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Polymorphic VT, Ischemic VF, and Torsade de Pointes
Quick Takes
- Different forms of polymorphic VT respond to different therapies.
- This paper reports ECG characteristics to consider when diagnosing torsade de pointes.
Study Questions:
Can different forms of polymorphic ventricular tachycardia (VT), which respond to different forms of therapy, be distinguished by their electrocardiographic (ECG) characteristics?
Methods:
The study group included 190 total patients out of which 84 patients had coronary artery disease and spontaneous polymorphic VT triggered by short coupled extrasystoles in the absence of myocardial ischemia: 32 of these patients were considered “pseudo torsade de pointes” (TdP) by virtue of polymorphic VT triggered by ectopic beats with short coupling interval in the context of a long QT interval (≥450 ms males, ≥460 ms females). Comparative groups were 50 patients who had ventricular fibrillation (VF) during acute myocardial infarction (“ischemic VF”, negative control) and 53 patients with drug-induced TdP (“true TdP”, positive control).
Results:
The true TdP group had the longest QTc (QTc 564.6 ± 75.6 ms) followed by the pseudo-TdP group (QTc 491.4 ± 25.2 ms) and the polymorphic VT with normal QT patients (447.3 ± 55.6 ms). Moreover, the coupling interval of the ectopic beat triggering the arrhythmia was significantly longer for the true TdP group (581.2 ± 95.3 ms) compared to the pseudo-TdP (359.1 ± 38.1 ms) and polymorphic VT with normal QT groups (356.6 ± 39.4 ms).
Conclusions:
The coupling interval of ectopy in true TdP is longer than other forms of polymorphic VT, a trait that can be used when diagnosing TdP.
Perspective:
Polymorphic VT in the context of a prolonged QT interval is usually suggestive of TdP; this study nicely highlights that not all long QT intervals and not all polymorphic VT are the same. In this study, the coupling interval, reflecting the timing of the beat initiating the VT, distinguished pseudo from true TdP, with 400 ms as a discriminating interval. Distinguishing between the two impacts the use of quinidine, shown to be effective therapy for pseudo-TdP but potentially dangerous in those with long QT. One limitation of the study is the lack of a standard definition of pseudo-TdP. Also, the ECG findings described cannot be applied to inherited long QT patients as only one was included in the study.
Clinical Topics: Arrhythmias and Clinical EP, Cardiovascular Care Team, Congenital Heart Disease and Pediatric Cardiology, Atherosclerotic Disease (CAD/PAD), Implantable Devices, EP Basic Science, Genetic Arrhythmic Conditions, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Congenital Heart Disease, CHD and Pediatrics and Arrhythmias, Novel Agents, Statins
Keywords: Arrhythmias, Cardiac, Cardiac Complexes, Premature, Coronary Artery Disease, Electrocardiography, Ischemia, Long QT Syndrome, Myocardial Infarction, Quinidine, Tachycardia, Ventricular, Torsades de Pointes, Ventricular Fibrillation
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