Elsevier

Heart Rhythm

Volume 8, Issue 10, October 2011, Pages 1629-1634
Heart Rhythm

Regular issue
Clinical: Imaging/mapping
Myocardial edema underlies dynamic T-wave inversion (Wellens' ECG pattern) in patients with reversible left ventricular dysfunction

https://doi.org/10.1016/j.hrthm.2011.04.035Get rights and content

Background

The Wellens' electrocardiogram (ECG) pattern of dynamic T-wave inversion in the anterior leads is observed in clinical conditions characterized by reversible left ventricular (LV) dysfunction (stunned myocardium), either ischemic or nonischemic. The pathophysiologic basis of this ECG pattern remains to be elucidated.

Objective

The purpose of this study was to report the contrast-enhanced cardiac magnetic resonance (CE-CMR) findings in 4 cases of Wellens' ECG pattern associated with transient LV dysfunction from a variety of clinical conditions such as myocardial bridge, coronary artery dissection, cholecystitis, and takotsubo syndrome.

Methods

All patients underwent CE-CMR at the time of acute clinical manifestations and after 6 to 8 weeks of follow-up to assess the presence and dynamics of LV myocardial changes.

Results

In all patients, the Wellens' ECG abnormalities were associated with increased signal intensity of the LV myocardium on T2-weighted sequences suggesting myocardial edema, in the absence of late enhancement on postcontrast sequences. Repolarization abnormalities and myocardial edema had a parallel time course with persistence beyond recovery of mechanical abnormalities. T-wave inversion was associated with transient prolongation of the QTc interval in all cases.

Conclusion

The study results suggest that myocardial edema rather than systolic dysfunction underlies the Wellens' ECG pattern, regardless of the causative mechanism.

Introduction

Wellens' syndrome is characterized by dynamic symmetric T-wave inversion in the precordial leads and QTc prolongation (Wellens' electrocardiogram [ECG] pattern) in the setting of acute coronary syndrome caused by atherosclerotic subocclusion of the left anterior descending coronary artery (LAD). This clinical scenario was regarded as unfavorable in the prerevascularization era due to the high incidence of recurrent ischemic symptoms and impending myocardial infarction.1 In the modern era, the development of transient, prominent inverted T-waves in the precordial leads after an acute coronary event has been interpreted as an ECG marker of ischemia-induced, reversible myocardial dysfunction.2, 3, 4, 5, 6 Moreover, the Wellens' ECG pattern has been recently described in other conditions unrelated to atherosclerotic disease of the LAD, such as takotsubo syndrome, LAD vasospasm, and intracranial bleedings.7, 8, 9 The pathophysiological basis of this ECG pattern remains to be elucidated. Contrast-enhanced cardiac magnetic resonance (CE-CMR) has recently emerged as a powerful tool that can noninvasively identify irreversible myocardial injury by late gadolinium enhancement (LGE) and myocardial inflammation by the presence of edema on T2-weighted images.10, 11, 12, 13, 14 We report 4 cases whose common denominator was the ECG pattern of dynamic deep anterior T-wave inversion and QT interval prolongation (Wellens' pattern) associated with negligible troponin I (TnI) release and transient left ventricular (LV) dysfunction. Coronary angiography showed that this clinical syndrome was caused by a variety of conditions other than the atherosclerotic LAD subocclusion originally reported by Wellens.1 All patients underwent CE-CMR at the time of acute clinical manifestations and after 6 to 8 weeks of follow-up to assess the presence and dynamics of ventricular myocardial changes.

Cardiac magnetic resonance was performed using a 1.5-Tesla scanner (Magnetom Avanto, Siemens Medical Solutions, Erlangen, Germany). Ventricular function was assessed by cine images that were acquired using true fast imaging with steady-state precession sequence (true FISP) cine loops in sequential short-axis and transverse long-axis views. Visualization of myocardial edema was performed using T2-weighted short tau-inversion recovery sequences. On T2-weighted images, myocardial edema was considered present when the signal intensity of the myocardium was >2 SD of the mean signal intensity of the remote region or pectoral muscle.15 After intravenous administration of contrast agent (gadobenate dimeglumine, Multihance, Bracco, 0.2 mmol/kg of body weight), 2-dimensional segmented fast low-angle shot inversion recovery sequences were acquired after at least 10 minutes in the same views of cine images. Late gadolinium enhancement was considered present when the signal intensity of hyperenhanced myocardium was >5 SD above the mean signal intensity of remote myocardium.16

Section snippets

Patient 1

A 78-year-old man was admitted for acute chest pain. The ECG on admission showed ST-segment elevation in V1-V5 leads. Repeated ECGs during the subsequent days revealed deep T-wave inversion in L1, L2, L3, aVF, and from V1 to V6 leads, in association with QTc prolongation (QTc = 510 ms) (Figure 1A). On cardiac catheterization, myocardial bridge of the second tract of LAD (Figures 2A and 2B) and apical hypokinesia with normal ejection fraction of the LV were observed. Two days after admission,

Patient 2

An 86-year-old woman was admitted for acute chest pain with evidence of ST-segment elevation in V2-V3 leads. Cardiac catheterization with coronary angiography demonstrated apical LV akinesia and subocclusion of the LAD due to spontaneous dissection (Figure 2C), subsequently confirmed by coronary computed tomography (Figure 2D). The coronary dissection was successfully treated with percutaneous coronary angioplasty and stent implantation. Afterward, T-wave inversion in L1, L2, L3, aVF, and V2 to

Patient 3

An 81-year-old woman was admitted for acute cholecystitis. The ECG on admission showed T-wave inversion in L1, L2, L3, aVL, aVF, and V2 to V6 leads, associated with QTc prolongation (QTc = 560 ms). (Figure 1C). A mild TnI increase was observed (2.01 μg/l). Cardiac catheterization with coronary angiography revealed mild LV systolic dysfunction (left ventricular ejection fraction [LVEF] = 52%) with midseptal and apical hypokinesia, in the absence of coronary artery disease. A CE-CMR performed 2

Patient 4

A 62-year-old woman was admitted for acute chest pain associated with diaphoresis after an emotional stress. The ECG showed ST-segment elevation in V1-V6 leads. Emergent cardiac catheterization showed apical and midwall akinesia, with basal hyperkinesia and moderate LV systolic dysfunction (LVEF 45%), in the absence of coronary artery disease. A diagnosis of takotsubo syndrome was made. Over the following days, diffuse T-wave inversion with QTc prolongation (QTc = 580 ms) was observed (Figure 1

Discussion

According to its original description, the Wellens' syndrome is characterized by: (1) a 12-lead ECG pattern of dynamic deep T-wave inversion usually localized in the anteroseptal leads, but occasionally extending to inferolateral leads (Wellens' ECG pattern) and (2) a subocclusion of LAD.1 Although the Wellens' ECG pattern was originally related to atherosclerotic subocclusion of the LAD, it was subsequently observed in other conditions characterized by a reversible LV dysfunction (stunned

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