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Patients who have pulmonary disorders, especially those with chronic obstructive pulmonary disease, often have atrial and ventricular arrhythmias. However, the pathogenesis of these arrhythmias is complex and may involve many factors. For example, these individuals often have anatomic cardiac abnormalities, such as right ventricular hypertrophy, with or without associated congestive heart failure. Cigarette smoking is protean in patients with chronic obstructive pulmonary disease, and, consequently, atherosclerotic heart disease may be present with its attendant complications. Hypoxia and hypercapnia occur in these patients and, under appropriate circumstances, can be arrhythmogenic. Patients may receive drugs that can cause arrhythmias. For example, diuretics may lead to hypokalemia, and aminophylline and adrenergic bronchodilator drugs may create the environment necessary for arrhythmias to emerge. Finally, patients with pulmonary disease are prone to any arrhythmias that occur in other people, for example, atrioventricular nodal reentry and Wolff-Parkinson-White reentry.

Patients with preexcitation syndromes may exhibit a variety of tachyarrhythmias [1]. The accessory pathway(s) associated with a particular preexcitation syndrome may be used as part of an atrioventricular (AV) reentrant tachycardia circuit (i.e., orthodromic or antidromic reciprocating tachycardia), or in certain arrhythmias such as atrial fibrillation the accessory pathway may not be needed to sustain tachycardia but is utilized to conduct impulses to the ventricle. Patients with preexcitation syndrome also may have tachycardias that do not involve conduction over the accessory pathway, such as ventricular tachycardia [2].

Transthoracic shocks using relatively low energy, for example, less than 40 joules, often can terminate organized sustained ventricular tachycardia. However, transthoracic shocks with these energy levels are painful and not tolerated by the awake patient. Previous investigations by Mirowski et al (1) demonstrated that ventricular fibrillation could be terminated in humans with an implantable defibrillator. We hypothesized that shocks applied directly to the myocardium via a catheter electrode might terminate sustained ventricular tachycardia with even lower energy levels than those used transthoracically or those necessary for internal defibrillation. These well-tolerated shocks would enable cardioversion in the awake alert patient. This report details the development of such a system.

Since the advent of catheter approaches to record His bundle activation, the use of such studies in patients who have ventricular tachycardia has been expanded to diagnose the arrhythmia, to evaluate its mechanism and response to treatment, and even to identify patients prone to developing ventricular tachycardia. Although the diagnosis of ventricular tachycardia often can be made from careful examination of the scalar ECG recorded during the arrhythmia, supraventricular tachycardia with aberrant conduction, especially left bundle branch aberrancy, as well as unusual forms of atrioventricular (AV) reentry utilizing one or more accessory pathways, may mimic ventricular tachycardia. In these circumstances, His bundle electrocardiography is very useful to differentiate ventricular from supraventricular tachycardia.

Many patients who survive the acute phase of a myocardial infarction are at risk of sudden cardiac death after hospital discharge, often in the first six months after leaving the hospital. Some factors that indicate high frequency of sudden death include substantial ventricular myocardial dysfunction [1] and the occurrence of “complex” premature ventricular depolarizations and nonsustained ventricular tachycardia [2–4]. However, the predictive value of these factors alone for sudden death is not sufficiently accurate for clinical usefulness. In patients who have coronary artery disease but no recent myocardial infarction, electrophysiologic stimulation has a high degree of sensitivity [5] for inducing the patient’s clinical arrhythmia, and serial electrophysiologic testing has proven useful for determining the drug therapy that will prevent recurrent arrhythmias [5–8]. Recently, electrophysiologic testing to initiate ventricular tachycardia has been advocated as a technique to identify patients in the postmyocardial infarction period most likely to have sudden cardiac death [9, 10].

Tachyarrhythmias may be treated effectively and safely with synchronized transthoracic direct current shocks (1). Further, an implantable defibrillator has been developed and used successfully in patients to terminate ventricular fibrillation (2,3). Recently, Jackman and Zipes (4) demonstrated that ventricular tachycardia could be terminated with shocks of ≤1.0 joule delivered through a catheter electrode placed in the right ventricular apex of dogs. Subsequently, we (5,6) reported our initial observations on the safety and usefulness of transvenous cardioversion of ventricular arrhythmias in humans. Extension of our preliminary results, including termination of supraventricular tachycardia, as well as methodology of transvenous cardioversion are discussed below.