Elsevier

Heart Rhythm

Volume 8, Issue 4, April 2011, Pages 555-561
Heart Rhythm

Clinical
General
Acquired long QT syndrome from stress cardiomyopathy is associated with ventricular arrhythmias and torsades de pointes

https://doi.org/10.1016/j.hrthm.2010.12.012Get rights and content

Background

Stress cardiomyopathy (SCM) is a syndrome of transient ventricular dysfunction triggered by severe emotional or physical stress, likely resulting from catecholamine-mediated myocardial toxicity. Repolarization abnormalities associated with other hyperadrenergic states can cause QT prolongation and lethal arrhythmia including torsades de pointes (TdP). Despite the development of repolarization abnormalities and QT prolongation in SCM, little is known about the risk of ventricular fibrillation (VF) and TdP.

Objective

The aim of this study was to assess the prevalence and clinical predictors of ventricular arrhythmias in a cohort of patients with SCM.

Methods

Data from a registry of consecutive patients with SCM from 2 institutions were reviewed. Patients who developed VF or TdP were identified. Clinical characteristics and outcomes were analyzed and compared with a control group of patients with SCM without VF/TdP.

Results

Of 93 patients with SCM, 8 (8.6%) experienced VF/TdP. Of these 8 patients, 2 presented with VF and were subsequently diagnosed with SCM. Six other patients experienced pause-dependent TdP or VF after SCM diagnosis in the setting of substantial QT prolongation. Prolongation of the corrected QT interval (QTc) was significantly associated with the occurrence of ventricular arrhythmia (odds ratio 1.28 for each 10 ms increase in QTc, 95% confidence interval 1.10 to 1.50).

Conclusion

SCM can be associated with life-threatening ventricular arrhythmia in over 8% of cases. SCM should be recognized among the causes of acquired long QT syndrome and can be associated with a risk of TdP.

Introduction

Stress cardiomyopathy (SCM) is a recently recognized syndrome characterized by transient ventricular dysfunction in the absence of obstructive coronary artery disease.1, 2, 3, 4 Also known as transient apical ballooning or Takotsubo syndrome, SCM most commonly occurs in the setting of severe emotional or physical stress. The exact mechanism of the transient cardiomyopathy remains unclear; however, it is believed that ventricular dysfunction results from catecholamine-mediated myocardial toxicity.5, 6, 7

The clinical profile of SCM has been described in several case series.1, 2, 3, 4, 8 On presentation, electrocardiographic changes resemble those seen in acute coronary syndromes, including ST-segment elevation. Within 24 to 48 hours from presentation, most patients with typical left ventricular apical involvement develop repolarization abnormalities, including diffuse T-wave inversions and QT prolongation, the latter often being quite pronounced.9 It is becoming evident that SCM should be considered among the causes of acquired long QT syndrome (LQTS).10, 11 LQTS is associated with sudden cardiac death (SCD) as a result of the distinctive reentrant polymorphic ventricular tachyarrhythmia, torsades de pointes (TdP), which can degenerate into ventricular fibrillation (VF).12, 13 VF has been previously described in the clinical presentation of SCM.7, 14 More recently, several case reports of TdP in the setting of SCM have been reported.11 However, despite the severe repolarization abnormalities seen in SCM, the mechanism of life-threatening arrhythmias remains incompletely understood, and the risk remains uncertain.

The purpose of this study was to determine the prevalence of malignant ventricular tachyarrhythmias and their association with QT prolongation in patients with SCM.

Section snippets

Methods

Between December 2001 and April 2008, consecutive SCM patients from 2 institutions in Massachusetts were registered in a database. A diagnosis of SCM was made on the basis of characteristic patterns of left ventricular dysfunction.15 Clinical characteristics supporting the diagnosis of SCM included the presence of a stressful physical or emotional trigger, mild elevations in cardiac troponin, absence of obstructive coronary disease by angiography, and the evolution of new characteristic

Patient characteristics

During the study period, a total of 93 patients were diagnosed with SCM. Eighty of the patients were female (86%), and the median age was 67 (range 55 to 78) years. The left ventricular ejection fraction (LVEF) at diagnosis was 28% (range 20% to 35%). The first measured QTc after diagnosis was 464 (range 436 to 503) ms and the peak QTc throughout the hospital course was 499 (range 470 to 534) ms (Table 1).

Of the 93 total patients, 8 (8.6%) had VF/TdP, whereas 85 patients did not show

Discussion

In this large series of consecutive patients diagnosed with SCM, we observed an 8.6% prevalence of life-threatening ventricular arrhythmias. The SCM patients with ventricular arrhythmias had a longer QTc on admission, and the QT prolongation was more severe during the early hospital course. The peak QTc was significantly associated with the occurrence of ventricular arrhythmias.

Six of the 8 patients (patients 3 to 8) developed VF and TdP in the setting of substantial QT prolongation. The

Conclusion

Ventricular arrhythmias can be seen in over 8% of patients with SCM. The underlying pathophysiology of ventricular arrhythmias on presentation with SCM is likely different than during the subacute phase, in which pause-dependent TdP can occur in the setting of severe QT prolongation. SCM should be considered among the causes of acquired LQTS. SCM patients in whom QT prolongation is observed should be monitored in a cardiac unit until shortening of the QT interval is documented.

References (30)

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  • QT Prolongation and In-Hospital Ventricular Arrhythmic Complications in Patients With Apical Ballooning Takotsubo Syndrome

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    In a retrospective cohort of 93 individuals with Takotsubo syndrome, Madias et al16 reported an incidence of ventricular tachycardia or fibrillation of approximately 10%. All patients with arrhythmia had some degree of QT prolongation, leading to a significant increase in the odds ratio for ventricular arrhythmia of 1.28 per each 10 ms increase in corrected QT.16 Similarly, in another retrospective study including 105 individuals, corrected QT prolongation was shown to reliably predict adverse events in hospital outcomes, including cardiogenic shock and in-hospital mortality.22

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