www.jecgonline.com

Journal of Electrocard

Transient pathologic Q waves in a case of apical ballooning

Pablo Robles, MD,4 Jose Julio Jimenez, MD, Isabel Monedero, MD, Ana Isabel Huelmos, MDDepartament of Cardiology, Fundacion Hospital Alcorcon, Madrid, Spain

Received 5 November 2006

Presentation

A 73-year-old woman with known mild systemic

hypertension was admitted to our hospital because of a 2-

hour history of chest pain. As a remarkable fact, her

husband had died that day. Physical examination showed a

normal blood pressure (130/60 mm Hg) and a heart rate of

100 beats per minute. Hematologic values and serum

creatinine levels were normal. Sodium and potassium serum

levels were also within normal limits. Initial serum creatine

kinase (CK) level was slightly increased (220 U/L; reference

range, 24-170 U/L), with a troponin I level of 11.8 lg/mL

(normal values up to 0.4 lg/mL). Chest x-ray was

unremarkable. The first electrocardiogram (EKG) was

performed when the patient still had chest pain and showed

Q waves and ST elevation in all the precordial leads and

leads I, II, and aVL (Fig. 1). Simultaneously, 2-dimensional

echocardiography was carried out showing apical akinesis

and mild ventricular dysfunction accompanied by ventric-

ular dilatation. With the diagnosis of extensive acute

anterior myocardial infarction (AMI), an urgent coronarog-

raphy was undertaken to perform a primary angioplasty, but

the coronary angiogram revealed a normal coronary tree.

Left ventriculogram demonstrated extensive apical akinesis

with hypercontractility of the basal segments (Fig. 2). An

ejection fraction of 0.35 was calculated. Peak CK and

troponin I serum levels were 2005 U/L and 31 lg/mL,

respectively. An EKG performed 5 days later showed deep

negative T waves in precordial leads, but Q waves could not

be observed (Fig. 3). Three weeks after admission, a 2-

dimensional echocardiography showed normal ventricular

function with no regional motion abnormalities. An almost-

normal EKG was obtained with absence of Q waves and

ST-T abnormalities (Fig. 4).

Diagnosis

The presence of pathologic Q waves in EKG is

traditionally considered as evidence of established AMI.

0022-0736/$ – see front matter D 2007 Elsevier Inc. All rights reserved.

doi:10.1016/j.jelectrocard.2007.02.003

4 Corresponding author. Pablo Robles, MD, Unidad de Cardiologıa,

Avda Budapest n8 1 28922, Alcorcon 28922, Madrid, Spain. Tel.: +34 91

6817330; fax: +34 916817330.

E-mail addresses: probles@fhalcorcon.es, problesve@yahoo.es

Abnormal Q waves are one of the most reliable markers of

myocardial necrosis. Pathologic and experimental studies

also support this assertion.

Although their disappearance on a long-term basis has

been well described in 5% to 25% of heart attacks and, more

often than not, in inferior AMI, their disappearance for brief

periods is an infrequent entity. Profound ischemia may not

result in necrosis but may cause myocardial stunning that

can induce transient cell damage and, as a consequence, a

loss of electrical forces.

We describe the case of a patient with suspected AMI

who developed transient pathologic Q waves. The exact

mechanism for regression or disappearance of abnormal

Q waves remains uncertain. Transient EKG changes

resembling AMI with Q waves and ST-segment elevation

have been reported in a variety of clinical situations in

which evidence for myocardial necrosis was not apparent.

Such EKG changes resolved to normal within minutes or

days. Few reports showed cases in which exercise testing

induced a painless reversible EKG abnormality identical to

acute anterior AMI, and subsequent angiography revealed a

severe stenosis in the proximal left coronary artery.1

In recent years, patients have been reported to have a

clinical picture that resembles AMI before some stressful

condition but have normal coronary arteries and a takot-

subo-shaped left ventricle on ventriculography or echocar-

diography. This type of stress cardiomyopathy is known as

bapical ballooningQ (AB)2 or btakotsubo cardiomyopathy,Q3

and it has been reported more frequently in Japan.

We present a case of AB with transient abnormal Q

waves (TAQ). Transient abnormal Q waves are defined as

abnormal Q waves that disappear within days. They are

most often seen in patients with ischemic heart disease but

are also described in other cardiac and noncardiac

conditions summarized in Table 1. Brief episodes of

myocardial ischemia give rise to reversible biochemical

and ultrastructural myocardial changes resulting in transient

EKG changes and provide an accepted theory for the

pathogenesis of TAQ. Investigations have shown that the

occurrence of exercise-induced TAQ may be a symptom of

ischemic heart disease.4

The etiology and clinical features of this form of

reversible left ventricular dysfunction remain unclear.

iology 40 (2007) 489–492

Fig. 1. Electrocardiogram 2 hours after admission. A QS pattern in leads V1 through V4 and ST elevation in leads I, aVL, and V2 through V6 were noted.

P. Robles et al. / Journal of Electrocardiology 40 (2007) 489–492490

Although provocative vasospasm has been confirmed in

some cases, multivessel epicardial spasm seems unlikely

because the abnormalities in contractility affect multiple

vascular territories. An alternative mechanism is microvas-

cular spasm. Abnormal coronary flow in the absence of

obstructive disease has recently been reported in patients

with stress-related myocardial dysfunction. Others have

demonstrated reduced coronary flow reserve and regional

defects on cardiac metaiodobenzylguanidine-enhanced im-

aging in such patients, suggesting the presence of sympa-

thetically mediated microcirculatory dysfunction.5

Some authors have demonstrated this kind of myocardial

ischemia without significant stenosis in an epicardial artery.

Management

The presence of Q waves in cases of AB were rarely

commented on in the literature. When this parameter was

Fig. 2. Left ventriculogram in systole showing extensive midventricul

analyzed, abnormal Q waves were present in between 20%

and 30% of patients.6

These abnormalities typically resolved in a few days

with restoration of normal R wave progression as in our

case. Also, the prolonged ST-segment elevation and

negative T waves observed in our patient have been related

to a severely dysfunctional but viable myocardium.

Furthermore, the persistent negative T waves have been

associated with denervation of the sympathetic nerve in

the jeopardized myocardium. Patients with AB compared

with those with AMI usually show asynergy in more

extensive areas and lower peak CK serum levels. Likewise,

patients with AB have a more rapid clinical and echocar-

diographic improvement.

The differentiation between patients with AB and those

with anterior acute AMI is difficult. Apical ballooning is an

acute cardiac syndrome that closely mimics ST-segment

elevation AMI leading to emergency thrombolysis or

coronary angiography in many patients. Previously pub-

ar and apical akinesis with hypercontractility of basal segments.

Fig. 3. Electrocardiogram 5 days later showed disappearance of Q waves, partial resolution of ST elevation, and development of giant negative Twaves in leads

with previous Q waves.

P. Robles et al. / Journal of Electrocardiology 40 (2007) 489–492 491

lished studies have tested the proposition that clinical and

EKG features may reliably differentiate AB from an acute

anterior AMI secondary to occlusion of the left anterior

descending coronary artery.7 Patients presenting with the

AB syndrome are usually postmenopausal women who

present with ischemiclike chest discomfort, ST-segment

elevation, small cardiac biomarker elevation, and charac-

teristic midventricular and apical wall motion abnormalities

in the absence of obstructive epicardial coronary disease.

Patients with AB develop symptoms proximate to an acute

emotional stress. The patients with AB have similar EKG

Fig. 4. Electrocardiogram 20 days later revealed a

findings to patients with anterior AMI infarct but with less

prominent ST-segment elevation in the anterior precordial

EKG leads. The clinical predictive value of the clinical and

EKG features in an individual patient was not sufficient to

reliably exclude AMI. The only reliable way to prospec-

tively distinguish AB from anterior AMI is coronary

angiography to document the absence or presence of

obstructive epicardial coronary atherothrombosis and left

ventriculography or echocardiography to demonstrate

the characteristic apical and midventricular wall motion

abnormalities.8

bsence of Q waves and ST-T abnormalities.

Table 1

Causes of transient Q waves

Extracardiac pathologies

Subarachnoid hemorrhage

Pancreatitis

Bronchial asthma

Phosphoric intoxication

Pulmonary embolism

Spontaneous pneumothorax

Ischemic heart disease

Treadmill tests

Angina crisis in Prinzmetal angina

Early reperfusion in acute coronary syndromes

Other cardiac disease

Myocarditis

Unknown mechanism

Apical ballooning syndrome

Technical problems

Electrode misplacement

P. Robles et al. / Journal of Electrocardiology 40 (2007) 489–492492

There is not a specific treatment for this entity. Some

authors recommend avoiding the use of pressor agents and

b-agonists because of the significant catecholamine release

observed in patients with AB.

Articles Appearing

Acquisition

What is inside the electrocardiograph?—Richard Gregg, MSEE;

MSEE; Karen Giuliano, PhD

Clinical diagnosis

Referral of patients with ST-elevation acute myocardial infarctio

teletransmission of 12-lead electrocardiogram—Martin Sillesen;

Freddy Lippert; Peter Clemmensen, MD

Mini-Symposium on ECG Waveform Ch

e-pub: Relation between P-wave dispersion and left ventricular geo

Mustafar Gur, MD; Remzi Yilmaz, MD; Recep Demirbag, MD; S

P-wave duration and dispersion in patients with coronary slow

Infarction frame count—Sait M. Dogan; Metin Gursurer; Must

e-pub: P-wave and QRS complex measurements in patients un

Madias, MD; Asma Yazidi, MD; Mohammed Bennani, MD; Ah

Tahiri, MD

Letter to the Editor: Interatrial block: a prevalent widely neglecte

David Spodick, MD

High prevalence of widened P waves among pediatric patien

Ariyarajah, MD; Debra O’Brien, CRT; Sirin Apiyasawat, MD; Dan

Relation of admission QRS duration with development of angiog

infarction treated with primary percutaneous interventions—O

MD; Hatice Selcuk, MD; Omer Alyan, MD; Tolga Aksu, MD; F

MD; Ahmet Demir, MD; Yucel Balbay, MD; Erdogan Ilkay, M

R-wave amplitude response to myocardial ischemia in hyper

Yoshiki Akakabe, MD; Michiyo Yamano, MD; Shigeyuki M

Kuribayashi, MD, PhD; Hiroki Sugihara, MD, PhD

References

1. West JN, Bennett MR, Pentecost BL. Association of transient abnormal

Q-waves during exercise testing with a stenosis of the main stem of the

left coronary artery. Int J Cardiol 1991;31:102.

2. Korlakunta HL, Thambidorai SK, Denney SD, Khan IA. Transient left

ventricular apical ballooning: a novel heart syndrome. Int J Cardiol

2005;102:351.

3. Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Musha H, Sasaka K.

123I-MIBG myocardial scintigraphy in patients with btakotsuboQcardiomyopathy. J Nucl Med 2004;45:1121.

4. Godballe C, Hoeck HC, Sorensen JA. Transient abnormal Q-waves.

Ugeskr Laeger 1990;152:92.

5. Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of

myocardial stunning due to sudden emotional stress. N Engl J Med

2005;352:539.

6. Donohue D, Movahed MR. Clinical characteristics, demographics and

prognosis of transient left ventricular apical ballooning syndrome. Heart

Fail Rev 2005;10:311.

7. Inoue M, Shimizu M, Ino H, et al. Differentiation between patients with

takotsubo cardiomyopathy and those with anterior acute myocardial

infarction. Circ J 2005;69:89.

8. Bybee KA, Motiei A, Syed I, et al. Electrocardiography cannot reliably

differentiate transient left ventricular apical ballooning syndrome from

anterior ST-segment elevation myocardial infarction. J Electrocardiol

2001;40:38, e1.

in Next Issue

Sophia Zhou, PhD; James Lindauer, MD; Eric Helfenbein,

n directly to the catheterization suite based on prehospital

Maria Sejersten; Soren Strange; Soren Loumann Nielsen;

anges in Common Clinical Syndromes

metric patterns in newly diagnosed essential hypertension—

elahattin Akyol, MD; Halil Altiparmak, MD

flow and its relationship with Thrombolysis in Myocardial

afa Aydin; Ezgi Kalaycioglu; Fatih Cam

dergoing hemodialysis—Abbdenasser Drighil, MD; John

med Bennis, MD; Beenyouness Ramdan, MD; Azzeddine

d and portenous abnormality—Vignendra Ariyarajah, MD;

ts in two separate hospitals—Ray Loo, MD; Vignendra

iel Silbert, MD; Stephen Katz, MD; David Spodick, MD, DSc

raphic no-reflow in acute ST-segment elevation myocardial

rhan Maden, MD; Fehmi Kacmaz, MD; Mehmet Selcuk,

atma Metin, MD; Omac Tufekcioglu, MD; Ramazan Atak,

D

trophic cardiomyopathy—Tatsuya Kawasaki, MD, PhD;

iki, MD, PhD; Tadaaki Kamitani, MD, PhD; Toshiro