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Improvements in medical therapy for advanced heart failure have improved prognosis. Nonetheless, mortality from both sudden and nonsudden death remains high. In addition, sudden death may occur in association with heart failure exacerbation. Clearly, avoidance of Type I antiarrhythmic agents and increased use of low dose amiodarone and transvenous ICD therapy decreases total mortality in a subset of patients. Further studies will help define the role of these therapies in sudden death prevention.

Although pharmacological therapy has ameliorated symptoms and improved the survival of patients with chronic heart failure (CHF), this chronic syndrome remains a progressive disease causing incremental morbidity and early mortality. A new therapy for the treatment of CHF should ideally decrease mortality, alleviate symptoms, and improve functional capacity. A growing body of evidence suggests that the use of implantable devices to resynchronize ventricular contraction may be a beneficial adjunct in the treatment of CHF.The Comparison of Medical Therapy, Pacing, and Defibrillation in Chronic Heart Failure (COMPANION) trial is a randomized, open-label, 3-arm study of patients in New York Heart Association class III or IV with an ejection fraction of 35% or less and a QRS duration of 120 milliseconds or less. The COMPANION study objectives are to determine whether optimal pharmacological therapy used with (1) ventricular resynchronization therapy alone or (2) ventricular resynchronization therapy combined with cardioverter-defibrillator capability is superior to optimal pharmacological therapy alone in reducing combined all-cause mortality and hospitalizations; reducing cardiac morbidity; improving functional capacity, cardiac performance, and quality of life; and increasing total survival.

Epidemiologic studies suggest that 20-30% of patients diagnosed with symptomatic congestive heart failure (CHF) have intraventricular conduction disorders characterized by a discoordinate contraction pattern and wide QRS. Biventricular pacing is an emerging therapy allowing simultaneous electrical stimulation of the right and left ventricles with the use of an implantable pacing system. The aim of this article is to describe 2 prospective randomized multicenter trials examining the effects of biventricular pacing on functional capacity, quality of life, and hemodynamic status in patients with dilated cardiomyopathy and intraventricular delay. The VIGOR CHF Trial is designed to assess functional and symptomatic improvement in heart failure patients with biventricular pacing and without a concomitant indication for conventional bradycardia pacemaker therapy. To assess for potential placebo effects, patients are randomized to receive either biventricular pacemaker therapy or no pacing therapy for the first 6 weeks, after which both groups receive pacing therapy. The VENTAK CHF trial uses an implantable cardioverter defibrillator system (ICD) designed to provide chronic biventricular pacing therapy in addition to treating ventricular tachyarrhythmias. All patients receive conventional ICD and CHF therapy throughout the study and are randomized in a 2-period crossover design to receive either no pacing or biventricular pacing for 3-month intervals. Patient enrollment in both studies is ongoing, with a closed analysis. The unique designs of these trials provide the opportunity to study this therapy in high-risk patients who have been optimally treated for heart failure.

Using a standardized induction protocol, we investigated the mechanism of initiation of atrial flutter, before ablation, to determine the site of initiating unidirectional block and to test the hypothesis that the direction of rotation of atrial flutter depends on the pacing site from which it initiates.The high recurrence rate of atrial flutter after presumed successful ablation may be due to difficulty in reinduction after termination. In addition, induction of clockwise flutter is currently of unknown clinical importance.Ten patients with documented typical flutter were studied before ablation. A standard protocol consisting of single and double extrastimuli followed by burst pacing was performed from four sites in the right atrium (high and low trabeculated and smooth right atrium) to assess efficacy at inducing atrial flutter. A 20-pole halo catheter placed around the tricuspid annulus and a decapole catheter placed in the coronary sinus were used for mapping during initiation to determine type of flutter induced and the site of unidirectional block during initiation.Atrial flutter was induced in 52 (6.2%) of 838 attempted inductions. Of these, 33 were counterclockwise and 20 were clockwise. Of the 20 inductions resulting in clockwise flutter, 18 were from the trabeculated right atrium, whereas all the counterclockwise inductions were from the smooth right atrium. In all but the two inductions, the site of unidirectional block was identified between the os of the coronary sinus and the low lateral right atrium for both counterclockwise and clockwise flutter, in the same isthmus at which ablation is targeted.Even in patients with clinical counterclockwise flutter, clockwise flutter is frequently induced before ablation and is dependent on the site of induction: Pacing from the smooth right atrium induces counterclockwise flutter, whereas pacing from the trabeculated right atrium induces clockwise flutter. The site of the unidirectional block during the initiation of either form of flutter is in the low right atrium isthmus.

The approach to localizing sites for catheter ablation of ventricular tachycardia foci depends on the type of tachycardia. In large reentry circuits such as those arising from infarct scars, areas of slow conduction in and around the scar should be targeted. During sinus rhythm, these can be suspected from the presence of fractionated electrograms and, at some sites, long stimulus to QRS delays during pacing. Slow conduction areas can be classified as: 1. central slow conduction zone sites, 2. exits from the slow conduction zone, 3. entrances to the slow conduction zone, and 4. bystander areas which are not involved in the tachycardia circuit. In the central slow conduction zone stimulation entrains or resets tachycardia with a long stimulus to QRS (S-QRS) delay (40 to greater than 300 ms) without altering the QRS morphology (entrainment with concealed fusion). At slow conduction zone exits, presystolic electrograms are recorded during VT, the pacemap matches the VT QRS morphology, and with pacing during VT the S-QRS interval is relatively short and VT may or may not be entrained. At entrances to the slow conduction zone electrogram timing is variable but early diastolic electrograms are expected and the pace-map QRS may differ from the VT QRS morphology. Relatively late stimuli or slow trains of stimuli entrain VT with concealed fusion with a relatively longer S-QRS interval than observed in the central slow conduction zone. Early stimuli may entrain VT while altering the QRS morphology due to propagation of the stimulated antidromic wavefront out of the scar from a site other than the tachycardia exit. At bystander sites electrogram timing, pace-mapping, and the effects of programmed stimulation are variable but may occasionally mimic reentry circuit sites. Relatively late stimuli are likely to capture the site without altering the VT. If discrete electrograms are present, analysis of these during pacing may provide further evidence that the site is not in the reentry circuit. Catheter ablation will probably be most effective at central slow conduction zone sites. When VT originates from a small focus surrounded by normal myocardium, such as is likely for idiopathic RV outflow tract and some idiopathic left ventricular tachycardias, presystolic electrical activity and pacemapping are likely to identify the tachycardia focus. For macroreentry involving the bundle branches, the right bundle branch can be easily targeted.

A patient failed to wean from mechanical ventilation. Her problem was unique in that she had a depressed central drive to breathe manifested by hypopnea when removed from the ventilator. After excluding the known problems that impair successful weaning, we empirically administered three separate infusions of doxapram, a respiratory stimulant. These infusions produced a dramatic improvement in spontaneous ventilation and led to successful weaning and hospital discharge.