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94 PART III Coronary Artery Disease
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with any increase in troponin who underwent early angiography
(within 4 to 48 hours) and revascularization (if appropriate)
achieved an approximately 55% reduction in the odds of
death or MI compared with patients undergoing conservative
management.
23
Prognosis. In addition to the diagnostic value of troponin,
cardiac troponins yield prognostic information. Prognosis
is related partly to the extent of the increase in troponin in
patients with an ischemic mechanism for myocardial injury.
24–26
Increased concentrations of troponin are associated with angiographic findings of greater lesion complexity, impaired blood
flow in the culprit artery, and decreased coronary microvascular
perfusion.
23
Cardiac troponin has also been proven to be a potent independent predictor of recurrent ischemic events and the risk of
death among patients presenting with ACS.27 The Thrombolysis
in Myocardial Ischemia Phase IIIB (TIMI IIIB) trial showed that
in patients presenting with ACS, mortality was consistently higher
among patients with elevated troponin I (>0.4 ng/mL) at the
time of admission. Additionally, there were statistically significant
increases in mortality with increasing levels of troponin I. Even
after adjustment for baseline variables known to be significantly
associated with an increased risk of cardiac events, elevated
troponin I was independently associated with increased risk of
mortality.28 Additionally, the Global Use of Strategies to Open
Occluded Coronary Arteries in Acute Coronary Syndromes
(GUSTO-IIa) trial found that elevated troponin T (>0.1 ng/mL)
was significantly predictive of 30-day mortality in patients with
acute myocardial ischemia even after adjusting for ECG changes
and CK-MB level.
29
Risk Stratification. Measuring cardiac troponin is a class I
recommendation for risk stratification in patients with ACS.8
Patients presenting with clinical evidence of myocardial ischemia
and elevated troponin, even at low levels, have worse outcomes
than patients without evidence of abnormal troponin.30 Peak
troponin T levels after primary percutaneous coronary intervention (PCI) for STEMI are a good indicator of infarct size and
an independent predictor of left ventricular function at 3 months
and major adverse cardiac events at 1 year.
25
Creatine Kinase MB
Creatine kinase (CK) is a cytosolic carrier protein for high-energy
phosphates.12 CK-MB is an isoenzyme of CK that is most
abundant in the heart. However, CK-MB also constitutes 1% to
3% of the CK in skeletal muscle and is present in a small fraction
in other organs, such as the small bowel, uterus, prostate, and
diaphragm.31 The specificity of CK-MB may be impaired in the
setting of major injury to these organs, especially skeletal muscle.
Although cardiac troponin is the preferred marker of myocardial necrosis, CK-MB by mass assay is an acceptable alternative
when cardiac troponin is unavailable.7 The diagnostic limit for
CK-MB is defined as the 99th percentile in a sex-specific reference
control group.5 All assays for CK-MB show a significant two-fold
to three-fold higher 99th percentile limit for men compared
with women. In addition, CK-MB can have two-fold to three-fold
higher concentrations in African Americans than whites. These
discrepancies have been attributed to physiologic differences in
muscle mass.10 It is recommended that two consecutive measurements of CK-MB above the diagnostic limit in a rise-and-fall
pattern be required for sufficient evidence of myocardial necrosis
because of the inherent lower tissue specificity of CK-MB
compared with troponin.
7
The temporal increase of CK-MB is similar to that of troponin
in that it occurs within 3 to 4 hours after the onset of myocardial
injury, but in contrast to troponin, CK-MB decreases to the
normal range by 48 to 72 hours (see Fig. 9.1). The rapid decline
of CK-MB to the reference interval by 48 to 72 hours allows for
the discrimination of early reinfarction when ischemic symptoms
recur between 72 hours and 2 weeks after the index acute MI;
during this time, troponin may still be elevated from the original
event.7 More recent data suggest, however, that serial troponin
I levels can diagnose reinfarction if a second sample obtained 3
to 6 hours after a first sample when reinfarction is suspected
increases by at least 20%.
5,32
Similar to troponin, the amount of
CK-MB released is useful for estimation of infarct size, which
correlates with left ventricular function, incidence of ventricular
arrhythmias, and prognosis.
13
Myoglobin
Myoglobin is a ubiquitous, heme-related, low-molecular-weight
protein present in cardiac and skeletal muscle. In the setting of
myocardial necrosis, myoglobin levels increase rapidly and are
detectable within the first 1 to 4 hours. Elevations persist for 12
to 24 hours before being excreted by the kidneys. Myoglobin
has a high sensitivity and a high negative predictive value for
myocardial cell death, making it an attractive tool for the early
exclusion of acute MI.7 Myoglobin is not specific for myocardial
necrosis, however, especially in the presence of skeletal muscle
injury and renal insufficiency.
13
A prospective study assessing the use of myoglobin in the
early evaluation of acute chest pain revealed that an elevated
myoglobin level was 100% sensitive for diagnosis of acute MI
at 2 hours; the negative predictive value was also 100% with
serial testing but the specificity was low, limiting the clinical
usefulness of myoglobin in the evaluation of acute MI.
myoglobin was directly compared with troponin in the early
detection of coronary ischemia, using the 99th percentile of
troponin I as a cutoff (0.07 µg/L), the cumulative sensitivity of
troponin was higher.34 A multimarker strategy including troponin
and myoglobin has not been shown to yield a superior overall
diagnostic performance compared with troponin alone; hence,
routine measurement of myoglobin is not recommended.
Adjunctive Biomarkers
Two emerging biomarkers that may be useful adjuncts in the
diagnosis and prognosis of acute MI are the natriuretic peptides
and inflammatory markers. BNP, a counter-regulatory peptide,
and its propeptide, NT-proBNP, are released from cardiac
myocytes in response to cardiac stretch. After transmural infarction, the plasma concentrations of BNP increase rapidly and
peak at approximately 24 hours.7 The peak value of BNP has
been found to be proportional to the size of the infarction.35 In
33
When
34
CHAPTER 9 Diagnosis of Acute Myocardial Infarction 95
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patients presenting with acute MI, elevated BNP and NT-proBNP
levels have been shown to predict a higher risk of death and
heart failure independent of other prognostic variables.
12
Increased concentrations of inflammatory biomarkers are
detectable in a substantial proportion of patients presenting with
acute MI; however, the precise basis for this relationship has not
been conclusively established. Studies have implicated inflammation as a contributor to plaque disruption in ACS.36 CRP, an
acute-phase reactant protein made in the liver, has been the
focus of much clinical investigation. In a cohort study of patients
with STEMI, patients with increased CRP were more likely to
have complications of acute MI.37 Similarly, several studies have
revealed high-sensitivity CRP to be an independent predictor
of short-term and long-term outcomes in patients with ACS.7
At this time, there are no therapeutic strategies specific to CRP
or BNP and NT-proBNP; however, these biomarkers, in conjunction with troponin, may be useful for risk assessment in patients
with acute MI.
Novel Cardiac Markers
Several novel markers of myocardial ischemia, such as ischemiamodified albumin, heart-type fatty acid-binding protein
(H-FABP), choline, copeptin, and cystatin C, are currently being
investigated in the setting of acute MI.12 Copeptin, part of the
prohormone that is cleaved to produce arginine vasopressin,
is among the most thoroughly investigated of these markers.
Current understanding suggests that endogenous stress, such as
myocardial ischemia, leads to arginine vasopressin and copeptin
release, thus allowing detection of acute ischemia and MI early
after symptom onset, when conventional troponin assays are
still normal. Studies have shown that when used in conjunction with conventional troponin assays, copeptin significantly
improves the diagnostic accuracy for MI and enables a more
expedient rule-out for MI.
38,39
The pursuit of new markers is
ongoing; which markers will become clinically useful depends on
several factors, including clinical efficacy, assay availability, and
cost-effectiveness.
CLINICAL EVALUATION
The evaluation of a patient presenting with acute MI should
begin with a targeted history that ascertains the following: (1)
characterization and duration of chest discomfort and any
associated symptoms; (2) prior episodes of myocardial ischemia,
MI, PCI, or coronary artery bypass surgery; (3) history of
hypertension, hyperlipidemia, diabetes mellitus, tobacco use,
cerebrovascular disease, and other cardiovascular risk factors;
and (4) assessment of bleeding risk and contraindications to
anticoagulation and reperfusion therapies.
The classic description of acute MI consists of crushing,
substernal chest pain or vice-like tightness with or without
radiation to the left arm, neck, jaw, interscapular area or epigastrium. This presentation is associated with an estimated 24%
probability of acute MI; the probability decreases to about 1%
if the pain is positional or pleuritic in a patient without a prior
history of coronary artery disease.41 Alternatively, the chest pain
may be described as burning like indigestion, or sharp and
40
stabbing, which are associated with a 23% and 5% probability
of acute MI, respectively.41 Patients may commonly deny pain
but describe a sensation of chest discomfort.40 The duration of
the discomfort is usually prolonged, lasting more than 30 minutes,
but may wax and wane or even remit completely. There may be
associated vagal symptoms of nausea, vomiting, lightheadedness,
and diaphoresis. The severity of chest pain, commonly graded
on a scale of 1 to 10, is not useful in discriminating ischemia or
infarction from other causes of pain and should be abandoned.
The performance of different chest pain characteristics in diagnosing ACS is shown in Table 9.3.
42
Elderly patients and women more commonly have atypical
presentations that mimic abdominal pathology or a neurologic
event (Table 9.4).43 One-third of all MIs are unrecognized,
especially in patients without prior history of MI, and about
half of these unrecognized MIs are associated with atypical
presentations.
44,45
Silent myocardial ischemia is defined as objective
TABLE 9.3 Performance of Chest Pain
Characteristics in Diagnosing Acute
Coronary Syndrome
Positive
Likelihood
Sensitivity,
Symptom
Radiation to both
arms
Pain similar to prior
ischemia
Change in pattern
over prior 24 hours
“Typical” chest pain 66 (58–74) 66 (49–83) 1.9 (0.94–2.9)
Worse with exertion 38–53 73–77 1.5–1.8
Radiation to neck or
jaw
Recent episode of
similar pain
Radiation to left arm 40 (28–54) 69 (61–76) 1.3 (1.2–1.4)
Radiation to right
arm
Associated
diaphoresis
Associated dyspnea 45 (42–49) 61 (59–63) 1.2 (1.1–1.3)
Abrupt onset 76 (71–80) 32 (30–34) 1.1 (1.0–1.2)
Any improvement
with nitroglycerin
“Typical” radiation 25–32 69–96 1.0–5.7
Burning pain 12–16 84–92 1.0–1.4
Associated nausea/
vomiting
Associated
palpitations
Associated syncope 9.0 (6.4–12) 84 (82–85) 0.55 (0.39–0.76)
Pleuritic pain 18–36 78–93 0.35–0.61
Modified from Fanaroff AC, Rymer JA, Goldstein SA, et al. Does this
patient with chest pain have acute coronary syndrome? The rational
clinical examination systematic review. JAMA. 2015;314:1955-1965.
CI, Confidence interval.
% (95% CI)
11 (8.3–15) 96 (95–96) 2.6 (1.8–3.7)
47 (42–53) 79 (77–80) 2.2 (2.0–2.6)
27 (23–32) 86 (85–88) 2.0 (1.6–2.5)
24 (15–36) 84 (76–90) 1.5 (1.3–1.8)
55 (50–60) 56 (54–59) 1.3 (1.1–1.4)
5.4 (3.4–8.3) 96 (95–97) 1.3 (0.78–2.1)
24–28 79–82 1.3–1.4
71 (23–95) 35 (44–86) (0.93–1.3)
21–22 77–80 0.92–1.1
6.0 (3.5–10) 91 (88–94) 0.71 (0.37–1.3)
Specificity,
% (95% CI)
Ratio
(95% CI)
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TABLE 9.4 Atypical Symptoms of
Myocardial Infarction in Elderly Patients
PERCENTAGE OF PATIENTS
WITH SYMPTOMS
Symptom
Chest pain 77 60 37
Shortness of breath 40 43 43
Sweating 34 23 14
Syncope 3 18 18
Acute confusion 3 8 19
Stroke 2 7 7
Modified from Bayer AJ, Chadha JS, Farag RR, et al. Changing
presentation of myocardial infarction with increasing old age. J Am
Geriatr Soc. 1986;34:263–266.
Age 65–74 y Age 75–84 y Age ≥85 y
documentation of myocardial ischemia in the absence of angina
or anginal equivalents.46 Diabetes and hypertension are known
to be associated with silent ischemia and infarction. The prognosis
of acute MI patients, whether symptomatic or asymptomatic,
is similar.
44
Response of chest pain to antacids, nitroglycerin, or analgesics
can be misleading and should not be relied on. Nitroglycerin
can reduce pain from esophageal spasm or pericarditis (by
reducing heart size) and, conversely, pain from acute MI may
not always respond well to nitroglycerin because the pain is due
to infarction rather than ischemia. Studies suggest that esophageal
stimulation can cause angina and reduce coronary blood flow
in patients with coronary artery disease. However, this response
is absent in patients with heart transplant, supporting the notion
of a cardioesophageal reflex, which can complicate further the
use of response to treatment as a diagnostic tool.
47
Physical Examination
Although an uncomplicated acute MI has no pathognomonic
physical signs, the physical examination is crucial in the early
assessment of the complications of acute MI and in establishing
a differential diagnosis for the chest pain. The general assessment
may reveal a restless and distressed patient with or without
confusion owing to poor cerebral perfusion. A clenched fist across
the chest, known as Levine sign, may be observed. The patient
may appear ashen, pale, or diaphoretic and may be cool and
clammy to the touch. Tachycardia and hypertension indicate
high sympathetic tone and are usually consistent with anterior
MI. Bradycardia and hypotension signify high vagal tone and
may be seen with inferior-posterior MI with or without right
ventricular involvement. Hypotension could also be secondary
to the development of cardiogenic shock or a result of medications, especially nitroglycerin, morphine sulfate, or beta-blockers.
Visualization of elevated jugular venous pressure may indicate
significant left or right ventricular dysfunction.
Auscultation for additional heart sounds, cardiac murmurs,
and friction rubs is mandatory. A soft S
left ventricular contractility and an S4 gallop indicates decreased
left ventricular compliance.40 Killip and Kimball proposed a
prognostic classification in 1967 that is still useful today for the
is heard with decreased
1
evaluation of patients with acute MI.48 The classification scheme
is based on the presence of a third heart sound (S3) and rales
on physical examination. Class I patients are without S3 or rales,
class II patients have rales over less than 50% of the lung fields
with or without S3, class III patients have pulmonary edema
with rales covering greater than 50% of the lung fields, and class
IV patients are in cardiogenic shock. Evidence of heart failure
on physical examination correlates with greater than 25% of the
myocardium being ischemic.40 A systolic murmur should prompt
an evaluation for complications of MI, such as mitral regurgitation
from papillary muscle rupture or the formation of a ventricular
septal defect, which may also be accompanied by a palpable
precordial thrill in half of cases. The chest wall should be palpated
to assess for its effect on chest pain. Significant worsening of
chest pain with palpation using moderate pressure is a clue that
supports a musculolskeletal etiology. All peripheral pulses should
be evaluated and documented. The finding of asymmetric or
absent pulses, especially in the presence of tearing chest pain
with radiation to the back, may indicate the presence of aortic
dissection as an alternative diagnosis.
Other causes of cardiac and noncardiac chest pain that may
be differentiated by physical examination include pericarditis,
pulmonary embolism, pneumothorax, peptic ulcer disease, and
acute cholecystitis. The initial clinical evaluation and physical
examination should be directed toward expeditiously identifying
the most likely etiology of each patient’s presentation. The rapid
triage of patients with ACS is crucial for the institution of the
most appropriate early reperfusion therapy.
Electrocardiogram
The ECG is paramount in the initial assessment of patients with
ACS. On arrival to the emergency department, the recommended
door-to-evaluation time, which includes performing and interpreting the ECG, is 10 minutes.40 The 12-lead ECG in the emergency
department is the lynchpin of the decision pathway. The ECG
aids in the diagnosis of acute MI, suggests the distribution of
the infarct-related artery, and estimates the amount of myocardium at risk.5 The presence of ST segment elevation in two
contiguous leads or a new LBBB identifies patients who benefit
from early reperfusion therapy, either fibrinolytic therapy or
primary PCI. In the absence of a bundle branch block, the more
abnormal the ECG leads, the greater the amount of ischemic
myocardium.
Initial performance measures for reperfusion therapy in
patients with STEMI were based on time elapsed since initial
arrival at a hospital. However, newer benchmarks use first medical
contact (FMC), such as arrival of emergency medical services
(EMS), as time zero, emphasizing the importance of early
reperfusion, which is strongly associated with outcomes.
Guidelines recommend EMS transport directly to a PCI-capable
hospital for primary PCI in patients with STEMI with an ideal
FMC-to-device time of 90 minutes or less. For patients with
STEMI that arrive at a non-PCI-capable hospital, immediate
transfer to a PCI-capable hospital for primary PCI is recommended with a goal FMC-to-device time of 120 minutes or less.
In the absence of contraindications, fibrinolytic therapy should
be given to patients with STEMI at non-PCI-capable hospitals
49–51
CHAPTER 9 Diagnosis of Acute Myocardial Infarction 97
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TABLE 9.5 Performance of the Electrocardiogram in Diagnosing Acute Coronary Syndrome
Electrocardiogram Finding Sensitivity, % (95% CI) Specificity, % (95% CI) Positive Likelihood Ratio (95% CI)
ST segment depression 25 (16–34) 95 (92–99) 5.3 (2.1–8.6)
Any T-wave inversion, ST segment depression
or Q waves
T-wave inversion 24 (15–38) 87 (69–95) 1.8 (1.3–2.7)
CI, Confidence interval.
Modified from Fanaroff AC, Rymer JA, Goldstein SA, et al. Does this patient with chest pain have acute coronary syndrome? The rational clinical
examination systematic review. JAMA. 2015;314:1955–1965.
32 (24–40) 91 (85–97) 3.6 (1.6–5.7)
when the anticipated FMC-to-device time with transfer to a
PCI-capable hospital exceeds 120 minutes. Once the decision is
made to give fibrinolytic therapy, this should be accomplished
within 30 minutes of hospital arrival.
50
New LBBB or anterior infarction are important predictors
of mortality.40 In patients being evaluated for ACS, ST segment
depression has a specificity of 95% and a sensitivity of 25%
for diagnosing ACS (Table 9.5).42 Conversely, the probability of
acute MI in patients with chest pain and an initially normal or
nonspecific ECG is low, approximately 3%.52 Comparison with
a previous ECG (if available) is indispensable and may help to
avoid unnecessary treatment in patients with an abnormal baseline
ECG.53 If the initial ECG is not diagnostic of STEMI, but the
patient remains symptomatic, serial ECGs at 15- to 30-minute
intervals should be performed to detect acute or evolving
changes.
5
The classic evolution of acute MI on ECG begins with an
abnormal T wave that is often prolonged, peaked, or depressed.
Most commonly, increased, hyperacute, symmetric T waves are
seen in at least two contiguous leads during the early stages
of ischemia.5 This is followed by ST segment elevation in the
leads facing the area of injury with ST segment depression in
the reciprocal leads. Increased R wave amplitude and width in
conjunction with S wave diminution are often seen in leads
exhibiting ST segment elevation.5 This evolution may conclude
with the formation of Q waves. The time course of development of these changes varies but usually occurs in minutes to
several hours. A more recent study revealed that among patients
presenting within 6 hours of symptom onset of STEMI, the
patients who exhibited Q waves on their baseline ECG had more
54
advanced disease with worse clinical outcomes.
This study underscores the need for early recognition of symptoms compatible
with acute MI not only by medical personnel but also in the
community.
In patients with inferior STEMI, right-sided ECG leads should
be obtained to screen for ST segment elevation suggestive of
right ventricle infarction (class I indication).40 Infarction of the
right ventricle associated with inferior acute MI has important
therapeutic and prognostic implications.55 Right ventricle infarction is likely when the ST segment is elevated 1 mm or more in
the right precordial leads from rV4 to rV6. This finding has a
sensitivity of about 90% and a specificity of 100% for proximal
right coronary artery occlusion.56 Other changes reported to be
associated with right ventricle infarction are (1) ST segment
elevation isolated to lead V1, (2) elevated ST segments in leads
V1 to V4, and (3) T wave inversion isolated to lead V2.56 The ECG
changes of right ventricle infarction are usually transient, persist
for hours, and then resolve within a day.
A normal ECG can be seen in 10% of cases of acute MI.57
One explanation for this apparent discrepancy is that the infarction may occur in an electrocardiographically silent area, such
as the posterior or lateral wall in the distribution of the left
circumflex artery.58 Acute posterior injury is suggested by marked
ST segment depression in leads V1 to V3 in combination with
dominant R waves (R/S ratio >1) and upright T waves. These
ECG findings are neither sensitive nor specific for posterior
infarction, however, and frequently are not evident on the initial
ECG.59 In the case of patients who present with clinical evidence
of acute MI but have a nondiagnostic ECG, the latest American
College of Cardiology/American Heart Association guidelines
state that it is reasonable to obtain supplemental posterior ECG
leads, V7 through V9, to assess for left circumflex occlusion (class
IIa indication).2 Several studies have shown that ST segment
elevation in leads V7 through V9 assists in the early identification
and treatment of patients who are having ischemic chest pain
due to acute posterior wall infarction but do not display ST
segment elevation on the standard 12-lead ECG.
55,58,59
Several conditions can potentially confound the ECG diagnosis
of acute MI or cause a pseudoinfarct pattern with Q waves or
QS complexes in the absence of MI. These include preexcitation,
obstructive or dilated cardiomyopathy, bundle branch block, left
and right ventricular hypertrophy, myocarditis, cor pulmonale,
and hyperkalemia.
5
Bundle Branch Block Patterns and Acute Myocardial Infarction. The presence of LBBB or ventricular pacing can mask the
ECG changes of acute MI. In the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary
Arteries (GUSTO)-1 trial, LBBB was seen in about 0.5% and
ventricular pacing in about 0.1% of patients with acute MIs.60
Based on this finding, Sgarbossa61 developed criteria to evaluate
for MI in the presence of left ventricular conduction abnormalities
(Table 9.6). These changes in the ST segment or T waves, although
very specific, are not seen in a significant proportion of patients:
other modalities, such as biomarkers and adjunctive imaging,
may be required for diagnosis of acute MI.
The same criteria used to assess for acute MI in the presence
of LBBB are also applicable to patients with endocardial ventricular pacemakers except for the T wave criteria. The most
indicative finding of acute MI in the presence of ventricular
98 PART III Coronary Artery Disease
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TABLE 9.6 Sensitivity and Specificity of
Electrocardiogram (ECG) Changes in Left
Bundle Branch Block for Diagnosis of Acute
Myocardial Infarction
Sensitivity
ECG Changes
ST segment elevation ≥
concordant with QRS polarity
ST segment depression ≥
leads V1, V2, V
ST segment elevation ≥
discordant with QRS polarity
Positive T waves in leads V
Modified from Sgarbossa EB. Recent advances in the
electrocardiographic diagnosis of myocardial infarction: left bundle
branch block and pacing. Pacing Clin Electrophysiol.
1996;19:1370–1379.
1 mm
1 mm in
3
5 mm
and V
5
(%)
73 92
25 96
31 92
6
26 92
pacing was ST segment elevation 5 mm or greater in the leads
with predominantly negative QRS complexes.61 In right bundle
branch block, the initial pattern of ventricular activation is normal;
hence, the classic pattern of acute MI on ECG is usually not
altered.
Specificity
(%)
Imaging Techniques
Noninvasive imaging can assist in the diagnosis and characterization of acute MI but should never delay reperfusion therapy in
the acute setting. Commonly used imaging techniques in acute
and chronic MI are echocardiography, radionuclide ventriculography, myocardial perfusion scintigraphy using single photon
emission computed tomography (SPECT), and magnetic resonance imaging (MRI).5 Imaging techniques are useful in the
diagnosis of MI by virtue of their ability to detect myocardial
viability and perfusion, either directly with radionuclide techniques or indirectly with echocardiography or MRI. In the
appropriate clinical setting and in the absence of nonischemic
causes, demonstration of a new loss of myocardial viability meets
the criteria for MI.
5
REINFARCTION
Reinfarction may be suspected when there are recurrent clinical
signs or symptoms of myocardial ischemia lasting 20 minutes
or longer within the first 28 days following an initial MI. The
incidence of reinfarction is reported to be less than 20%.32 In
patients who show evidence of reinfarction, an immediate
measurement of cardiac troponin is recommended, followed by
a second sample 3 to 6 hours later. When the first sample is
elevated, reinfarction is diagnosed if there is an increase of at
least 20% in the second sample; if the first sample is normal,
then the criteria for a new acute MI apply.5 Traditionally, CK-MB
has been used to assess for reinfarction. However, there is increasing evidence that troponin values yield similar information;
hence, it remains the preferred cardiac biomarker for diagnosing
reinfarction.32 The ECG diagnosis of reinfarction should be
considered when ST segment elevation greater than 0.1 mV recurs
in a patient previously having a lesser degree of ST segment
elevation or with the development of new Q waves in at least
two contiguous leads.5 The reelevation of the ST segments can
also be seen in threatened myocardial rupture and acute pericarditis. Their presence should prompt an expeditious evaluation
for the complications of acute MI.
CONCLUSION
The rapid recognition and diagnosis of acute MI is crucial for
the early institution of therapy to restore perfusion, minimize
myocardial damage, and preserve cardiac function. Abnormal
cardiac biomarkers, particularly troponin, have become the
hallmark of acute MI but must always be interpreted in the
context of the clinical scenario and ECG.
Acknowledgment
We acknowledge the contributions of Drs. Melissa Daubert and
Allen Jeremias, who were coauthors of this chapter in the previous
edition.
The full reference list for this chapter is available at
ExpertConsult.com.
CHAPTER 9 Diagnosis of Acute Myocardial Infarction 98.e1
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OUTLINE
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Introduction, 99
Inferior Myocardial Infarction, 99
Right Ventricle Myocardial Infarction, 99
Anterior Myocardial Infarction, 100
10
Use of the Electrocardiogram in
Acute Myocardial Infarction
Jason Matos, Roderick Tung, Peter Zimetbaum
Left Main Occlusion, 100
Diagnosis in Bundle Branch Block, 101
Absence of ST Elevations, 101
INTRODUCTION
The term electrocardiogram was first coined by Einthoven at the
Dutch Medical Meeting of 1893. In 1901, he successfully developed
a new string galvanometer with very high sensitivity, which he
used in his electrocardiograph. His device weighed 600 pounds
(Fig. 10.1). Sir Edward Schafer of the University of Edinburgh
was the first to buy a string galvanometer electrograph for clinical
use in 1908. The first electrocardiogram (ECG) machine was
introduced to the United States in 1909 by Dr. Alfred Cohn at
Mt. Sinai Hospital, New York. In 1924, Einthoven was awarded
the Nobel Prize in physiology and medicine for the invention
of the electrocardiograph. By 1930, the importance of the ECG
in differentiating cardiac from noncardiac chest pain was well
recognized; in fact, some patterns were considered so characteristic
that the ECG alone could be used to confirm the diagnosis of
myocardial infarction (MI).1 This chapter reviews the contemporary use of the ECG in the diagnosis of acute MI.
INFERIOR MYOCARDIAL INFARCTION
In 80% of cases, the culprit vessel in inferior MI is the right
coronary artery. The left circumflex artery is the culprit vessel
in all other cases, with the rare exception of a distally extending
inferoapical “wraparound” left anterior descending artery, which
is suggested when there is concomitant ST segment elevation in
the precordial leads.
the magnitude of elevation in lead II with reciprocating ST
segment depressions in I and aVL of greater than 1 mm strongly
suggests the right coronary artery as the culprit over the circumflex
artery. The ST segment vector is directed toward the right when
the right coronary artery is involved, which accounts for the
elevation in lead III greater than lead II (Fig. 10.2). The added
findings of ECG evidence of right ventricle (RV) MI increases
the specificity for the right coronary artery and localizes the
occlusion to a proximal location.
1
ST segment elevation in lead III that exceeds
2
Conversely, the left circumflex artery is suggested when ST
segment elevation in lead III is not greater than lead II and by
the absence of ST segment depression in leads I and aVL.
isoelectric or depressed ST segment with a negative T wave in
lead V4R is very specific but insensitive for proximal left circumflex
artery occlusion.
has been reported to be specific for the left circumflex artery,
although a dominant right coronary artery can produce similar
findings. The presence of ST depression in leads V1 and V2 with
a prominent R wave in lead V2 can be nonspecific and can suggest
involvement of the left ventricular posterior wall or concomitant
disease in the left anterior descending artery. Performing an
ECG with posterior leads (V7–V9) can show a primary posterior
wall injury pattern with ST segment elevation. A localization
schema for inferior MI is summarized in Table 10.1.
6,7
ST segment depression in leads V1 and V2
3–5
An
RIGHT VENTRICLE MYOCARDIAL INFARCTION
In the setting of inferior MI, right-sided precordial lead recordings
are strongly indicated. The presence of RV involvement portends
a worse prognosis and enables the clinician to identify a subgroup
of inferior MI patients with a propensity toward hemodynamic
instability and shock, leading to increased in-hospital mortality.
RV MI is always associated with a proximal occlusion of the
right coronary artery before the takeoff of the right ventricular
marginal branches. The most sensitive sign is 1 mm of ST segment
elevation in lead V4R.9 This sign is not fully specific for RV MI,
however, because ST segment elevation in lead V4R can be seen
in acute pulmonary embolus, anteroseptal MI, and pericarditis.
ST segment elevation in lead V1 in association with elevation in
leads II, III, and aVF is highly correlated with the presence of
RV infarction.
easily confused with anterior wall infarction owing to the anterior
location of the RV, with ST segment elevation manifest only in
the early precordial leads (V1–V3).
2,10
Isolated RV infarction, although rare, can be
11
8
99
CHAPTER 10 Use of the Electrocardiogram in Acute Myocardial Infarction 99.e1
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Keywords
electrocardiogram
myocardial infarction
ST segment elevation
bundle branch block
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