Electrocardiographic ST Segment Elevation:

Left Ventricular Aneurysm

JOHN ENGEL, MD, WILLIAM J. BRADY, MD, AMAL MATTU, MD,†

AND ANDREW D. PERRON, MD

Left ventricular aneurysm (LVA), also described as dyskinetic left ven- the emergency department (ED) with substernal chest pain.
tricular segment, is defined as a localized area of infarcted myocardium The pain, which was intermittent in occurrence, had ap-
that bulges outward during both systole and diastole. LVAs most often peared approximately 10 days before arrival in the ED and
are noted after large anterior wall events but may also be encountered was described as a pressure-like sensation. The patient
status after inferior and posterior wall injuries. In most cases, LVA is
stated that the pain was associated with occasional nausea.
manifested electrocardiographically by varying degrees of ST segment
elevation (STE), which may be difficult to distinguish from ST segment The physical examination was remarkable for bibasilar rales
changes caused by acute myocardial infarction. The STE is generally and significant lower extremity edema. A 12-lead ECG (Fig
associated with well-developed, completed Q waves in the anterior pre- 1) revealed normal sinus rhythm with ST segment elevation
cordial leads, and there will not be reciprocal ST depression in the in leads in V1 to V3; past ECGs were not available for
contralateral leads. This article focuses on the electrocardiographic find- comparison. The concern of early anterior wall AMI was
ings useful in making the diagnosis of left ventricular aneurysm as well raised as the patient was treated. The patient received anti-
as distinguishing LVA from other STE syndromes. (Am J Emerg Med anginal therapy with resolution of the chest discomfort. The
2002;20:238-242. Copyright 2002, Elsevier Science (USA). All rights re- ECG did not show any change with chest pain disappear-
served.) ance.
Additional questioning did not uncover any additional
Left ventricular aneurysm (LVA), also described as dys- medical issues; circumstances surrounding the past MI were
kinetic ventricular segment, is defined as a localized area of unknown. The patient was admitted to the hospital and
infarcted myocardium that bulges outward during both sys- underwent rule out MI with serial cardiac enzyme and ECG
tole and diastole. LVAs most often are noted after large analysis, which did not reveal AMI; the repeat ECGs did not
anterior wall events but may also be encountered status after show change. The patient underwent an echocardiogram,
inferior and posterior wall myocardial infarctions. In most which revealed a prominent dyskinetic segment in the an-
cases, the LVA is manifested electrocardiographically by terior region consistent with anterior wall aneurysm. A
varying degrees of ST segment elevation (STE), which may resting sestamibi scan showed a fixed defect in the anterior
be difficult to distinguish from ST segment changes caused wall. The patient underwent cardiac catheterization, which
by acute myocardial infarction, particularly in the chest pain revealed findings as noted on the echocardiogram as well as
patient with known past myocardial infarction (MI).1 The minimal irregularities in the left anterior descending artery
actual STE itself is believed to result from either an injury and 95% occlusion of the mid right coronary artery; this
current originating from viable yet ischemic myocytes in the right coronary artery lesion was successfully opened by
aneurysm or from mechanical wall stress caused by traction angioplasty with placement of a intracoronary stent. The
on the normal, adjacent myocardium. patient was discharged without incident with diagnoses of
The following article focuses on LVA as a cause of unstable angina, old LVA, and chest pain likely of esoph-
non–acute MI (AMI) STE and includes the electrocardio- ageal origin.
graphic changes useful in making this diagnosis as well as
distinguishing LVA from other syndromes encountered on Case 2
the electrocardiogram (ECG). A 65-year-old man with a history of diabetes mellitus,
hypertension, and MI presented to the ED with chest pain of
CASE PRESENTATIONS 2 hours’ duration. The chest discomfort was described as
Case 1 left sided in location, “aching” in quality, and radiating to
the left shoulder; he also noted diaphoresis and nausea. The
A 59-year-old woman with a past medical history signif- physical examination was unremarkable. The initial 12-lead
icant for past MI and congestive heart failure presented to ECG (Fig 2) showed ST segment elevation in the antero-
lateral leads. The patient received nitroglycerin, morphine,
aspirin, heparin, and beta-adrenergic blocker with continued
From the *Department of Emergency Medicine, University of Vir-
ginia, Charlottesville, VA, and †Division of Emergency Medicine,
pain. An extensive anterolateral AMI was suspected.
Department of Surgery, University of Maryland School of Medicine, A comparison to an old ECG obtained during a routine
Baltimore, MD. office visit as well as a review of serial ECGs revealed
Manuscript received September 8, 2001, accepted September 8, similar findings. Serial ECGs (Fig 3) showed no further
2001. change in the anterolateral distribution other than a reduc-
Reprints are not available.
Copyright 2002, Elsevier Science (USA). All rights reserved. tion in the heart rate. With continued therapy, the patient’s
0735-6757/02/2003-0019$35.00/0 pain resolved; the ECG did not reveal any change with the
doi:10.1053/ajem.2002.32634 pain-free status. The results of the previously mentioned
238
ENGEL ET AL ■ ELECTROCARDIOGRAPHIC MANIFESTATIONS OF LV ANEURYSM 239

FIGURE 1. Case 1. Normal sinus rhythm with STE in leads V1 FIGURE 3. Case 2. After therapy, including beta-blockade, the
to V3 with accompanying Q waves; T wave inversions are noted patient’s pain lessened. The heart rate is reduced, yet the magni-
in leads V3 to V5. The STE is potentially ominous in appearance, tude and morphology of the STE is unchanged.
worrisome for AMI; its cause is in fact because of LVA.

The patient’s pain spontaneously resolved before any

electrocardiographic analysis suggested that the changes medical therapy. The patient was admitted to the ED-based
were felt to represent a noninfarction origin, namely a LVA. chest pain center and underwent rule out MI with serial
Cardiology consultation was requested; arrangements were cardiac enzyme and ECG analysis, which did not reveal MI;
then made for urgent diagnostic cardiac catheterization. No the repeat ECGs did not show any change. Furthermore, an
significant coronary lesions were seen. Furthermore, the left ECG obtained 2 years before during a routine examination
ventriculogram showed aneurysm of the anterior wall. Car- revealed similar findings. The patient underwent a nuclear
diac enzymes were not elevated. A past ECG was eventually stress test, which was normal; he was discharged with a
located, which revealed ST segment elevation similar to that diagnosis of chest wall pain and past MI with LVA.
seen in Figures 2 and 3; past medical history was also noted
to include LVA of the anterior wall. The patient was ulti- DISCUSSION
mately discharged with the diagnoses of unstable angina
The evaluation and treatment of chest pain patients in the
and past LVA.
ED has undergone tremendous change in the past 20 years.
The benefits of early diagnosis and rapid revascularization
Case 3
in the setting of AMI are now widely recognized. This
A 61-year-old man with past medical history significant advancement in acute cardiac care has placed a greater
for MI with LVA presented to the ED with left chest pain. emphasis on the role of the emergency physician (EP) and
The pain, which was intermittent in occurrence, had ap- his/her competence and ability to interpret ECGs in a rapid,
peared approximately 3 weeks before arrival in the ED and timely, knowledgeable manner.
was worsened on inspiration and with upper extremity STE can indicate an acute coronary ischemic event and
movement; no associated symptoms were noted. The phys- remains an important criterion for the initiation of revascu-
ical examination was normal; chest wall tenderness was larization therapy, including thrombolysis or primary angio-
found, which reproduced the pain. A 12-lead ECG (Fig 4) plasty.2 STE itself, however, is not a sensitive marker of
revealed normal sinus rhythm with minimal ST segment AMI.3 Other noninfarction syndromes that cause STE on
elevation in leads V1 to V3 with pathologic Q waves in the ECG include left bundle branch block, left ventricular
leads V1 and V2, which were believed to be consistent with hypertrophy, and LVA. These syndromes occur with in-
past LVA.

FIGURE 2. Case 2. Sinus tachycardia with STE in leads I, aVl, FIGURE 4. Case 3. STE in leads V1 to V3 with a concave
and V2 to V6. morphology is seen here in this patient with known LVA.
240 AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 3 ■ May 2002

other diagnostic studies, and consultants. The study design

clearly removed these options from the physician partici-
pants.
STE syndromes can be misdiagnosed as acute infarction
that then may subject the patient to unnecessary, potentially
dangerous therapies and procedures. Sharkey et al8 report
that 11% of patients receiving a thrombolytic agent were not
in fact experiencing AMI.8 Appropriate therapy delivered in
an expeditious manner is only possible if the correct diag-
nosis, both clinically and electrocardiographically, is estab-
lished in rapid fashion by the EP.
The incidence of LVA after MI is estimated between 3%
and 15% from postmortem studies. Ventricular aneurysms
were found angiographically in 7.6% of patients with cor-
FIGURE 5. Pronounced STE with significant Q waves is seen in onary artery disease in the CASS registry. Although LVAs
leads V1 to V3 in this patient with an initially misdiagnosed chest most commonly occur after a transmural MI, they may also
pain syndrome. On initial presentation, the ECG was felt to rep-
resent an STE AMI. Further review of the patient’s past medical occur after blunt chest trauma, Chagas disease, and sarcoid.
records revealed the presence of LVA. More than 80% of LVAs are located anterolaterally and are
usually associated with total occlusion of the left anterior
descending artery.10 Inferior and posterior aneurysms are
creased frequency in patients with known coronary artery less common. In the CASS registry, risk factors for devel-
disease and may confound the ED evaluation of the chest oping an aneurysm were previous MI and MI with resultant
pain patient presenting with a potential acute ischemic ejection fraction less than 50%. Among patients with LVA,
event. Other patterns, such as benign early repolarization Dubnow et al11 found that men predominated by a 4:1 ratio.
and acute pericarditis, are not necessarily associated with Pathologically, the aneurysm is characterized by a transmu-
ischemic heart disease, although they may resemble acute ral scar that is significantly thinned and is clearly delineated
infarction ST segment waveforms. from the adjacent ventricular muscle.12 Associated findings
In the ED setting, STE is encountered in approximately on autopsy included severe coronary artery disease, scarred
20% of chest pain patients. The most frequent origins for pappillary muscle, pulmonary edema, pericardial thicken-
this STE involve left ventricular hypertrophy and bundle ing, and mural thrombi. The mechanism responsible for
branch block; LVA is an uncommon ST segment elevation persistent ST elevation is not known but is thought to from
entity seen in this patient population, accounting for only mechanical stress caused by traction on the normal myocar-
3% to 4% of all patients with STE.4,5 Although LVA-related dium surrounding the aneurysm.13
STE is an uncommon form of STE, it represents a not LVA is characterized electrocardiographically by persis-
infrequent cause of error in diagnosis and management of tent STE observed several weeks after AMI. Because LVA
ED chest pain patients with ST segment abnormality.6,7 In a is frequently anterior in its location, STE is usually observed
retrospective review of EP electrocardiographic readings, in leads I, aVl, and V1 through V6 (Figs 1 through 6). Of
LVA was the most frequently misinterpreted pattern in ED course, the inferior wall LVA would be manifested on the
chest pain patients.6 Two-hundred two patients presented surface ECG by STE in the inferior leads (Fig 7); such STE,
with chest pain and electrocardiographic STE; 2 of 5 pa- however, is usually less pronounced than the ST segment
tients with LVA-related STE had initial ECG misinterpre- changes noted in the anterior leads. Posterior wall aneurysm
tations. In another investigation7 of electrocardiographic is more difficult to detect electrocardiographically because
STE, EPs were given a series of ECGs with STE; they were
asked to determine the cause of STE and, if related to AMI,
would they prescribe a thrombolytic agent for presumed
AMI. In this study, LVA was again found to be a frequent
cause of error. In fact, LVA was the leading electrocardio-
graphic entity among misinterpreted patterns with 72% of
instances diagnosed incorrectly by the ECG. Both more
importantly and more ominously, the LVA pattern in this
study accounted for a very high rate of inappropriate throm-
bolysis with 28% application of a fibrinolytic agent for
non-AMI syndromes.7 The questionnaire structure of this
study was a hypothetical, contrived situation, which was
highly artificial, and very much unlike the actual ED en-
counter. In a real-time interpretation of the ECG, the EP
would have had numerous other diagnostic tools that would
have assisted in arriving at the correct origin of the STE,
such as an expanded history, past medical history, the
physical examination, both prior and serial ECGs, various FIGURE 6. STE in the anterior distribution resulting from LVA.
ENGEL ET AL ■ ELECTROCARDIOGRAPHIC MANIFESTATIONS OF LV ANEURYSM 241

FIGURE 7. Inferior wall LVA with pathologic Q waves in leads FIGURE 9. STE caused by LVA in A through F. Note the
II and III. Pathologic Q waves are also seen in leads V1 and V2. variation in the magnitude and morphology of the elevated ST
segment.

the usual 12-lead ECG’s view of the posterior wall of the

left ventricle from the anterior perspective. diagnosis of AMI makes it an ideal tool for ruling in AMI
The actual ST segment abnormality caused by the LVA in the patient with chest pain and STE. The predictive
may present with varying morphologies, ranging from ob- values of this electrocardiographic tool are also rather high,
vious, convex ST segment elevation (Figures 1 to 3 and 5 to in particular the positive predictive value. Positive predic-
7) to minimal, concave elevations (Fig 7). The vast majority tive value is the probability of disease presence in a patient
of patients with LVA seen in 1 ED population of chest pain with a positive or abnormal test finding; in this case, the
patients with ST segment elevation showed a concave mor- finding of a nonconcave ST segment morphology suggests
phology of the elevated ST segment.5 Patients with LVA, AMI with a very high probability.5 In fact, in an ED chest
usually the result of extensive anterior wall infarction, will pain population with STE, all patients with the LVA elec-
frequently also have significant Q waves in the same distri- trocardiographic pattern had concave STE.5
bution. STE and Q waves in the inferior or lateral leads in Reciprocal change, which is a not infrequent electrocar-
the proper clinical setting correlate with the less common diographic feature of AMI, strongly suggests that the cur-
inferior and lateral LVAs, respectively. The loss of R wave rent ST segment changes results at least in part from acute
deflection in standard leads may also correlate with the infarction.16,1 In patients with LVA, usually the result of
presence of LVA.14 It has been shown that patients with extensive anterior wall infarction, will frequently also have
larger LVAs have a wider distribution of Q waves; further- significant Q waves in the same distribution. The simulta-
more, the amount of STE does not correlate with the size of neous appearance of the Q wave is not a feature which
the LVA, and the QRS duration increases with the age of the unquestionably supports the electrocardiographic diagnosis
aneurysm.15 The distinction from STE in the patient with of LVA; the emergency physician must recall that Q waves
AMI may be difficult.1 may appear as early as 2 hours after the onset of transmural
The application of ST segment morphologic analysis has AMI. The dynamic nature of AMI-related ST segment ele-
been suggested as a useful tool in distinguishing between vation compared with the often-static ST segment character
AMI and non-AMI causes of STE.5 The use of this mor- in LVA makes both a comparison to past ECGs as well as
phologic analysis has a very high specificity for the diag-
nosis of AMI with a disappointing sensitivity.5 This elec-
trocardiographic interpretative tool is therefore a poor
choice to rule out acute infarction in a patient with chest
pain and STE. Conversely, its quite high specificity for the

FIGURE 10. Serial ECG in a chest pain patient with known LVA
(lead V3 seen). Over time, no change in the morphology or the
FIGURE 8. Single ECG complex from lead V3 showing concave magnitude of the STE is seen, suggesting a nonischemic origin of
STE caused by LVA. the elevated ST segment.
242 AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 20, Number 3 ■ May 2002

2. Hedges JR, Rouan GW, Toltzis R, et al: Use of cardiac en-

zymes identifies patients with acute myocardial infarction otherwise
unrecognized in the emergency department. Ann Emerg Med 1987;
16:248-53
3. Rouan GW, Hedges JR, Toltzis P, et al: A chest pain clinic to
improve the follow-up of patients released from an urban university
teaching hospital emergency department. Ann Emerg Med 1987;16:
1145-50
FIGURE 11. Serial ECG in a chest pain patient with known LVA 4. Brady WJ, Perron AD, Martin ML, et al: Electrocardiographic
(lead V3 seen). Over time, a significant change in both the mor- ST segment elevation in emergency department chest pain center
phology and the magnitude of the STE is seen, suggesting an patients: Etiology responsible for the ST segment abnormality. Am J
ischemic origin of the elevated ST segment. The patient was Emerg Med 2001;19:25-8
diagnosed with recurrent AMI and past LVA. 5. Brady WJ, Syverud SA, Beagle C, et al: Electrocardiographic
ST segment elevation: The diagnosis of AMI by morphologic anal-
ysis of the ST segment. Acad Emerg Med 2001;8:961-967
6. Brady WJ, Perron A, Ullman E: Errors in Emergency Physician
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considerable diagnostic value. Acad Emerg Med 2000;7:1256-60
There are several clinical, nonelectrocardiographic clues 7. Brady WJ, Perron A, Chan T: Electrocardiographic ST segment
useful for detecting an aneurysm. The patient’s history will elevation: Correct identification of AMI and non-AMI syndromes by
emergency physicians. Acad Emerg Med 2001;8:349-60
most often indicate a prior MI, with anterior transmural 8. Muller DW, Topol EJ: Selection of patients with acute myocar-
infarcts increasing the likelihood of LVA. On physical dial infarction for thrombolytic therapy. Ann Intern Med 1990;113:
examination, an abnormal cardiac impulse and third or 949-60
fourth heart sounds are common physical findings.17 The 9. Faxon DP, Ryan TJ, Davis KB, et al: Prognostic significance of
chest roentgenogram may reveal a bulge of the silhouette of angiographically documented left ventricular aneurysm from
the Coronary Artery Surgery Study (CASS). Am J Cardiol 1982;50:
the left ventricle. Echocardiography has a sensitivity and 157-64
specificity of 93 and 94%, respectively, for detecting LVA. 10. Elliott MA, Braunwald E: Acute myocardial infarction. In
Cardiac catheterization remains the gold standard for diag- Braunwald B (ed): Heart Disease. Philadelphia, WB Saunders Com-
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LVA is a less frequent cause of STE among ED chest management of patients with acute myocardial infarction. In Alex-
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graphic appearance of LVA is quite varied, ranging from the lar aneurysm. Am Heart J 1949;37:267-77
nonthreatening, minimally elevated, concave STE to the 15. Cokkinos DV, Hallman GL, Cooley DA, et al: Left ventricular
ominous significant convex elevation. aneurysm: Analysis of electrocardiographic features and postres-
section changes. Am Heart J 1971;82(2):149-57
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