than 90 minutes,
then the optimal approach is to administer thrombolytics within 12 hours of onset of
symptoms in patients with ST-segment elevation greater than 0.1 mV in 2 or more
contiguous ECG leads, new left bundle-branch block (LBBB), or anterior ST depression
consistent with posterior infarction. Tissue plasminogen activator (t-PA) is superior to
streptokinase in achieving a higher rate of coronary artery patency; however, the key to
efficacy lies in the speed of the delivery of therapy.
• Aspirin and/or antiplatelet therapy
o Aspirin has been shown to decrease mortality and re-infarction rates after
myocardial infarction. Administer aspirin immediately, which the patient should
chew if possible upon presentation. Continue aspirin indefinitely unless an
obvious contraindication, such as a bleeding tendency or an allergy, is present.
Clopidogrel may be used as an alternative in cases of a resistance or allergy to
aspirin. Recent data from the CLARITY trial (CLopidogrel as Adjunctive
ReperfusIon Therapy Thrombolysis in Myocardial Infarction [TIMI] 28) suggest
that adding clopidogrel to this regimen is safe and effective.7 The clopidogrel dose
used was 300 mg. Further studies suggest that a higher dose of clopidogrel may
have added benefit.8
o Administer a platelet glycoprotein (GP) IIb/IIIa-receptor antagonist, in addition to
acetylsalicylic acid and unfractionated heparin (UFH), to patients with continuing
ischemia or with other high-risk features and to patients in whom a percutaneous
coronary intervention (PCI) is planned. Eptifibatide and tirofiban are approved for
this use. Abciximab9,10 also can be used for 12-24 hours in patients with unstable
angina or NSTEMI in whom a PCI is planned within the next 24 hours.
• Heparin (and other anticoagulant agents) has an established role as an adjunctive agent
in patients receiving t-PA, but not in patients receiving streptokinase. Heparin is also
indicated in patients undergoing primary angioplasty. Few data exist with regard to
efficacy in patients not receiving thrombolytic therapy in the setting of acute myocardial
infarction. Low molecular-weight heparins (LMWHs) have been shown to be superior to
UFHs in patients with unstable angina or NSTEMI. Bivalirudin (a direct thrombin inhibitor)
has shown some promise in the setting of STEMI if combined with high-dose clopidogrel
load and may be an appropriate alternative strategy.
• Nitrates have no apparent impact on mortality rate in patients with ischemic syndromes.
Their utility is in symptomatic relief and preload reduction. Administer to all patients with
acute myocardial infarction within the first 48 hours of presentation, unless
contraindicated (ie, in RV infarction).
• ACE inhibitors reduce mortality rates after myocardial infarction. Administer ACE
inhibitors as soon as possible as long as the patient has no contraindications and
remains in stable condition. ACE inhibitors have the greatest benefit in patients with
ventricular dysfunction. Continue ACE inhibitors indefinitely after myocardial infarction.
Angiotensin-receptor blockers may be used as an alternative in patients who develop
adverse effects, such as a persistent cough, although initial trials need to be confirmed.
• Beta-blockers may reduce the rates of reinfarction and recurrent ischemia. Administer to
patients with myocardial infarction unless a contraindication is present. However, a large
Chinese trial showed no benefit to beta-blockade. This has created some doubt as to the
benefit and may lead to a change in the guidelines.11

Exercise training
Myocardial infarction is a major cause of morbidity and mortality. Quick and evidence-based
management of myocardial infarction is essential in the care of patients. A study on patients with
recent myocardial infarction demonstrated better cardiac survival for those who showed
improvement in heart rate recovery after exercise training.12

Surgical Care

• Percutaneous coronary intervention


o PCI is the treatment of choice in most patients with STEMI, assuming a door to
balloon time of less than 90 minutes in at least 75% of the patients presenting
with STEMI. PCI provides greater coronary patency (>96% thrombolysis in
myocardial infarction [TIMI] 3 flow), lower risk of bleeding, and instant knowledge
about the extent of the underlying disease. Studies have shown that primary PCI
has a mortality benefit over thrombolytic therapy. Door to balloon times correlate
closely with mortality rates, making this the key measurement for any successful
interventional program.
o The choice of primary PCI should be individualized to each institution and to the
patient's presentation and timing. PCI in patients with occluded arteries for more
than 24 hours appears to offer no added benefit over medical treatment.
o The widespread use of stenting and adjunctive IIb/IIIa therapy are improving the
results of primary PCI. One trial showed that, in patients with acute myocardial
infarction, coronary stenting and abciximab lead to a greater degree of
myocardial salvage and a better clinical outcome than fibrinolysis with
thrombolytic therapy.13 Improvement of long- and short-term outcomes, however,
depends highly on the speed with which reperfusion is achieved.
o Primary PCI is also the treatment of choice in patients with cardiogenic shock,
patients in whom thrombolysis failed, and those with high risk of bleeding or
contraindications to thrombolytic therapy.
o Only an experienced operator should perform primary PTCA, and PTCA should
be performed only where the appropriate facilities are available. Operators
should have at least 75 cases per year, while the center should perform at least
200 cases per year as per the recommendations of the ACC.
o Cantor et al studied high-risk patients with ST-segment elevated myocardial
infarction (STEMI) who received fibrinolytic therapy in hospitals that do not have
percutaneous coronary intervention (PCI) capabilities.14
 This study randomized 1059 patients to either standard treatment (ie, if
needed, included rescue PCI, or delayed angiography) or immediate
transfer to another hospital and PCI within 6 hours following fibrinolysis.
 All patients received aspirin, tenecteplase, and anticoagulation (heparin
or enoxaparin), and clopidogrel was recommended.
 The study’s primary endpoint was a composite of death, reinfarction,
recurrent ischemia, new or worsening congestive heart failure, or
cardiogenic shock within 30 days. The primary end point occurred in 11%
of patients in the group that was immediately transferred compared with
17.2% of patients randomized to the standard treatment (P=0.004).
 A significant decrease in ischemic complications was observed in high-
risk patients with STEMI who were treated with fibrinolysis and
transferred for PCI within 6 hours following fibrinolysis.
• Emergent or urgent coronary artery graft bypass surgery is indicated in patients in whom
angioplasty fails and in patients who develop mechanical complications such as a VSD,
LV, or papillary muscle rupture.

Consultations

• Emergency department personnel should initiate evaluation and treatment, including


administering a thrombolytic agent.
• Obtain cardiology consultation immediately if primary PCI is considered. Otherwise,
cardiology consultation may be obtained as needed and upon admission. Consultation
may be obtained sooner if the patient presents with significant heart failure, mechanical
complications, arrhythmias, or other complicating factors.

Diet

• Initially, keep the patient on nothing by mouth (NPO) until his or her condition has been
stabilized and treated. Following initial therapy and admission, a dietitian should instruct
the patient regarding appropriate diet, as recommended by the AHA.
• A low-salt, low-fat, and low-cholesterol diet is generally recommended.

Activity

• Confine patients to bed rest to minimize oxygen consumption until reperfusion and initial
therapy are complete. This usually lasts about 24-48 hours; after that, the patient's
activity may be accelerated slowly as tolerated and as the clinical situation allows.
• Initiate cardiac rehabilitation prior to discharge.

Medication

The goals of pharmacotherapy for myocardial infarction are to reduce morbidity and to prevent
complications.

Salicylates
The antiplatelet effects of these agents may improve mortality rate.

Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Early administration of aspirin in patients with acute MI has been shown to reduce cardiac
mortality rate by 23% in first mo.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult

160-325 mg PO or chewed
Pediatric

10-15 mg/kg/dose PO q4-6h

Antiplatelet agent
Strong mortality benefit. Increased risk of bleeding in case of emergent CABG.

Clopidogrel (Plavix)

Selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and subsequent
ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet
aggregation.

May have a positive influence on several hemorrhagic parameters and may exert protection
against atherosclerosis, not only through inhibition of platelet function but also through changes in
the hemorrhagic profile.

Shown to decrease cardiovascular death, MI, and stroke in patients with acute coronary
syndrome (ie, unstable angina, non-Q-wave MI).

• Dosing
• Interactions
• Contraindications
• Precautions
Adult
Loading dose: 300 mg PO once or 600 mg once
Maintenance: 75 mg PO qd administered with aspirin 75-325 mg/d PO

Pediatric
Not established

Anticoagulants
Unfractionated intravenous heparin and fractionated low molecular weight subcutaneous heparins
are the two choices for initial anticoagulation therapy.

Bivalirudin (Angiomax)

Synthetic analogue of recombinant hirudin. Inhibits thrombin. Used for anticoagulation in unstable
angina undergoing PTCA. With provisional use of glycoprotein IIb/IIIa inhibitor (GP IIb/IIIa
inhibitor) indicated for use as anticoagulant in patients undergoing PCI. Potential advantages over
conventional heparin therapy include more predictable and precise levels of anticoagulation,
activity against clot-bound thrombin, absence of natural inhibitors (eg, platelet factor 4,
heparinase), and continued efficacy following clearance from plasma (because of binding to
thrombin).

• Dosing
• Interactions
• Contraindications
• Precautions
Adult

0.75 mg/kg IV bolus initially; followed by 1.75 mg/kg/h IV for 4 h for duration of procedure

Pediatric

Not established

Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not
actively lyse but is able to inhibit further thrombus formation. Prevents reaccumulation of clot after
spontaneous fibrinolysis.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult

70 IU/kg IV bolus, followed by 15 mcg/kg/h infusion, adjust to maintain aPTT 1.5-2 times control

Pediatric

Loading dose: 50 IU/kg/h IV


Maintenance infusion: 15-25 mcg/kg/h IV; increase dose by 2-4 IU/kg/h q6-8h prn using aPTT
results

Enoxaparin (Lovenox)

Enhances inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition,
preferentially increases inhibition of factor Xa.
Indicated for treatment of acute STEMI managed medically or with subsequent PCI. Also
indicated as prophylaxis of ischemic complications caused by unstable angina and non-Q-wave
MI.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult

Treatment regimens include aspirin (75-325 mg/d) if not contraindicated


NSTEMI
1 mg/kg SC bid
CrCl <30 mL/min: 1 mg/kg SC qd
STEMI
<75 years: 30 mg IV single bolus plus 1 mg/kg SC, then 1 mg/kg SC q12h; not to exceed 100
mg/dose for first 2 SC doses
<75 years and CrCl <30 mL/min: 30 mg IV single bolus plus 1 mg/kg SC, then 1 mg/kg SC qd;
not to exceed 100 mg/dose for first 2 SC doses
>75 years: 0.75 mg/kg SC q12h (no initial IV bolus administered), not to exceed 75 mg/dose for
first 2 doses
>75 years and CrCl <30 mL/min: 1 mg/kg SC qd (no initial IV bolus administered)
With PCI: If last enoxaparin dose administered >8 h before balloon inflation, administer an
additional IV bolus of 0.3 mg/kg
With thrombolytic agent: Give dose specified for age and renal function between 15 min before
and 30 min after the start of fibrinolytic therapy

Pediatric
Not established

Platelet aggregation inhibitors


These agents prevent acute cardiac ischemic complications in unstable angina unresponsive to
conventional therapy.

Abciximab (ReoPro)

Chimeric human-murine monoclonal antibody. Binds to receptor with high affinity and reduces
platelet aggregation by 80%. Inhibition of platelet aggregation persists for as long as 48 h after
infusion stopped.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult

0.25 mcg/kg bolus IV, followed by 0.125 mcg/kg/min infusion for 12 h

Pediatric

Not established

Tirofiban (Aggrastat)

Nonpeptide antagonist of glycoprotein IIb/IIIa receptor. Reversible antagonist of fibrinogen


binding. When administered IV, >90% of platelet aggregation inhibited.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult

0.4 mcg/kg/min IV for 30 min, then continue at 0.1 mcg/kg/min; administer half dose in patients
with severe renal insufficiency (CrCl <30 mL/min)
Pediatric

Not established

Eptifibatide (Integrilin)

Cyclic peptide that reversibly inhibits platelet aggregation by binding to IIb/IIIa receptor.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult

Unstable angina:
180 mcg/kg IV bolus, followed by 2 mcg/kg/min continuous infusion until discharge or surgery

Patients undergoing PCI:


135 mcg/kg IV bolus before PCI, followed by 0.5 mcg/kg/min continuous infusion

Pediatric

Not established

Vasodilators
These agents relieve chest discomfort by improving myocardial oxygen supply, which in turn
dilates epicardial and collateral vessels, improving blood supply to the ischemic myocardium.

Nitroglycerin (Nitro-Bid)

Causes relaxation of vascular smooth muscle via stimulation of intracellular cyclic guanosine
monophosphate production, causing decrease in BP.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult
400 mcg SL or spray q5min, repeat up to 3 times; if symptoms persist, 5-10 mcg/min IV infusion;
titrate to 10% reduction in MAP or symptom relief, limiting adverse effects of hypotension

Pediatric
Not established

Beta-adrenergic blockers
This category of drugs has the potential to suppress ventricular ectopy due to ischemia or excess
catecholamines. In the setting of myocardial ischemia, beta-blockers have antiarrhythmic
properties and reduce myocardial oxygen demand secondary to elevations in heart rate and
inotropy.

Metoprolol (Lopressor)

Selective beta1-adrenergic receptor blocker that decreases automaticity and contractions. Goals
of treatment are reduction in heart rate to 60-80 bpm. During IV administration, carefully monitor
BP, heart rate, and ECG.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult
5 mg IV slow infusion q5min; not to exceed 15 mg or desired heart rate
25 mg PO bid usual initial dose, up to 100 mg bid; titrate to desired effect

Pediatric
Not established

Esmolol (Brevibloc)

Useful drug for patients at risk of experiencing complications from beta-blockers, particularly
reactive airway disease, mild-to-moderate LV dysfunction, and peripheral vascular disease. Its
short half-life of 8 min allows for titration to desired effect with ability to stop quickly if necessary.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult
0.1 mg/kg/min IV starting maintenance dose, titrate in increments of 0.05 mg/kg/min q10-15min to
total dose of 0.2 mg/kg/min

Pediatric
Not established

Angiotensin-converting enzyme (ACE) inhibitors


These agents may prevent conversion of angiotensin I to angiotensin II, a potent vasoconstrictor,
resulting in lower aldosterone secretion.

Captopril (Capoten)

Has short half-life, which makes it important drug for initiation of ACE inhibitor therapy. Can be
started at low dose and titrated upward as needed and as patient tolerates.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult

6.25 mg PO tid initially; may titrate to total 450 mg/d

Pediatric

Not established

Thrombolytics
The main objective is to restore circulation through a previously occluded vessel by the rapid and
complete removal of a pathologic intraluminal thrombus or embolus that has not been dissolved
by the endogenous fibrinolytic system.

Alteplase, t-PA (Activase)

Fibrin-specific agent with brief half-life of 5 min. Adjunctive therapy with IV heparin necessary to
maintain patency of arteries recanalized by t-PA, especially during first 24-48 h.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult
15 mg IV initial bolus, followed by 50 mg IV over next 30 min, and then 35 mg IV over next h; total
dose not to exceed 100 mg

Pediatric
Not established

Streptokinase (Kabikinase, Streptase)

Acts with plasminogen to convert plasminogen to plasmin. Plasmin degrades fibrin clots,
fibrinogen, and other plasma proteins. Increase in fibrinolytic activity that degrades fibrinogen
levels for 24-36 h occurs with IV infusion of streptokinase. Adjunctive therapy with heparin not
needed.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult
1.5 million IU in 50 cc D5W IV over 60 min

Pediatric
Administer as in adults

Reteplase (Retavase)

Recombinant plasminogen activator that forms plasmin after facilitating cleavage of endogenous
plasminogen. In clinical trials, has been comparable to alteplase in achieving TIMI 2 or 3 patency
at 90 min. Heparin and aspirin usually administered concomitantly and after reteplase.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult
10 IU IV over 2 min, followed by second 10-IU IV dose after 30 min

Pediatric
Not recommended

Anistreplase (Eminase)

Non–fibrin-specific agent that activates conversion of plasminogen to plasmin and has half-life of
90 min. However, does not have any benefit over streptokinase, although has higher rate of
allergic and bleeding complications. Easier to administer than t-PA, has lower cost ($1500), and
does not require heparinization.

• Dosing
• Interactions
• Contraindications
• Precautions
Adult
30 IU over 2-5 min

Pediatric
Not established

Analgesics
Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote
pulmonary toilet, and have sedating properties, which are beneficial for patients who experience
pain.

Morphine sulfate (Duramorph, Astramorph, MS Contin)

DOC for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of
reversibility with naloxone. Administered IV, may be dosed in a number of ways and commonly is
titrated until desired effect.
• Dosing
• Interactions
• Contraindications
• Precautions
Adult

2 mg IV q5-15min, titrate to symptomatic relief or adverse effects (eg, lethargy, hypotension,


respiratory depression)

Pediatric

0.1-0.2 mg/kg IV q2-4h prn

Follow-up

Further Inpatient Care

• Admit patients with myocardial infarction to a coronary care unit. Monitor patients
carefully for arrhythmia, recurrent ischemia, and other possible complications. The patient
may be transferred to a telemetry unit 24-48 hours after admission if no complications
occur. Hospitalize the patient for approximately 4-5 days after myocardial infarction.
Patients who undergo primary PCI or have an immediate cardiac catheterization may be
discharged sooner if their hospital course is without incident.
• Perform a coronary angiography on high-risk patients prior to discharge to evaluate their
need for revascularization.
• In the case of patients who have not had a cardiac catheterization and have no
complications, perform a submaximal stress test prior to discharge to assess their
subsequent risk.
• To stratify mortality risk after PCI for acute myocardial infarction, Negassa et al have
developed a prognostic classification model. Patients can be readily stratified into risk
categories using this tree-structured model.15

Further Outpatient Care

• Arrange for follow-up within 2 weeks of discharge.


• Arrange for cardiac rehabilitation.

Inpatient & Outpatient Medications

• The long-term use of aspirin in patients who have had an myocardial infarction results in
significant reduction in subsequent mortality rate.
• Beta-blocker therapy has confirmed therapeutic benefit in survivors of acute myocardial
infarction. This therapy is most beneficial in patients with the highest risk.
• ACE inhibitor use in patients with known coronary artery disease has been shown to
reduce mortality rate.
• Many trials have shown a clear benefit of lipid-lowering therapy in the secondary and
primary prevention of coronary artery disease. The National Cholesterol Education Panel
has set guidelines for target cholesterol levels. In general, patients who have experienced
myocardial infarction should achieve low-density lipoprotein (LDL) level less than 100
mg/dL, high-density lipoprotein (HDL) level greater than 40 mg/dL, and triglyceride level
less than 200 mg/dL. High-risk patients should be treated to a target LDL level of less
than 70 mg/dL.
• Schwartz et al recently showed in the MIRACL trial that initiating atorvastatin during
hospitalization for an acute coronary syndrome, irrespective of lipid levels, reduces the
frequency of recurrent ischemic events. This treatment significantly reduced the
frequency of the combined end point of death, recurrent death, myocardial infarction, or
worsening unstable angina requiring hospitalization.16
• Clopidogrel should be prescribed for a year following discharge if the patient has no
contraindications and cost is not prohibitive. To reduce the risk of bleeding, the aspirin
dose can be reduced to 81 mg.

Transfer
A patient in whom thrombolytic therapy fails should be transferred to a facility where cardiac
catheterization and angioplasty facilities are available.

Deterrence/Prevention

• Smoking cessation
o Cigarette smoking is a major risk factor for coronary artery disease. Risk of
recurrent coronary events decreases 50% at 1 year after smoking cessation.
o Provide all patients who smoke with guidance, education, and the support
needed to avoid smoking.
o Bupropion has been shown to increase the chances of patients' success in
achieving smoking cessation.
• Alcohol consumption
o Mild alcohol consumption has been associated with a decreased risk of stroke
and myocardial infarction.
o Cautiously consider recommending and discussing alcohol use on a case-by-
case basis.
• Antioxidant therapy, including vitamin E, has not shown clear benefit in the prevention of
coronary events.
• Do not use long-term anticoagulant (ie, warfarin) therapy routinely in post–myocardial
infarction patients but as an alternative in patients who cannot take antiplatelet agents.
Patients with known LV thrombus, atrial fibrillation, or severe wall motion abnormalities
have shown benefit from long-term anticoagulation, maintaining the international
normalized ratio (INR) between 2 and 3.
• Low-dose aspirin has shown substantial benefit for primary prevention of myocardial
infarction and stroke, but its use must be weighed against the risk for hemorrhagic stroke
and gastrointestinal bleeding.
o The Antithrombotic Trialists’ (ATT) Collaboration conducted meta-analyses of
serious vascular events, including myocardial infarction, stroke, and vascular
death, and major bleeds in 6 primary prevention trials and in 16 secondary
prevention trials that compared long-term aspirin versus control.17 The primary
prevention trials included 95,000 individuals at low average risk, and the
secondary prevention trials included 17,000 individuals at high average risk.
o Aspirin was associated with significant reduction (12% proportional reduction) for
serious vascular events (0.51% aspirin vs 0.57% control annually, p = 0.0001),
but the net effect on stroke was not significant. This reduction was largely due to
a 20% reduction in nonfatal myocardial infarction (0.18% vs 0.23% annually, p
<0.0001). Aspirin increased risk for major gastrointestinal and extracranial
bleeding. The use of aspirin for primary prevention must be advised in context
with the patient’s personal risks and history.
• Do not start post–myocardial infarction patients on postmenopausal hormone therapy
(HT). Patients already taking HT for more than 1 year may be continued on this therapy
without increased risk.

Complications

• A number of arrhythmias occur after myocardial infarction, ranging from benign to fatal.
Arrhythmias are common in the setting of myocardial infarction and are a major cause of
morbidity and mortality. Close monitoring and immediate treatment of arrhythmias may
be the most important part of the treatment of a post–myocardial infarction patient within
the first 48 hours. Pay close attention to exacerbating factors, such as electrolyte
disturbances (especially potassium and magnesium), hypoxemia, drugs, or acidosis, and
correct them accordingly.
• Ventricular fibrillation and/or ventricular tachycardia occurring within the first 48 hours
may be due to ischemia; however, if ventricular arrhythmias occur later, then further
workup is indicated. Immediate cardioversion is the treatment of choice. Accelerated
idioventricular arrhythmia is a ventricular arrhythmia that may occur in response to
reperfusion. This rhythm has a benign prognosis and usually does not require therapy.
• Supraventricular arrhythmias are also common. Sinus bradycardia may be due to drugs,
ischemia, or a vagal response. Sinus tachycardia may be due to pain, anxiety, drugs, or
other causes. Atrial fibrillation and other atrial tachycardias may also occur. Treat any
tachycardia by correcting the cause first or by pharmacotherapy, because persistent
tachycardias may lead to further ischemia.
• Conduction abnormalities may result from ischemia, necrosis, or chronotropic drugs, or
as a vagal response. Recognition and treatment of these abnormalities are important in
short- and long-term outcomes. Possible therapies include medications, such as atropine,
or even placement of a transvenous pacemaker if indicated. Conduction disturbances are
seen more commonly in the setting of inferior myocardial infarction but are more ominous
when seen with an anterior infarct.
• Recurrent ischemia may be due to incomplete reperfusion. Postinfarct angina occurs in
20-30% of patients. This is an indication to proceed to cardiac catheterization followed by
mechanical revascularization as needed.
• Congestive heart failure can be due to systolic dysfunction or diastolic dysfunction in the
setting of myocardial infarction. The severity of the heart failure and systolic dysfunction
depends on the extent of the infarct and the presence of any other complications, such as
acute mitral regurgitation. Aggressive treatment is indicated to avoid worsening of the
situation. Treatment may include any or all of the following: nitrates, morphine, diuretics,
ACE inhibitors, and other vasodilators if needed. Digoxin has no role in the setting of
acute congestive heart failure due to ischemia.
• Cardiogenic shock is defined as a systolic BP less than 90 mm Hg in the presence of
organ hypoperfusion. The mortality rate due to cardiogenic shock is as high as 70% in
some series. Patients usually require inotropic agents, such as dopamine or dobutamine,
and occasionally an intraaortic balloon pump is required. Patients presenting with
cardiogenic shock should proceed directly to the catheterization lab, if available, for
mechanical revascularization.
• Acute mitral regurgitation is most common in the setting of an inferoposterior myocardial
infarction. This is secondary to ischemia, necrosis, or rupture of the LV papillary muscle
(especially the posteromedial papillary muscle). This can lead to mild-to-severe mitral
regurgitation with congestive heart failure. Diagnosis can be made on physical
examination, but an echocardiogram is necessary to confirm the diagnosis and assess
the severity, which helps in the choice of therapy. Treatment consists of aggressive
afterload reduction, intraaortic balloon pump insertion, and immediate surgical repair.
• Ventricular rupture occurs in the interventricular septum or the LV free wall. Both are
catastrophic events with mortality rates greater than 90%. Prompt recognition,
stabilization, and surgical repair are crucial to any hope of survival. Ventricular rupture is
more common in women, patients with hypertension, and those receiving NSAIDs or
steroids. An echocardiogram can usually define the abnormality, and a right heart
catheterization can show an oxygen saturation step-up in the case of a septal rupture.
• Other complications include pericarditis, ventricular aneurysms, mural thrombi, and
hypertension. Recognition and treatment can be life saving.

Prognosis

• Acute myocardial infarction is associated with a 30% mortality rate; half of the deaths
occur prior to arrival at the hospital.
• An additional 5-10% of survivors die within the first year after their myocardial infarction.
• Approximately half of all patients with an myocardial infarction are rehospitalized within 1
year of their index event.
• Overall, prognosis is highly variable and depends largely on the extent of the infarct, the
residual LV function, and whether the patient underwent revascularization.

Patient Education

• Diet
Diet plays an important role in the development of coronary artery disease.
o
Educate post – myocardial infarction patients about the role of a low-cholesterol
and low-salt diet.
o Educate patients about the AHA dietary guidelines regarding a low-fat, low-
cholesterol diet.
o A dietitian should see and evaluate all patients post myocardial infarction prior to
their discharge.
• Smoking cessation
o Educate all patients post myocardial infarction regarding the critical role of
smoking in the development of coronary artery disease.
o Smoking cessation classes should be offered to help patients avoid smoking
after their myocardial infarction.
• For excellent patient education resources, visit eMedicine's Cholesterol Center. Also, see
eMedicine's patient education articles High Cholesterol, Understanding Your Cholesterol
level, Lifestyle Cholesterol Management, Understanding Cholesterol-Lowering
Medications, Chest Pain, Coronary Heart Disease, andHeart Attack.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnosis a myocardial infarction is the leading cause of litigation


against emergency department clinicians and cardiologists.
• Consider atypical presentations in elderly patients, patients with diabetes, and women.
Assess all patients carefully, especially if they have significant cardiac risk factors.
• Review all ECGs that are obtained in a prompt fashion because time is crucial.
• Obtain cardiology consultation whenever the diagnosis is questionable.
• Consider an echocardiogram to assess wall motion abnormalities in difficult cases with
nondiagnostic ECGs, such as with an LBBB.

Special Concerns

• Right ventricular infarction


o Approximately one third of patients with inferior myocardial infarction develop RV
infarction. RV infarction presents a special challenge because the adjunctive
therapy, other than reperfusion, is somewhat different.
o A right-sided ECG with greater than 1 mm ST elevation in V 3 R or V 4 R leads
describes an RV infarct. An echocardiogram may be helpful in confirming the
diagnosis. On physical examination, signs of right heart failure, such as elevated
jugular venous pulsation, right-sided S 3 , Kussmaul sign, or hypotension, may be
present, and the patient may have clear lung fields.
o The patient becomes volume dependent to maintain adequate LV and RV filling.
Occasionally, dobutamine may be needed, or even an intraaortic balloon pump
for hemodynamic support.
o Avoid nitrates or any medications that lower preload in this setting. A pulmonary
artery catheter can be helpful in guiding therapy.
• Elderly patients
o Elderly patients with acute myocardial infarction are at increased risk of
developing complications. Treat these patients aggressively.
o Elderly patients have an increased risk of bleeding with thrombolytic therapy, but
they also have the most to gain from this therapy.
o Very elderly patients should undergo primary angioplasty if available, but they
should receive thrombolytics if excessive delay is anticipated before angioplasty
can be performed.
Multimedia

Media file 1: Acute anterior myocardial infarction.

(Enlarge Image)

Media file 2: Acute inferior myocardial infarction.

(Enlarge Image)

Media file 3: Poster

(Enlarge Image)