Woman With Persistent ECG Abnormalities After Chest Pain Resolves

December 31, 2006

A56-year-old woman with chest pain and emesis is brought to the hospitalby ambulance. En route, the pain resolves after nitrates, morphine,and aspirin are administered.

A 56-year-old woman with chest pain and emesis is brought to the hospital by ambulance. En route, the pain resolves after nitrates, morphine, and aspirin are administered.Results of a physical examination are normal. A 12-lead ECG is obtained; the tracing is shown here.Serum markers are measured every 4 hours; all levels are normal.Although the patient remains pain-free, the findings on a second ECG are unchanged. A nuclear cardiac stress imaging study is ordered.Which of the following best explains the ECG findings?A. Acute pulmonary embolism.
B. Wellens syndrome.
C. Persistent juvenile T-wave pattern.
D. Left ventricular hypertrophy.
E. Subarachnoid hemorrhage.

The ECG shows invertedT waves in leads V2 through V6 butnormal ST segments (Figure 1).T waves are deeply inverted in V3through V5. In a pain-free patientwho has normal serum marker levels,these findings suggest Wellenssyndrome (B), in which the T-wavechanges in the precordium are associatedwith critical, proximal leftanterior descending (LAD) arterystenosis.1 The syndrome is also referredto as "LAD coronary T-wavesyndrome."Wellens and colleagues1 firstdescribed this syndrome in a subgroupof patients hospitalized forunstable angina who were at highrisk for anterior wall myocardial infarction(MI). A prominent, commonfeature in these patients wasthe pattern of ECG changes thatinvolved the T wave, with occasionalabnormality of the ST segment.There were 2 basic patterns ofECG changes:

  • An isoelectric or minimally elevatedST segment leading into a symmetric,deeply inverted T wave(Figures 1 and 2).2
  • Biphasic T waves (Figure 3).3

Approximately 20% of patientsin the initial study demonstratedthese ECG patterns.


Moreover, allof the patients with these ECGchanges had significant disease ofthe proximal LAD artery. Seventyfivepercent of these patients did notundergo coronary revascularization,and extensive anterior wall infarctiondeveloped in these patientswithin a few weeks after admission.


In a second, prospective investigation,Wellens and colleagues


found that approximately 15% of patientswith unstable angina presentedwith these characteristic ECGchanges. In all patients in whomsuch changes were evident, urgentcoronary angiography demonstratedsignificant LAD artery obstruction.

Features of Wellens syndrome.

The criteria for Wellens syndromeinclude T-wave changes plus a historyof ischemic chest pain withoutserum marker abnormalities


These criteria essentially describea pain-free patient with continuedECG abnormalities who has nothad an acute MI. Additional featuresof the syndrome may include:

  • T-wave abnormalities (deeplyinverted or biphasic T waves) inthe right to mid precordial leads.
  • Minimal or no ST-segmentelevation.
  • Normal precordial R-waveprogression.
  • Absence of Q waves.

The T-wave abnormalities arevery apparent on the ECG and are akey feature of this ECG syndrome.The T-wave changes may have 1 of2 patterns:

  • T waves are deeply inverted andsymmetric in contour. As the STsegment terminates, the T wave assumesa very negative angle relativeto the isoelectric baseline; this anglemay approach 90 degrees (see Figures1 and 2). This is the morecommon of the 2 patterns and isseen in approximately 75% of affectedpatients.
  • T waves are biphasic (see Figure3). This is the less common variant,seen in 25% of patients with Wellenssyndrome.1,2

The T-wave changes are presentin leads V2 and V3; in certaincases, the changes may also involveleads V1 and V4. T-wave abnormalitiesmay persist for hours to weeksdespite the resolution of chest discomfort.In the second study byWellens and associates


, 60% of patientsin whom the syndrome wasdiagnosed demonstrated the characteristicECG changes on admission.After admission, the classic ECG abnormalitiesdeveloped in a majorityof the remaining patients.Neither significant ST-segmentelevation nor Q waves are evident onthe ECGs of patients with Wellenssyndrome. The ST segment itself isoften normal (ie, isoelectric). If theST segment is abnormal, it is minimallyelevated-usually less than1 mm, with a high take-off from theQRS complex (see

Figure 3

). ElevatedST segments are usually eitherconvex or obliquely straight; however,concave morphologies are alsoseen.


Differential diagnosis of invertedT waves.

Interpreting theECG in the context of the clinicalpresentation can help the cliniciandistinguish between Wellens syndromeand a number of other causesof T-wave inversions. In thiswoman, acute pulmonary embolism
(A) can be ruled out because of thelack of dyspnea and tachycardia;cerebrovascular accident(B), because of the lack of headache andfocal neurologic issues; and a persistentjuvenile pattern(C), becauseof her age. Left ventricular hypertrophy(LVH) (D) can be excluded becauseof the absence of prominentQRS complexes consistent with LVHon this patient's ECG.Other entities in the electrocardiographicdifferential diagnosisof inverted T waves are listed in

Table 2.

Of these, acute myocarditisand pericarditis can often be distinguishedfrom Wellens syndrome onthe basis of the clinical picture. Inacute myocarditis, acute congestiveheart failure is normally present.In pericarditis, the typical chest painpattern is different from that seen inWellens syndrome. Wolff-Parkinson-White (WPW) syndrome and bundle-branch block (BBB) can usuallybe differentiated from Wellens syndromebased on the presence of additionalECG abnormalities not usuallyseen in the latter entity (deltawaves and widened QRS complexesin WPW syndrome and an abnormalQRS morphology and width inBBB)Past MI cannot be distinguishedfrom Wellens syndrome onthe basis of either clinical informationor electrocardiographic features.In patients in whom Wellenssyndrome is a possible diagnosis,past MI should be considered aswell. Always keep in mind, however,that this ECG pattern, with T-waveabnormalities in the right to midprecordial leads, is strongly associatedwith proximal LAD artery obstructionand anterior wall MI.

Significance of Wellens syndrome.

The importance of this syndromelies in its clinical presentationand natural history. Patients havehad recent chest discomfort but appearwell; ECG abnormalities continueafter the pain resolves. The naturalhistory is essentially anteriorwall infarction with associated morbidityand mortality.The ECG findings that characterizeWellens syndrome may bethe only indication of an impendingextensive anterior wall acute MI inan otherwise asymptomatic patient.Thus, it is vital to recognize thesechanges and to be aware of theirassociation with critical LAD arteryobstruction and significant, shorttermrisk of anterior wall MI.Stress imaging may not be themost appropriate testing modality inpatients with Wellens syndrome;such testing may precipitate anacute MI. Definitive management ofthe stenosis (through eithercatheter-based or surgical therapy)leads to resolution of the ECGchanges.

Outcome of this case.

After acardiology consultation, the diagnosticplan was altered. Cardiac catheterizationrevealed a near-total occlusionof the LAD artery. Angioplastywith stent placement was performedsuccessfully. The patient was dischargedwithout incident, and 1 yearlater she remains in good health.




de Zwaan C, Bar FW, Wellens HJ. Characteristicelectrocardiographic pattern indicating a criticalstenosis high in left anterior descending coronary arteryin patients admitted because of impending myocardialinfarction. Am Heart J. 1982;103:730-736.


de Zwaan C, Bar FW, Janssen JH, et al. Angiographicand clinical characteristics of patients withunstable angina showing an ECG pattern indicatingcritical narrowing of the proximal LAD coronaryartery. Am Heart J. 1989;117:657-665.


Tandy TK, Bottomy DP, Lewis JG. Wellens’ syndrome.Ann Emerg Med. 1999;33:347-351.