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Available online at www.sciencedirect.com
ScienceDirect
journal homepage: www.elsevier.com/locate/ihj
Case Report
'Action potential-like' ST elevation following
pseudo-Wellens' electrocardiogram
Fatih Oksuz, Baris Sensoy, Fatih Sen, Ethem Celik, Ozcan Ozeke
*,Orhan Maden
Turkiye Yuksek Ihtisas Training and Research Hospital,
Department of Cardiology, Ankara, Turkey
a r t i c l e i n f o
Article history:
Received 8 December 2014
Accepted 29 May 2015
Available online 4 August 2015
Keywords:
Vasospastic angina
ST segment elevation
Wellens' syndrome
a b s t r a c t
Coronary artery vasospasm is an important cause of chest pain
syndromes that can lead to
myocardial infarction, ventricular arrhythmias, and sudden
death. In 1959, Prinzmetal et al
described a syndrome of nonexertional chest pain with ST-segment
elevation on electro-
cardiography. Persistent angina is challenging, and repeated
coronary angioplasty may be
required in this syndrome. Calcium antagonists are extremely
effective in treating and
preventing coronary spasm, andmay provide long-lasting relief
for the patient.Whereas the
Wellens' syndrome is characterized by symmetrically inverted
T-waves with preserved R
waves in the precordial leads suggestive of impendingmyocardial
infarction due to a critical
proximal left anterior descending stenosis, the pseudo-Wellens'
syndrome caused by
coronary artery spasm has also rarely been reported in
literature. We present a pseudo-
Wellens syndrome as a cause of vasospastic angina, and a diffuse
ST segment elavation on
electrocardiogram resembling the Greek letter lambda, called
also 'action potential-like' ECG
in a patient with vasospastic-type Printzmetal angina.
# 2015 Cardiological Society of India. Published by Elsevier
B.V. All rights reserved.
1. Introduction
Restingangina isoneof themost frequentsymptomsofpatientsin the
emergency room.1 Many patients with chest pain whohave no
obstructive stenoses at diagnostic angiography aremisclassified as
having noncardiac chest pain.2 Variant anginais a form of angina
pectoris that shows transient ST-segmentelevation on
electrocardiogram during an attack of chest pain.Ischemic episodes
of variant angina show circadian variationand often occur at rest
from midnight to early morning.3 Thedemonstration of either
spontaneous or provoked coronary
* Corresponding author at: Türkiye Yüksek İhtisas Hastanesi,
KardiyoE-mail address: [email protected] (O. Ozeke).
http://dx.doi.org/10.1016/j.ihj.2015.05.0250019-4832/# 2015
Cardiological Society of India. Published by Elsevie
spasm proves coronary hypercontractility and thus the diagno-sis
of variant angina4 Coronary spasm could be documented innearly 50%
of the suspected ACS in emergency departmants.5
Risk stratification of patients with recurrent chest pain
andnormal coronary angiogram is a relevant but still
definitelyunsolved clinical problem.6 Although coronary artery
vaso-spasm can be suspected clinically, proof cannot usually
beobtained by non-invasive means but is easily available
duringcardiac catheterization. Patients with vasospastic angina
arerepeatedly exposed to this invasive procedure as
mostcardiologists suspect a coronary lesion (requiring
intervention)as the cause of the patient's resting angina.7
loji Klinigi, Ankara, 06100, Turkey. Tel.: +90 505 383 67
73.
r B.V. All rights reserved.
http://crossmark.crossref.org/dialog/?doi=10.1016/j.ihj.2015.05.025&domain=pdfhttp://crossmark.crossref.org/dialog/?doi=10.1016/j.ihj.2015.05.025&domain=pdfhttp://dx.doi.org/10.1016/j.ihj.2015.05.025mailto:[email protected]://www.sciencedirect.com/science/journal/00194832www.elsevier.com/locate/ihjhttp://dx.doi.org/10.1016/j.ihj.2015.05.025
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[(Fig._1)TD$FIG]
Fig. 1 – The 12 lead ECG taken emergency department showing ST-T
wave changes suggesting acute coronary syndrome.
i n d i a n h e a r t j o u rn a l 6 7 ( 2 0 1 5 ) 4 7 2 – 4 7 5
473
2. Case report
A 33-year-old man presented with substernal, crushing chestpain
that lasted intermittenly for 60 min. He had none of theclassical
risk factors for coronary artery disease, and didnot usealcohol,
tobacco, or cocaine. He had a history of
emergencycoronaryangiogramonemonthbeforedue tosimilar chestpain.An
electrocardiogram (ECG) revealed sinus rhythm, biphasic Twaveswith
preserved Rwaves inV1–V4 precordial leads (Fig. 1);but these
appearances were similar to those noted before hisrecent discharge
from the hospital (Fig. 2).We decided to followthe patient.
However, in the early morning hours about 5.5 hafter admission, his
severe chest pain restarted, and hisECG showed lamda-like diffuse
ST segment elevation with
[(Fig._2)TD$FIG]
Fig. 2 – The 12 lead ECG taken one month
reciprocal ST depression in aVR and V1 (Fig. 3).
Immediatelyafter starting intravenous nitroglycerine, his diffuse
'actionpotential-like' STsegmentelevationreturned tobaseline
(Fig.4),concomitant with his pain subsiding. Sincewe did not have
theprevious angiogram data; we planned to perform immediatecoronary
angiography, which showed normal coronary arteriesexcept mild
lesion at mid left anterior descending coronaryartery. The next
day, his previous coronary angiogram takenonemonth earlier revealed
that the angiographic findingsweresimilar to those noted before his
recent discharge from theoutside hospital. The clinical and ECG
pictures pointed to thediagnosis of a vasospastic-type Printzmetal
angina, and thepatient responded well to calcium blockers and
long-termnitroglycerin therapy and remained symptom-free
throughouta 6-month follow-up.
before showing ST-T wave changes.
-
[(Fig._3)TD$FIG]
Fig. 3 – The 12 lead ECG during severe chest pain shows the
diffuse ST segment elevation resembling the Greek letter
lambda,called also 'action potential-like' shape or ‘‘tomb
shape-like’’ in precordial leads.
i n d i a n h e a r t j o u r n a l 6 7 ( 2 0 1 5 ) 4 7 2 – 4 7
5474
3. Discussion
Coronary artery spasm is a hyper-contraction of coronarysmooth
muscle triggered by an increase of intracellularCa2+ in the
presence of an increased Ca2+ sensitivity.8
[(Fig._4)TD$FIG]
Fig. 4 – The 12 lead ECG immediately after starting intravenous
nreturned to baseline.
Electrocardiographically, the attacks of coronary spasm
areassociatedwith either ST segment elevation or depression,
ornegative U wave on ECG.8 Whereas the Wellens' syndrome
ischaracterized by symmetrically inverted T-waves withpreserved R
waves in the precordial leads suggestive ofimpending myocardial
infarction due to a critical proximal
itroglycerine showing the his diffuse ST segment elevation
-
i n d i a n h e a r t j o u rn a l 6 7 ( 2 0 1 5 ) 4 7 2 – 4 7 5
475
left anterior descending stenosis,9 the pseudo-Wellens'syndrome
caused by coronary artery spasm has also beenrarely reported in
literature.10–13 These T-wave changesrepresent stunning and
reperfusion of the myocardium.10–13 Complete or near-complete
occlusion of LAD causes severemyocardial ischemia and angina. When
coronary flow isrestored, reperfusion injury related repolarization
abnormal-ities will be seen in precordial leads with inverted or
biphasicT-waves. Absolute recovering of stunnedmyocardium resultsin
normalized T-waves. Not only severe stenosis, any cause ofcoronary
flow interruption, including spasm, could causecharacteristic
T-wave changes.13 Our patient had a pseudo-Wellens sign on ECG at
first admission, and a diffuse STsegment elevation on
electrocardiogram resembling theGreek letter lambda, called also
'action potential-like' shapeor ‘‘tomb shape-like’’ in precordial
leads (Fig. 3).14–16 Thisspecific ST segment elevation was
accompanied by an up-sloping ST segment depression in aVR and V 1.
ACS patientswithout culprit lesion and proof of coronary spasm have
anexcellent prognosis in terms of survival and coronary eventsafter
3 years compared with patients with obstructive ACS;however,
persistent angina represents a challenging problemin these
patients, leading in some cases to repeated
coronaryangiography.5
Conflicts of interest
The authors have none to declare.
r e f e r e n c e s
1. Lee TH, Goldman L. Evaluation of the patient with acutechest
pain. N Engl J Med. 2000;342:1187–1195.
2. Titterington JS, Hung OY, Wenger NK. Microvascular angina:an
update on diagnosis and treatment. Future
Cardiol.2015;11:229–242.
3. Kusama Y, Kodani E, Nakagomi A, et al. Variant angina
andcoronary artery spasm: the clinical spectrum,
pathophysiology, and management. J Nippon Med
Sch.2011;78:4–12.
4. Auch-Schwelk W. Coronary spasm—a clinically relevantproblem?
Herz. 1998;23:106–115.
5. Ong P, Athanasiadis A, Borgulya G, Voehringer M, SechtemU.
3-year follow-up of patients with coronary artery spasmas cause of
acute coronary syndrome: the CASPAR (coronaryartery spasm in
patients with acute coronary syndrome)study follow-up. J Am Coll
Cardiol. 2011;57:147–152.
6. Takagi Y, Takahashi J, Yasuda S, et al.
Prognosticstratification of patients with vasospastic angina:
acomprehensive clinical risk score developed by theJapanese
coronary spasm association. J Am Coll
Cardiol.2013;62:1144–1153.
7. Sechtem U, Ong P, Athanasiadis A, Vohringer M, Merher
R,Yilmaz A. Coronary vasospasm: is it a myth? Am J CardiovascDrugs.
2010;10(suppl 1):19–26.
8. Yasue H, Nakagawa H, Itoh T, Harada E, Mizuno Y.
Coronaryartery spasm—clinical features, diagnosis, pathogenesis,and
treatment. J Cardiol. 2008;51:2–17.
9. de Zwaan C, Bar FW, Wellens HJ.
Characteristicelectrocardiographic pattern indicating a critical
stenosishigh in left anterior descending coronary artery in
patientsadmitted because of impending myocardial infarction.
AmHeart J. 1982;103:730–736.
10. Dhawan SS. Pseudo-Wellens' syndrome after crack cocaineuse.
Can J Cardiol. 2008;24:404.
11. Abulaiti A, Aini R, Xu H, Song Z. A special case of
Wellens'syndrome. J Cardiovasc Dis Res. 2013;4:51–54.
12. Kukla P, Korpak-Wysocka R, Dragan J, et al.
Pseudo-Wellenssyndrome in a patient with vasospastic angina.
Kardiol Pol.2011;69:79–81. discussion 2.
13. Langston W, Pollack M. Pseudo-Wellens syndrome in acocaine
user. Am J Emerg Med. 2006;24:122–123.
14. Riera AR, Ferreira C, Schapachnik E, Sanches PC, Moffa
PJ.Brugada syndrome with atypical ECG: downsloping ST-segment
elevation in inferior leads. J Electrocardiol.2004;37:101–104.
15. Gussak I, Bjerregaard P, Kostis J.
Electrocardiographic‘‘lambda’’ wave and primary idiopathic
cardiacasystole: a new clinical syndrome? J
Electrocardiol.2004;37:105–107.
16. Kukla P, Jastrzebski M, Sacha J, Bryniarski L. Lambda-like
STsegment elevation in acute myocardial infarction - a newrisk
marker for ventricular fibrillation? Three case reports.Kardiol
Pol. 2008;66:873–877. discussion 7–8.
http://refhub.elsevier.com/S0019-4832(15)00180-7/sref1http://refhub.elsevier.com/S0019-4832(15)00180-7/sref1http://refhub.elsevier.com/S0019-4832(15)00180-7/sref2http://refhub.elsevier.com/S0019-4832(15)00180-7/sref2http://refhub.elsevier.com/S0019-4832(15)00180-7/sref2http://refhub.elsevier.com/S0019-4832(15)00180-7/sref3http://refhub.elsevier.com/S0019-4832(15)00180-7/sref3http://refhub.elsevier.com/S0019-4832(15)00180-7/sref3http://refhub.elsevier.com/S0019-4832(15)00180-7/sref3http://refhub.elsevier.com/S0019-4832(15)00180-7/sref4http://refhub.elsevier.com/S0019-4832(15)00180-7/sref4http://refhub.elsevier.com/S0019-4832(15)00180-7/sref5http://refhub.elsevier.com/S0019-4832(15)00180-7/sref5http://refhub.elsevier.com/S0019-4832(15)00180-7/sref5http://refhub.elsevier.com/S0019-4832(15)00180-7/sref5http://refhub.elsevier.com/S0019-4832(15)00180-7/sref5http://refhub.elsevier.com/S0019-4832(15)00180-7/sref6http://refhub.elsevier.com/S0019-4832(15)00180-7/sref6http://refhub.elsevier.com/S0019-4832(15)00180-7/sref6http://refhub.elsevier.com/S0019-4832(15)00180-7/sref6http://refhub.elsevier.com/S0019-4832(15)00180-7/sref6http://refhub.elsevier.com/S0019-4832(15)00180-7/sref7http://refhub.elsevier.com/S0019-4832(15)00180-7/sref7http://refhub.elsevier.com/S0019-4832(15)00180-7/sref7http://refhub.elsevier.com/S0019-4832(15)00180-7/sref8http://refhub.elsevier.com/S0019-4832(15)00180-7/sref8http://refhub.elsevier.com/S0019-4832(15)00180-7/sref8http://refhub.elsevier.com/S0019-4832(15)00180-7/sref9http://refhub.elsevier.com/S0019-4832(15)00180-7/sref9http://refhub.elsevier.com/S0019-4832(15)00180-7/sref9http://refhub.elsevier.com/S0019-4832(15)00180-7/sref9http://refhub.elsevier.com/S0019-4832(15)00180-7/sref9http://refhub.elsevier.com/S0019-4832(15)00180-7/sref10http://refhub.elsevier.com/S0019-4832(15)00180-7/sref10http://refhub.elsevier.com/S0019-4832(15)00180-7/sref11http://refhub.elsevier.com/S0019-4832(15)00180-7/sref11http://refhub.elsevier.com/S0019-4832(15)00180-7/sref12http://refhub.elsevier.com/S0019-4832(15)00180-7/sref12http://refhub.elsevier.com/S0019-4832(15)00180-7/sref12http://refhub.elsevier.com/S0019-4832(15)00180-7/sref13http://refhub.elsevier.com/S0019-4832(15)00180-7/sref13http://refhub.elsevier.com/S0019-4832(15)00180-7/sref14http://refhub.elsevier.com/S0019-4832(15)00180-7/sref14http://refhub.elsevier.com/S0019-4832(15)00180-7/sref14http://refhub.elsevier.com/S0019-4832(15)00180-7/sref14http://refhub.elsevier.com/S0019-4832(15)00180-7/sref15http://refhub.elsevier.com/S0019-4832(15)00180-7/sref15http://refhub.elsevier.com/S0019-4832(15)00180-7/sref15http://refhub.elsevier.com/S0019-4832(15)00180-7/sref15http://refhub.elsevier.com/S0019-4832(15)00180-7/sref16http://refhub.elsevier.com/S0019-4832(15)00180-7/sref16http://refhub.elsevier.com/S0019-4832(15)00180-7/sref16http://refhub.elsevier.com/S0019-4832(15)00180-7/sref16
`Action potential-like' ST elevation following pseudo-Wellens'
electrocardiogram1 Introduction2 Case report3 DiscussionConflicts
of interestReferences