The Natural History of Untreated Monomorphic Ventricular Tachycardia

DOI: 10.19102/icrm.2012.030309

DAVID F. KATZ, MD, DUY T. NGUYEN, MD and WILLIAM H. SAUER, MD

Section of Cardiac Electrophysiology, University of Colorado, Aurora, CO

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KEYWORDS. ventricular assist device, ventricular fibrillation, ventricular tachycardia.

The authors report no conflicts of interest for the published content.
Manuscript received January 20, 2012, final version accepted February 7, 2012.
Address correspondence to: David Katz, MD, Section of Cardiac Electrophysiology, University of Colorado, 12401 East 17th Avenue, B136, Aurora, CO 80045. E-mail: David.Katz@ucdenver.edu

A 53-year-old man with recent myocardial infarction and refractory cardiogenic shock underwent placement of temporary right and left non-pulsatile ventricular assist devices (VADs) (Thoratec CentriMag, Thoratec Corporation, Pleasanton, CA). While in the surgical intensive care unit he was noted to have the arrhythmia shown above. While the patient was previously in sinus rhythm with ectopy, the arterial-line tracing demonstrated pulsatile flow with every fourth ventricular depolarization. A single ventricular ectopic beat resulted in 5 beats of polymorphic ventricular tachycardia (VT) which organized into monomorphic VT. After 2 min the monomorphic VT degenerated into coarse polymorphic VT and then to ventricular fibrillation (VF). During VT and VF, all pulsatile flow was lost, but the patient’s mean arterial pressure was unchanged. He remained awake and alert throughout. Sedation was administered and the patient was electively cardioverted with a single 200-J biphasic external shock. Patients with VADs have previously been reported to demonstrate hemodynamic tolerance of ventricular arrhythmias.¹ Here we demonstrate the natural progression of monomorphic VT to fine VF. The relatively slow progression from monomorphic VT to fine VF observed in this patient may be due to a delay in the development of ventricular ischemia as a result of the hemodynamic support provided by the VADs. Thankfully this sequence, described previously in ischemic dog hearts,² is rarely seen in the era of prompt defibrillation of hospitalized patients.

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