Glenn N.

Levine, MD, FACC, FAHA

CHAPTER 18

ST SEGMENT ELEVATION MYOCARDIAL

INFARCTION
1. W
 hat are the electrocardiograph (ECG) criteria for the diagnosis of ST
segment elevation myocardial infarction (STEMI)?
Criteria for the diagnosis of STEMI can derive from criteria established for the administration of
thrombolytic therapy, which evolved in the late 1980s and 1990s. ECG criteria for suspected coronary
artery occlusion include:
n American College of Cardiology Foundation/American Heart Association (ACCF/AHA) criteria
for STEMI consist of ST segment elevation greater than 0.1 mV (one small box) in at least two
contiguous leads (e.g., leads III and aVF, or leads V2 and V3). The European Society of Cardiology
(ESC) STEMI guidelines require 0.2 mV or greater ST elevation when analyzing leads V1 through
V3 (but similarly, 0.1 mV elevation for other leads and/or territories). Figure 18.1 demonstrates
the ECG finding of ST elevation in a patient with acute myocardial infarction.
n New or presumably new left bundle branch block (LBBB)
2. Is intracoronary thrombus common in STEMI?
Yes. The majority of STEMI is due to plaque rupture, fissure, or disruption, leading to superimposed
thrombus formation and vessel occlusion. Angioscopy demonstrates coronary thrombus in more than
90% of patients with STEMI (as opposed to 35% to 75% of patients with nonST segment elevation
acute coronary syndrome [NSTE-ACS] and 1% of patients with stable angina).
3. W
 hat is primary PCI?
Primary percutaneous coronary intervention (PCI) refers to the strategy of taking a patient who presents with STEMI directly to the cardiac catheterization laboratory to undergo mechanical revascularization using balloon angioplasty, coronary stents, aspiration thrombectomy, and other measures. Patients
I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Figure 18-1. ST elevation in a patient with acute myocardial infarction (MI). There are 3 to 4 mm ST elevation in the
anterior leads (V2 through V4 ), with lesser degrees of ST elevation in the lateral leads (I, aVL, V5, V6).

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are not treated with thrombolytic therapy in the emergency room (or ambulance) but preferentially
taken directly to the cardiac catheterization laboratory for primary PCI. Studies have demonstrated
that primary PCI is superior to thrombolytic therapy when it can be performed in a timely manner by a
skilled interventional cardiologist with a skilled and experienced catheterization laboratory team.
4. W
 hat are considered to be contraindications to thrombolytic therapy?
Several absolute contraindications to thrombolytic therapy and several relative contraindications (or
cautions) must be considered in deciding whether to treat a patient with lytic agents. As would be
expected, these are based on the risks and consequences of bleeding resulting from thrombolytic
therapy. These contraindications and cautions are given in Box 18-1.

BOX 18-1.CONTRAINDICATIONS AND CAUTIONS OR RELATIVE CONTRAINDICATIONS FOR FIBRINOLYTIC

THERAPY, AS GIVEN BY THE AMERICAN COLLEGE OF CARDIOLOGY/AMERICAN HEART
ASSOCIATION (ACC/AHA) AND BY THE EUROPEAN SOCIETY OF CARDIOLOGY (ESC)
ACC/AHA
Absolute Contraindications:
n Any prior intracranial hemorrhage (ICH)
n Known structural cerebral vascular lesion (e.g.,
arteriovenous malformation)
n Known malignant intracranial neoplasm (primary or
metastatic)
n Ischemic stroke within 3 months (except acute ischemic
stroke within 4.5 hours)
n Suspected aortic dissection
n Active bleeding (excluding menses) or bleeding diathesis
n Significant closed-head or facial trauma within 3 months

Cautions/Relative Contraindications:
n
n

n
n
n
n
n

 istory of chronic, severe, poorly controlled hypertension

H
Severe uncontrolled hypertension of presentation (systolic
blood pressure [SBP] > 180 mm Hg or diastolic blood
pressure [DBP] > 110 mm Hg)
Traumatic or prolonged (>10 minutes) cardiopulmonary
resuscitation (CPR) or major surgery within 3 weeks
Recent (within 2-4 weeks) internal bleeding
Noncompressible vascular punctures
Pregnancy
Active peptic ulcer
Current use of anticoagulants with high international normalized
ratio (INR); the higher the INR, the higher the risk of bleeding
For streptokinase or anistreplase: prior exposure (more than
5 days ago) or prior allergic reaction to these agents

ESC
Absolute Contraindications:
Hemorrhagic stroke or stroke
of unknown origin at any time
n Ischemic stroke in preceding
6 months
n Central nervous system (CNS)
damage or neoplasms
n Recent major trauma/
surgery/head injury (within
preceding 3 weeks)
n Gastrointestinal bleeding
within the last month
n Known bleeding disorder
n Aortic dissection
n

Relative Contraindications:
n

n
n

n
n
n

n
n
n

T ransient ischemic attack in

preceding 6 months
Oral anticoagulant therapy
Pregnancy or within 1 week
post-partum
Non-compressible punctures
Traumatic resuscitation
Refractory hypertension (SBP
> 180 mm Hg)
Advanced liver disease
Infective endocarditis
Active peptic ulcer

Modified from Antman EM, Anbe DT, Armstrong PW, etal: ACC/AHA guidelines for the management of patients
with ST-elevation myocardial infarction. J Am Coll Cardiol 44:E1-E211, 2004, and from Van de Werf F, Ardissino
D, Betriu A, etal: Management of acute myocardial infarction in patients presenting with ST-segment elevation.
The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology.
Eur Heart J 24:28-66, 2003.

ST SEGMENT ELEVATION MYOCARDIAL INFARCTION

5. W
 hat is door-to-balloon time?
Door-to-balloon time is a phrase that denotes the time it takes from when a patient with STEMI sets foot
in the emergency room until the time that a balloon is inflated in the occluded, culprit coronary artery.
More recently, the concept of medical contact-to-balloon time has been emphasized, given that STEMI
may first be diagnosed in the transporting ambulance in some cases. Because balloon angioplasty is
no longer always the first intervention performed on an occluded artery, the term has further evolved to
medical contact-to-device time. The generally accepted medical contact-to-device time goal is 90 minutes or less in cases in which the patient presents or is taken directly to a hospital that performs PCI. In
cases in which the patient must be transferred from a hospital that does not perform PCI to a hospital
that does perform PCI, the goal is a medical contact-to-device time of no more than 120 minutes.
6. W
 hat is door-to-needle time?
Door-to-needle time is a phrase that denotes the time it takes from when a patient with STEMI sets
foot in the emergency room until the beginning of thrombolytic therapy administration. The generally
accepted goal for door-to-needle time is 30 minutes or less.
7. In patients treated with thrombolytic therapy, how long should antithrombin
therapy be continued?
Patients who are treated with unfractionated heparin (UFH) should be treated for 48 hours. Studies of
low-molecular-weight heparins (EXTRACT, CREATE) and of direct thrombin inhibitors (OASIS-6) have
suggested that patients treated with these agents should be treated throughout their hospitalizations,
up to 8 days maximum. Guidelines for adjunctive antiplatelet and antithrombin therapy in patients
treated with thrombolytic therapy are given in Table 18-1.
8. W
 hich patients with STEMI should undergo cardiac catheterization?
Patients with STEMI who should undergo immediate coronary angiography include those who are
candidates for primary PCI, those with severe heart failure or cardiogenic shock (if they are suitable
candidates for revascularization), and many of those with moderate to large areas of myocardium
at risk and evidence of failed fibrinolysis. Cardiac catheterization is reasonable in hemodynamically
stable patients with evidence of successful fibrinolysis. Recommendations from the 2011 ACCF/AHA/
Society for Cardiovascular Angiography and Interventions (SCAI) Guidelines on PCI regarding coronary
angiography in patients with STEMI are given in Table 18-2.
9. W
 hich patients with STEMI should undergo primary PCI?
Primary PCI should be performed in patients with STEMI who present within 12 hours of symptom
onset, in patients with severe heart failure or cardiogenic shock, and in those with contraindications
to fibrinolytic therapy. PCI can also be considered in those who have clinical evidence for fibrinolytic failure or infarct artery reocclusion after fibrinolytic failure, as well as those treated with likely
successful fibrinolytic failure. Recommendations from the 2011 ACCF/AHA/SCAI Guidelines on PCI
regarding PCI in patients with STEMI are given in Table 18-3.
10. W
 hat is facilitated PCI?
Facilitated PCI refers to a strategy of planned PCI immediately or shortly after administration of an initial
pharmacologic regimen intended to improve coronary artery patency before the PCI procedure. Such
regimens have included full-dose or reduced-dose thrombolytic therapy, glycoprotein IIb/IIIa inhibitors,
antithrombin agents, and combinations of agents. The concept is to restore at least some coronary blood
flow as the cardiac catheterization laboratory is getting activated and the patient is being transported to the
hospitals catheterization laboratory. Although this strategy is intuitively appealing, studies of such a strategy
generally have not demonstrated any advantage of facilitated PCI over primary PCI and it is no longer generally recommended. The term itself is controversial, and there has been a movement to abolish this phrase.
11. W
 hat is rescue PCI?
Rescue PCI is the performance of PCI after thrombolytic therapy has failed in a patient. Studies of
rescue PCI versus medical management generally have shown a modest benefit with rescue PCI

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TABLE 18-1.2013 ACCF/AHA GUIDELINES FOR ADJUNCTIVE ANTITHROMBOTIC THERAPY

TO SUPPORT REPERFUSION WITH FIBRINOLYTIC THERAPY
COR

LOE

Antiplatelet therapy
Aspirin
n

162- to 325-mg loading dose

81- to 325-mg daily maintenance dose (indefinite)

81 mg daily is the preferred maintenance dose

IIa

A (14 d)
C (up to 1 y)

P2Y12 receptor inhibitors

n

Clopidogrel:

Age 75 y: 300-mg loading dose

Followed by 75 mg daily for at least 14 d and up to 1 y in
absence of bleeding

Age >75 y: no loading dose, give 75 mg

Followed by 75 mg daily for at least 14 d and up to 1 y in

absence of bleeding

A (14 d)
C (up to 1 y)

Anticoagulant therapy
n

UFH:

Enoxaparin:

 egardless of ages, if CrCl < 30 mL/min: 1 mg/kg

R
subcutaneously every 24 h

 uration: For the index hospitalization, up to 8 d or until

D
revascularization

Fondaparinux:

Initial dose 2.5 mg IV, then 2.5 mg subcutaneously daily

starting the following day, for the index hospitalization up to
8 d or until revascularization

Contraindicated if CrCl < 30 mL/min

 eight-based IV bolus and infusion adjusted to obtain aPTT

W
of 1.5 to 2.0 times control for 48 h or until revascularization.
IV bolus of 60 U/kg (maximum 4000 U) followed by an infusion
of 12 U/kg/h (maximum 1000 U) initially, adjusted to maintain
aPTT at 1.5 to 2.0 times control (approximately 50 to 70 s) for
48 h or until revascularization
If age <75 y: 30-mg IV bolus, followed in 15 min by 1 mg/kg
subcutaneously every 12 h (maximum 100 mg for the first 2
doses)
If age 75 y: no bolus, 0.75 mg/kg subcutaneously every 12 h
(maximum 75 mg for the first 2 doses)

Reproduced with permission from OGara P, Kushner FG, Ascheim D, et al. 2013 ACCF/AHA Guideline for the
Management of ST-Elevation Myocardial Infarction. J Am Coll Cardiol 2013;61(4):e78-e140.
ACC, American College of Cardiology; AHA, American Heart Association; aPPT, activated partial thromboplastin
time; COR, Class of Recommendation; CrCl, creatinine clearance; IV, intravenous; LOE, Level of Evidence; N/A,
not available; STEMI, ST segment elevation myocardial infarction; UFH, unfractionated heparin.

ST SEGMENT ELEVATION MYOCARDIAL INFARCTION

TABLE 18-2.RECOMMENDATIONS FROM THE 2011 ACCF/AHA/SCAI GUIDELINES ON PCI REGARDING

CORONARY ANGIOGRAPHY IN PATIENTS WITH STEMI
Indications

COR

LOE

Immediate Coronary Angiography

Candidate for primary PCI

Severe heart failure or cardiogenic shock (if suitable revascularization

candidate)

Moderate to large area of myocardium at risk and evidence of failed fibrinolysis IIa

Coronary Angiography 3 to 24 Hours after Fibrinolysis

Hemodynamically stable patients with evidence for successful fibrinolysis

IIa

IIb

III: No
benefit

Coronary Angiography before Hospital Discharge

Stable patients
Coronary Angiography at Any Time
Patients in whom the risks of revascularization are likely to outweigh the
benefits or the patient or designee does not want invasive care

Modified from Levine GN, Bates ER, Blankenship JC, etal. 2011 ACCF/AHA/SCAI Guideline for Percutaneous
Coronary Intervention. A report of the American College of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. J Am Coll
Cardiol 58:e44-e122, 2011.
ACCF, American College of Cardiology Foundation; AHA, American Heart Association; COR, class of recommendation; LOE, level of evidence; PCI, percutaneous coronary intervention; SCAI, Society for Cardiovascular
Angiography and Interventions; STEMI, ST segment elevation myocardial infarction.

in appropriately selected patients. The problem with rescue PCI is that clinical and electrocardiographic criteria for predicting which patients have actually failed thrombolytic therapy (have not had
successful lysis of coronary thrombosis and restoration of coronary perfusion) are imprecise. Thus,
some patients with continued occluded arteries may not be referred for rescue PCI and some patients
with successful reperfusion will be referred for unnecessary cardiac catheterization. As with the term
facilitated PCI, some have advocated for elimination of the term rescue PCI.
12. W
 hich patients should not be treated with beta-adrenergic blocking agent
(-blocker) therapy?
-Blockers have been a mainstay of STEMI therapy for decades. However, in the Clopidogrel and
Metoprolol in Myocardial Infarction Trial/Second Chinese Cardiac (COMMIT/CCS-2) study, the potential
benefits of -blocker therapy were offset by an increased incidence of cardiogenic shock and shockrelated death with -blocker therapy. Therefore, in patients with signs of heart failure, evidence of a
low-output state, or increased risk for cardiogenic shock, -blocker therapy should not be initiated.
Risk factors for cardiogenic shock include age older than 70 years, systolic blood pressure less than
120 mm Hg, sinus tachycardia greater than 110 beats/min, and heart rate less than 60 beats/min.
Other contraindications to initiating -blocker therapy include PR interval more than 0.24 seconds,
second- or third-degree heart block, active asthma, or severe reactive airway disease.
13. W
 hich patients should be treated with nitrate therapy?
Sublingual (SL) nitroglycerin (0.4 mg) every 5 minutes, up to three doses, should be administered for ongoing ischemic discomfort. Intravenous nitroglycerin is indicated for relief of
ongoing ischemic discomfort that responds to nitrate therapy, for control of hypertension, and

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TABLE 18-3.RECOMMENDATIONS FROM THE 2011 ACCF/AHA/SCAI GUIDELINES ON PCI REGARDING

PCI IN PATIENTS WITH STEMI
Indications

COR

LOE

Primary PCI
STEMI symptoms within 12 hours

I
I

A
B

Severe heart failure or cardiogenic shock

Contraindications to fibrinolytic therapy with ischemic symptoms

<12 hours

Asymptomatic patient presenting between 12 and 24 hours after

symptoms onset and higher risk

IIB

Noninfarct artery PCI at the time of primary PCI in patients without

hemodynamic compromise

III: Harm

Delayed or elective PCI in patients with STEMI (i.e., nonprimary PCI)

Clinical evidence for fibrinolytic failure or infarct artery reocclusion

IIA

Patient infarct artery 3 to 24 hours after fibrinolytic therapy

IIA

Ischemia on noninvasive testing

IIA

Hemodynamically significant stenosis in a patient infarct artery >24

hours after STEMI

11B

Totally occluded infarct artery >24 hours after STEMI in a

hemodynamically stable asymptomatic patient without evidence of
severe ischemia

III: No benefit

Modified from Levine GN, Bates ER, Blankenship JC, etal. 2011 ACCF/AHA/SCAI Guideline for Percutaneous
Coronary Intervention. A report of the American College of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. J Am Coll
Cardiol 58:e44-e122, 2011.
ACCF, American College of Cardiology Foundation; AHA, American Heart Association; COR, class of recommendation; LOE, level of evidence; PCI, percutaneous coronary intervention; SCAI, Society for Cardiovascular
Angiography and Interventions; STEMI, ST segment elevation myocardial infarction.

for management of pulmonary edema. Nitrates should not be administered to patients who have
received a phosphodiesterase inhibitor for erectile dysfunction within 24 to 48 hours (depending
on the specific agent). Nitrates should also not be administered to those with suspected right
ventricular (RV) infarction, systolic blood pressure less than 90 mm Hg (or 30 mm Hg or more
below baseline), severe bradycardia (less than 50 beats/min), or tachycardia (more than
100 beats/min) (Box 18-1).
14. S
 hould patients with STEMI be continued on nonselective nonsteroidal
antiinflammatory drugs (NSAIDs) (other than aspirin) or COX-2 inhibitors?
No. Use of these agents has been associated with increased risk of reinfarction, hypertension, heart
failure, myocardial rupture, and death. Therefore, such agents should be discontinued at the time of
admission.
15. What are the main mechanical complications of myocardial infarction?
n Free wall rupture: Acute free wall rupture is almost always fatal. In some cases of subacute
free wall rupture, only a small quantity of blood initially reaches the pericardial cavity and

ST SEGMENT ELEVATION MYOCARDIAL INFARCTION

RV1

RV4

RV2

RV5

RV3

RV6

Figure 18-2. Right-sided leads demonstrating ST segment elevation (arrows) in leads RV4 through RV6, highly
suggestive of right ventricular infarction.

begins to cause signs of pericardial tamponade. Emergent echocardiography and immediate

surgery are indicated.
Ventricular septal rupture: A ventricular septal defect (VSD) caused by myocardial infarction and septal rupture occurred in 1% to 2% of all patients with infarction in older series,
though the incidence in the fibrinolytic age is 0.2% to 0.3%. Patients may complain of a chest
pain somewhat different than their MI pain and will usually develop cardiogenic shock. A new
systolic murmur may be audible, often along the left sternal border. Mortality without surgery is
54% in the first week and up to 92% within the first year.
Papillary muscle rupture: Papillary muscle rupture leads to acute and severe mitral regurgitation. It occurs in approximately 1% of STEMI patients. Because of the abrupt elevation in left
atrial pressure, there may not be an audible murmur of mitral regurgitation. Pulmonary edema
and cardiogenic shock usually develop. Treatment is urgent or emergent mitral valve replacement (or in rare cases, mitral valve repair).

16. W
 hat is the triad of findings suggestive of RV infarction?
The triad of findings suggestive of RV infarction is hypotension, distended neck veins, and clear lungs.
Clinical RV infarction occurs in approximately 30% of inferior MI patients. Because the infarcted
right ventricle is dependent on preload, administration of nitroglycerin (or morphine), which leads to
venous pooling and decreased blood return to the right ventricle, may lead to profound hypotension.
When such hypotension occurs, patients should be placed in reverse Trendelenburg position (legs
above chest and head) and treated with extremely aggressive administration of several liters of fluid
through large-bore intravenous needles. Those who do not respond to such therapy may require
treatment with agents such as dopamine.
In patients with inferior MI, a right-sided ECG should be obtained. The precordial leads are placed
over the right side of the chest in a mirror-image pattern to normal. The finding of 1 mm or greater
ST elevation in leads RV4 through RV6 is highly suggestive of RV infarction (Fig. 18-2), although the
absence of this often-transient finding should not be used to dismiss a diagnosis of RV infarction
made on clinical grounds.

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17. B
 esides plaque rupture and thrombotic occlusion, what are other causes of
STEMI?
Although plaque rupture with subsequent thrombus formation is the most common etiology of STEMI,
other causes to consider include:
n Coronary vasospasm, such as what can occur with cocaine use
n Coronary artery embolism, such as in a patient with atrial fibrillation, left ventricular thrombus, endocarditis, or cardiac or valvular tumor
n Spontaneous coronary artery dissection
n Ascending thoracic aortic dissection with compromise of the right coronary artery ostium
n Tako-tsubo cardiomyopathy (stress cardiomyopathy, broken heart syndrome)

BIBLIOGRAPHY, SUGGESTED READINGS, AND WEBSITES

1. Antman EM: ST-elevation myocardial infarction: management. In Libby P, Bonow R, Mann D, editors: Braunwalds
heart disease: a textbook of cardiovascular medicine, ed 8, Philadelphia, 2008, Saunders.
2. Antman EM, Anbe DT, Armstrong PW, etal: ACC/AHA guidelines for the management of patients with ST-elevation
myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction), J Am Coll Cardiol 44:E1E211, 2004.
3. Antman EM, Hand M, Armstrong PW, etal: focused update of the ACC/AHA 2004 guidelines for the management
of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines, J Am Coll Cardiol 51:210247, 2007. 2008.
4. Zafari AM: Myocardial infarction. Available at: http://emedicine.medscape.com/article/155919-overview. Accessed
March 28, 2013.
5. CM Gibson, JP Carrozza, RJ Laham, Primary PCI versus Fibrinolysis (Thrombolysis) in Acute ST Elevation (Q Wave)
Myocardial Infarction: Clinical Trials. Available at: http://www.uptodate.com/contents/primary-percutaneouscoronary-intervention-versus-fibrinolysis-in-acute-st-elevation-myocardial-infarction-clinical-trials. Accessed
March 28, 2013.
6. GS Reeder, HL Kennedy, RS Rosenson, Overview of the Management of Acute ST Elevation (Q Wave) Myocardial
Infarction. Available at: http://www.uptodate.com/contents/overview-of-the-acute-management-of-st-elevationmyocardial-infarction. Accessed March 28, 2013.
7. Van de Werf F, Ardissino D, Betriu A, etal: Management of acute myocardial infarction in patients presenting with
ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society
of Cardiology, Eur Heart J 24:2866, 2003.