Asian Cardiovasc Thorac Ann 2003;11:263-265
© 2003 Asia Publishing EXchange Ltd
Early Repolarization Pattern Occurring With the Wolff-Parkinson-White Syndrome
Kian Keong Poh, MRCP,
Adrian Low, MRCP,
Huay Cheem Tan, MRCP,
Boon Lock Chia, FRACP
Cardiac Department, National University Hospital Singapore, Republic of Singapore
For reprint information contact: Boon Lock Chia, FRACP Tel: 65 6772 5211 Fax: 65 6872 2998 email: mdccbl{at}nus.edu.sg Cardiac Department, National University Hospital, Lower Kent Ridge Road, Singapore 119074, Republic of Singapore.
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ABSTRACT
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A 35-year-old male presented with the combined ECG abnormality of the early repolarization pattern and the Wolff-Parkinson-White syndrome. This has not been previously reported.
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INTRODUCTION
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The early repolarization electrocardiographic pattern is a normal variant occurring in young, healthy individuals. In most cases, ST-segment elevation is seen in the precordial leads, V3 to V6.1,2 To the best of our knowledge, the coexistence of the early repolarization pattern with the Wolff-Parkinson-White (WPW) syndrome has not been described in the literature as yet.
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CASE REPORT
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A 35-year-old Chinese male presented with a food allergy. An examination of his cardiovascular system showed no abnormalities and the blood pressure was 120/80 mm Hg. The results of routine haematological and biochemistry investigations were also normal and a chest x-ray showed no abnormalities. However, the 12-lead electrocardiogram (ECG) showed the presence of the WPW syndrome as well as an early repolarization pattern. Two-dimensional and Doppler echocardiography were both normal. A treadmill exercise stress test was subsequently performed (Figures 1
and 2).
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Figure 1. Resting 12-lead ECG recorded before commencement of the exercise stress test. Note: (i) WPW syndrome as reflected by a short P-R interval of about 0.08 seconds and delta waves in leads V2 to V6, I, II, III and aVF and (ii) ST segment elevation, tall T-waves and notching of the downstroke of the R-wave or J point in leads V2 to V6, II, III and aVF reflecting early repolarization pattern (see text).
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Figure 2. ECG recorded during Stage III of the Bruce exercise stress test protocol. Note: (i) sinus tachycardia (166/minute). The WPW syndrome is still present and (ii) upward-sloping ST-segment depression in leads V3 to V6, II, III and aVF (see text).
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ELECTROCARDIOGRAPHIC ANALYSIS
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Figure 1
shows the resting 12-lead ECG recorded before the commencement of the exercise stress test. The WPW syndrome is observed as a short P-R interval (about 0.08 seconds) and delta waves, which are seen in leads V2 to V6, I, II, III and aVF. In addition, there is a ST-segment elevation (1–3 mm), tall T-waves and notching of either the downstroke of the R-wave or the J point in leads V2 to V6, II, III and aVF. All of these reflect the early repolarization pattern. Figure 2 was recorded during peak exercise at Stage III of the Bruce protocol. It shows sinus tachycardia (166/minute). The WPW syndrome, however, is not as marked as in Figure 1. An upward-sloping ST-segment depression of approximately 2–3 mm is seen in leads V3 to V6, II, III and aVF. Figure 3, recorded about 6 months later, shows the early repolarization pattern as reflected by ST-segment elevation and notching of the downstroke of the R-wave or the J point in leads V3 to V6. However, the WPW syndrome is absent in this ECG.
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Figure 3. 12-lead ECG which was recorded 6 months later. Note that the WPW syndrome is now absent. However, the ECG still shows the early repolarization pattern as reflected by ST-segment elevation, tall T-waves and notching of either the downstroke of the R-wave or the J point in leads V3 to V6 (see text).
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DISCUSSION
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The early repolarization ECG pattern is a normal variant seen mainly in healthy young individuals. The characteristic features are a raised ST-segment that concaves upwards, merging with tall T-waves, tall R-waves and, prominent notching of either the downstroke of the R-wave or the J point. All the ECG changes are seen predominantly in the precordial leads V3 to V6. Reciprocal ST-segment depression is absent.1,2,3 Because of the elevated ST-segment and tall T-waves, the ECG pattern may be misdiagnosed as acute pericarditis or ST-elevation myocardial infarction (MI).1,2
The ECG pattern of the WPW syndrome has been well described in the literature. It manifests as a short P-R interval (< 0.12 seconds), a delta wave, and a broad QRS complex. In addition, prominent Q-waves may be seen in either the limb leads or the praecordial leads and therefore frequently misdiagnosed as MI. Tall R-waves are also common, occurring in the left praecordial leads when the accessory pathway is right-sided, and the right praecordial leads when the accessory pathway is left-sided. These tall R-waves often result in a wrong diagnosis of either left, or right, ventricular hypertrophy. 4
ST-segment and T-wave changes are frequently present in the WPW syndrome and have been attributed to the abnormal intra-ventricular conduction seen in this condition. The secondary ST-segment/T-wave changes usually manifest as ST-segment depression and, T-wave inversion in the leads where the QRS complex is dominantly positive.1,5,6 Primary ST-segment changes have also been described in the WPW syndrome. Here, the ST shift is in the same direction as the QRS complex resulting in ST-segment elevation in the leads where the QRS complexes are upright. Unlike secondary ST-segment changes, primary ST-segment changes manifesting as ST-segment elevation in the WPW pattern are usually considered to be abnormal, such as in patients with acute myocardial infarction.7
Guler et al recently described a patient who was successfully resuscitated from ventricular fibrillation and whose initial ECG showed ST-segment elevation in leads V1 to V6 suggesting an acute anterior myocardial infarction.8 On the fourth day, the ECG showed WPW syndrome but no ST-segment elevation. Myocardial infarction was excluded from the diagnosis after performing biochemical tests, echocardiography and coronary angiography.
To the best of our knowledge, the simultaneous occurrence of the early repolarization pattern and the WPW syndrome has not been previously reported. In our patient, the early repolarization pattern occurred in the presence as well as in the absence of the WPW syndrome (Figures 1 and 3). The absence of chest pain during the exercise stress test and the very low pre-test likelihood of coronary artery disease suggests that, the ST-segment depression, seen at peak exercise, represents a false positive result. This phenomenon has been well described in patients presenting with the WPW syndrome.1,2
This case illustrates that primary ST-elevation in patients presenting with the WPW pattern is not always due to a pathological aetiology and may occasionally be due to a normal variant. This knowledge is clinically important in this current era of reperfusion therapy, because a misdiagnosis of acute MI in this situation may result in incorrect treatment involving thrombolytic therapy.
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REFERENCES
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- Schamroth L. The 12 Lead Electrocardiogram. Oxford: Blackwell Scientific Publications 1989;1:145–223.
- Goldberger AL. Myocardial Infarction. St Louis: The C.V. Mosby Co 1984;177–179.
- Mehta M, Jain A, Mehta A. Early repolarization. Clin Cardio 1999;22:59–65.
- Khan IA, Shaw IS. Pseudo ventricular hypertrophy and pseudo myocardial infarction in Wolff-Parkinson-White syndrome. Am J Emerg Med. 2000;18:807–9.[Medline]
- Goldberger AL. Pseudo-infarct patterns in the Wolff-Parkinson-White syndrome: importance of Q wave-T wave vector discordance. J Electrocardiol. 1980;13:115–8.[Medline]
- Wang K, Asinger R, Hodges M. Electrocardiograms of Wolff-Parkinson-White syndrome simulating other conditions. Am Heart J 1996;132:152–5.[Medline]
- Brackbill T A, Dove J T, Murphy G W, Barold S. The diagnosis of myocardial infarction in the Wolff-Parkinson-White syndrome. Chest 1974;65:493–9.[Abstract/Free Full Text]
- Guler N, Eryonucu B, Bilge M, Erkoc R, Turkoglu C. Wolff-Parkinson-White syndrome mimicking acute anterior myocardial infarction in a young male patient – a case report. Angiology 2001;52:293–5.
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ABSTRACT
Introduction
