JAOA • Vol 108 • No 7 • July 2008 • 344-349
Pulmonary Embolism Mimicking Anteroseptal Acute Myocardial Infarction
Gregory T. Wilson, DO;
Frederick A. Schaller, DO
From the Department of Internal Medicine at the Plaza Medical Center of
Fort Worth (Dr Wilson) in Tex, and Touro University Nevada College of
Osteopathic Medicine (Dr Schaller) in Henderson.
Address correspondence to Gregory T. Wilson, DO, Attn: Kay Washington, Plaza
Medical Center of Fort Worth, 900 Eighth Ave, Fort Worth, TX
76104-2100.E-mail:
gregwilson{at}lscom.net
Pulmonary embolism (PE) is a potentially lethal condition that presents in
patients with chest pain or shortness of breath. Although electrocardiograms
(ECGs) typically demonstrate abnormalities associated with PE, ST-segment
elevation, which can indicate anteroseptal acute myocardial infarction (AMI),
has—on rare occasions—been noted on ECGs of patients with acute
PE. The current report documents the case of a 57-year-old man who presented
to the emergency department with chest pain. Findings from an ECG suggested
anteroseptal AMI; however, cardiac catheterization indicated that the patient
did not have critical ischemic heart disease. On further examination, the
patient was found to have a massive bilateral PE. The present report
emphasizes that physicians must investigate PE in all patients presenting with
chest pain, dyspnea, or both, even in the face of ECG changes that are
suggestive of a cardiac etiology. A brief discussion of the current theories
of ST-segment elevation in the setting of PE is also included.
Acute pulmonary embolism (PE), common in patients presenting with chest
pain and dyspnea, can be lethal, particularly if the condition is not
diagnosed. Electrocardiograms (ECGs) are typically used to diagnose PE in
patients. Sinus tachycardia, complete or incomplete right bundle-branch block,
the S1Q3T3 pattern (prominence of the S wave in lead I, Q wave in lead III,
and T wave in lead III), and ST-segment depression in the precordial leads are
among the most common ECG findings characteristic of this condition
(Figure
1).1
On rare occasions, ST-segment elevation, which can indicate anteroseptal acute
myocardial infarction (AMI), is associated with acute
PE.2-4
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Figure 1. Typical electrocardiogram changes associated with pulmonary embolism. This
figure was adapted from Electrocardiography in Clinical Practice: Adult and
Pediatric.1
Copyright Elsevier, 2008. Abbreviations: S1Q3, prominence of the S wave in
lead I and the Q wave in lead III; S1Q3T3, prominence of the S wave in lead I,
Q wave in lead III, and T wave in lead III.
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The present report describes a man who demonstrated dramatic and dynamic
ST-segment elevation suggestive of anteroseptal AMI. However, diagnostic
testing revealed a large bilateral PE. In addition, we review the changes in
ECG results that are typically associated with PE and summarize the theory of
ST-segment elevation in such cases.
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Report of Case
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A 57-year-old man presented to the emergency department after he had a
syncopal episode while at home alone. The patient stated that he had no
prodrome and was unaware as to how long he was unconscious. He described
substantial midsternal chest pain and shortness of breath on awakening.
Although he had a history of coronary artery disease, the chest discomfort
differed from his typical angina. The patient stated that, in the weeks before
presenting to the emergency department, he had increasing fatigue as well as
episodic chest pain and shortness of breath unrelated to physical
activity.
The patient's medical history was significant for coronary artery disease,
hyperlipidemia, hypertension, depression, and renal insufficiency. The patient
had three intracoronary stents placed more than 3 years earlier: two in the
left anterior descending artery and one in the right coronary artery. The
patient had no known history of myocardial infarction, cardiomyopathy,
arrhythmia, or central nervous system disease. He had a 6-year history of
minimal tobacco use (approximately 1 pack per year), admitted to occasional
alcohol consumption, and denied illegal drug use. His prescribed medications
included clopidogrel bisulfate, 75 mg/d, for coronary artery disease;
metoprolol tartrate, 50 mg twice a day, for hypertension; isosorbide
mononitrate, 60 mg/d, for angina; lansoprazole, 30 mg/d, for heart burn;
amitriptyline hydrochloride, 25 mg at bedtime, and citalopram hydrobromide, 20
mg/d, for depression; inhaled beclomethasone dipropionate, 42 µg twice a
day, as a prophylaxis for asthma; and aspirin, 325 mg/d, for cardiac
protection.
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Figure 2. Laboratory test results of a 57-year-old man presenting with chest pain
suggestive of anteroseptal acute myocardial infarction.
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On examination, the patient's blood pressure was 123/80 mm Hg in the supine
and orthostatic positions; oxygen saturation, 96%; and heart rate, 111 beats
per minute and regular. He appeared to be well nourished. Although he was in
mild respiratory distress, the patient was able to complete full sentences.
His trachea was midline and his lung fields were clear. No jugular venous
distension was noted. Cardiac examination revealed tachycardia and a grade 1
or 2 early-peaking systolic murmur at the lower left sternal border without an
audible third heart sound and no parasternal heave. Findings from the
abdominal examination were unremarkable. The patient's extremities were warm
with normal pulses and without edema.
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Figure 3. Initial electrocardiogram of a 57-year-old man shows sinus rhythm with
incomplete right bundle-branch block and anterior and inferior T-wave
inversions consistent with anterior and inferior myocardial ischemia. In the
inferior leads, Q waves were also noted, suggesting age-indeterminate inferior
myocardial infarction.
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Laboratory data revealed near-baseline serum electrolyte levels and
unremarkable complete blood cell count
(Figure 2). The
patient had a mildly elevated creatinine level of 1.6 mg/dL and a brain-type
natriuretic peptide level of 21 pg/mL. Troponin I was normal (0.03 ng/mL).
Results from the initial ECG demonstrated sinus tachycardia with first-degree
block in the interval from atrial stimulus to succeeding ventricular stimulus,
incomplete right bundle-branch block, and subtle ST-segment elevation in the
anteroseptal leads. Inverted T waves were noted in the right precordial and
inferior leads (Figure
3). Chest X-ray findings were unremarkable.
The patient was admitted to the telemetry unit for further laboratory
testing, including serial cardiac enzyme measurements. Intravenous heparin was
administered as a 5000 U bolus dose followed by an infusion of 1000 U/hr.
Partial thromboplastin time was measured after 1 hour, and the infusion was
adjusted according to a previously established nomogram. Several hours later,
the patient again experienced substantial midsternal chest discomfort (rated 8
on a 10-point scale, with 10 being "the worst pain imaginable")
and shortness of breath similar to that prompting his admission. After
initiating transdermal nitroglycerin therapy, the patient's blood pressure
decreased from 110/70 mm Hg to 78/40 mm Hg. Nitroglycerin was removed, and
intravenous fluids were administered. A second ECG revealed substantial
ST-segment elevation and pathologic Q waves consistent with AMI
(Figure 4). As a
result, therapy for acute coronary syndrome was initiated and arrangements
were made for emergency cardiac catheterization for suspected acute coronary
occlusion.
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Figure 4. Second electrocardiogram (ECG) taken several hours after the initial ECG of
a 57-year-old man demonstrates substantial ST-segment elevation and pathologic
Q waves in the anterior and inferior leads consistent with anteroseptal acute
myocardial infarction.
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Results from an angiogram, however, failed to reveal critical obstructive
coronary disease. In fact, all of the patient's stents were widely patent with
only mild to moderate atherosclerotic disease in the left anterior descending
coronary artery, circumflex artery, and right coronary artery
(Figure 5). Although
the ECG changes suggested compromised anterior circulation, the patient's
response to nitroglycerin suggested right ventricular injury. However, the
angiogram revealed a preserved vascular supply to the right ventricle.
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Figure 5. Cardiac catheterization images of a 57-year-old man suspected of having
acute coronary occlusion. However, results revealed only (A) minor distal
irregularities of the left anterior descending coronary artery (arrow); (B)
moderate plaque in the circumflex artery (arrow) without substantial
obstruction and no substantial left main coronary disease; and (C) moderate
plaque in the right coronary artery (arrow).
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After cardiac catheterization, transthoracic echocardiogram revealed
dramatic right ventricular enlargement and displacement of the
interventricular septum into the left ventricle
(Figure 6); however,
left ventricular systolic function was normal. In addition, cardiac pressures
on the right side were elevated, and right ventricular systolic function was
mildly reduced. The patient did not demonstrate "McConnell's
sign," which is described as ventricular freewall hypokinesis with
preservation of right ventricular apical
function.5
McConnell's sign has been reported in instances of massive
PE.5
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Figure 6. Echocardiographic images of a 57-year-old man after cardiac catheterization
did not reveal acute coronary occlusion. Short-axis two-dimensional
transthoracic echocardiogram (A) reveals an enlarged right ventricle (RV) and
leftward displacement of the interventricular septum (IVS) during diastole.
Compression of the left ventricle (LV) suggests elevated pulmonary pressures
on the right side. Spectral Doppler echocardiogram of the tricuspid
regurgitant jet (B) reveals elevated right ventricular systolic pressure (41
mm Hg).
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As a result of the patient's renal insufficiency and contrast load from
angiography, a ventilation-perfusion (V/Q) scan was promptly ordered instead
of a computed tomography scan to evaluate for PE. The V/Q scan demonstrated
large bilateral ventilation-perfusion mismatches highly suggestive of PE
(Figure 7). The
patient's troponin I level increased to a peak of 2.6 ng/mL, and creatine
kinase-MB increased to 18.3 ng/mL.
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Figure 7. Ventilation-perfusion scans used to evaluate a 57-year-old man for
suspected pulmonary embolism. The resulting multiple, bilateral segmental, and
lobar perfusion defects (arrows) visible in the perfusion scan (A) and
consistent in the ventilation scan (B) reveal a high probability for massive
bilateral pulmonary embolism.
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After continuation of intravenous heparin therapy and hydration, the
patient's condition stabilized. The remainder of the patient's hospital stay
was unremarkable. Three days after presentation, a second echocardiogram
revealed normalization of the right ventricular cavity size and a decrease in
estimated pulmonary artery pressures
(Figure 8). Likewise,
the anterior ST-segment changes and conduction defects resolved without the
occurrence of pathologic Q waves. The right precordial T-wave inversions also
improved (Figure 9).
All cardiac enzyme markers normalized. Ten grams of coumadin was adminstered
on the day before discharge, and 7.5 mg on the day of patient's discharge.
Arrangements were made with the patient's internist for follow-up care.
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Figure 8. A second set of echocardiographic images from a 57-year-old man after
treatment for pulmonary embolism. Short-axis two-dimensional transthoracic
echocardiogram (A) shows improvement in the size of the right ventricle (RV)
and a return of the left ventricle (LV) to a normal circular shape. Spectral
Doppler echocardiography of the tricuspid regurgitant jet (B) reveals interval
improvement in right ventricular systolic pressure (34 mm Hg). Abbreviation:
IVS, interventricular septum.
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Figure 9. Follow-up electrocardiogram (ECG) taken 3 days after patient presentation
to the emergency department demonstrates interval resolution of the anterior
and inferior ST changes without Q waves. The incomplete right bundle-branch
block noted in the initial ECG has also resolved.
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Discussion
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As stated previously, ST-segment elevation associated with PE is rare, and
the direct relationship remains unclear. Anteroseptal ST-segment elevation was
noted in one case2
involving a 42-year-old woman with echocardiographic evidence of right
ventricular pressure overload, which resolved after administration of
thrombolytics (80 mg of tenecteplase). Another
report3 described a
62-year-old man with substantial anteroseptal ST-segment elevation. Autopsy
revealed that the patient had a massive PE without significant coronary artery
atherosclerotic lesions. The distribution and contour of ST-segment elevation
in each of these
cases2,3
are similar to those in the present case. However, those two
reports2,3
do not describe the patients' metabolic status—particularly potassium
and pH levels—at the time of ECG.
The anteroseptal leads visible on ECGs are most likely to show ST-segment
elevation. Paradoxical embolization of a venous clot across an atrial septal
defect or across a patent foramen ovale into a coronary vessel represents one
possible mechanism of ST-segment elevation in patients with deep venous
thrombosus and PE.4
In such patients, coronary angiography will likely demonstrate a filling
abnormality consistent with embolic debris. Furthermore, most ECG
abnormalities associated with PE are thought to be a consequence of a sudden
pressure load on a noncompensatory right
ventricle.3 This
additional strain may induce global or focal myocardial ischemia. Therefore,
another potential theory suggests that ST-segment elevation in PE results from
epicardial or microvascular coronary vasospasm induced by such
strain.3 A third
theory suggests that severe hypoxemia induces a catecholamine surge, which
increases myocardial workload and results in
ischemia.3
Several metabolic abnormalities, including hyperkalemia, have also been
associated with ST-segment elevation evidenced on
ECGs.6 Severe
acidosis—specifically diabetic acidosis—has also been associated
with ST-segment elevation, which is believed to be caused by potassium shifts
into extracellular
spaces.6 As
described in one case
report6 where
substantial anteroseptal ST-segment elevation was present, the patient had a
serum bicarbonate level of 4 mEq/L; pH, 7.06; and potassium, 8.9 mEq/L.
Elevation of the ST segment in patients with hyperkalemia typically slopes
down.7 This
characteristic can be helpful to physicians attempting to differentiate it
from myocardial injury, in which the ST segment typically has a plateau,
shoulder, or upsloping
elevation.7
Potassium levels, when associated with ST-segment elevation, are typically
high and are joined by other ECG abnormalities (eg, peaked T waves, widening
of the QRS complex, loss of atrial P
waves).7 Although
the mild increase in potassium in our patient was unlikely to result in such
dramatic ST-segment elevation, the second ECG demonstrated downsloping
elevation and narrow-based T waves, which are similar to changes documented in
hyperkalemia.7 The
serum potassium level in our patient at the time of the ECG was 5.5 mEq/L,
lower than that seen in previous cases of ST-segment
elevation.6 In
addition the severity of metabolic acidosis in our patient (bicarbonate, 21
mEq/L) is less than that seen in other cases associated with ST elevation
attributed to metabolic
derangements.6
Troponin elevation in the setting of PE has a clinically significant effect
on patient
prognosis.8 The
rapid and significant rise in right ventricular pressure with PE can lead to
right ventricular myocardial ischemia and troponin release, which correlates
with increased risk of
mortality.8 In one
prospective study9
of 56 patients with confirmed PE, elevated troponin T (
0.1 µg/L) was
associated with an increased risk of in-hospital death (odds ratio [OR], 29.6;
95% confidence interval [CI], 3.3-265.3) and was an independent predictor of
30-day mortality (OR, 15.2; 95% CI, 1.22-190.4). Although troponin I was
measured in our patient rather than troponin T, it is plausible that troponin
I elevation portends a poorer outcome than in patients without elevation of
either cardiac biomarker.
The present report is particularly interesting for several reasons. When
viewed retrospectively, the patient's initial ECG demonstrates several
potential signs of PE. Specifically, the subtle S1Q3T3 pattern, incomplete
right bundle-branch block, and nonspecific anterior T-wave inversions were
potential signs of PE. The patient also had several risk factors for PE,
including chronic tobacco use, chronic coronary artery disease, and
hypertension.10
Although PE was an early consideration, initial evaluation and clinical
management focused on a cardiac etiology for the patient's symptoms because of
his history of coronary problems. Furthermore, though the dramatic
anteroseptal ST-segment elevation in our patient likely represented true
myocardial injury given the increase in cardiac enzymes, angiography did not
reveal critical coronary lesions, making paradoxical embolization
unlikely.
One potential explanation for the ECG findings in the present report is
intense coronary vasospasm superimposed on nonobstructive atherosclerosis in
the anterior circulation—which together could result in myocardial
injury and cause the ECG changes noted. The fact that the ECG abnormalities
resolved concomitantly with a reduction in right ventricular pressures and
chamber dimensions implies a potential link between right ventricular dynamics
and the anterior ECG findings as demonstrated by the patient's response to
nitroglycerin. The right ventricle is dependent on adequate venous return and
preload to maintain forward flow against the elevated pulmonary pressures. In
the present report, as a result of nitroglycerin, venous dilation reduced
preload and caused hemodynamic deterioration.
Because most patients with acute coronary syndromes are treated with early
heparin therapy—either low molecular weight or
unfractionated—patients would theoretically be treated for nonlethal PE
as well as for emergent coronary conditions. However, patients with PE would
require long-term anticoagulation therapy, which is not a standard treatment
after myocardial infarction. Therefore, though initial management of these two
conditions may be similar, the diagnosis of PE substantially changes postacute
care from that of coronary disease and may prompt a work-up for coagulopathy.
Clearly, the diagnosis of PE in those with chest pain has clinically
significant treatment implications.
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Conclusion
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Specific abnormal findings on ECGs may provide clues to the diagnosis of PE
in patients presenting with chest pain, dyspnea, or both. Typically, these
changes involve nonspecific precordial ST-segment depression, T-wave
inversion, or changes consistent with right ventricular strain. However, the
present case illustrates the rare association of PE with ST-segment elevation,
particularly in the anteroseptal leads. Therefore, we recommend that
physicians consider the presence of PE in patients with chest pain or dyspnea,
even when ST-segment elevation is present.
Submitted June 11, 2007;
revision received August 30, 2007;
accepted September 17, 2007.
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References
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Report of Case
Discussion
