ClinicalGeneralAcquired long QT syndrome from stress cardiomyopathy is associated with ventricular arrhythmias and torsades de pointes
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.
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