Abstract
The “modern” era of the treatment of ventricular tachyarrhythmias with device-based therapy may have begun in 1899, when Prevost and Battelli noted, almost as an afterthought, that direct current shock could terminate ventricular fibrillation (VF) in dogs.1 Three decades later, pioneering work in the field of defibrillation concluded that the passage of electrical current across the heart can both initiate and terminate VF.2,3 Still, little attention was paid to this phenomenon, as evidenced by Paul Dudley White’s Heart Disease , which devoted less than half a page to VF and characterized the arrhythmia as “a condition of little importance so far as we know now.”4 In 1947, the thoracic surgeon Claude Beck saved the first human life by the successful use of cardiac defibrillation in a 14-year-old boy who developed VF during a thoracic surgical procedure and went on to achieve a full recovery.5 These early accomplishments provided the foundation for the landmark work of Mirowski and Mower that ultimately led to the development of the implantable cardioverter-defibrillator (ICD) and its introduction in humans in 1980.6 Pacing may prevent sudden cardiac death due to bradyarrhythmias and in certain circumstances such as torsade de pointes associated with congenital long-QT syndrome (LQTS) and pause-dependent ventricular tachycardia (VT). Although no controlled studies exist, retrospective analyses suggest that recurrent torsade de pointes in patients with LQTS may be prevented by continuous pacing.7 Early clinical data on small numbers of patients suggested that the combination of β-adrenergic blockade plus continuous pacing reduced the number of syncopal events and the anticipated rate of sudden death in high-risk LQTS patients.8 The beneficial effects of pacing may be limited to patients with LQT2 and LQT3, in which the transmural dispersion of repolarization worsens steeply during bradycardia.9 Genotype-phenotype correlation confirms that …
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