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Notes: Multisite pacing for the treatment of heart failure has added a new dimension to the electrocardiographic evaluation of device function. During left ventricular (LV) pacing from the appropriate site in the coronary venous system, a correctly positioned lead V1 registers a right bundle branch block pattern with few exceptions. During biventricular stimulation associated with right ventricular (RV) apical pacing, the QRS is often positive in lead V1. The frontal plane QRS axis is usually in the right superior quadrant and occasionally in the left superior quadrant. Barring incorrect placement of lead V1 (too high on the chest), lack of LV capture, LV lead displacement or marked latency (exit block or delay from the stimulation site), ventricular fusion with the spontaneous QRS complex, a negative QRS complex in lead V1 during biventricular pacing involving the RV apex probably reflects different activation of an heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation in view of the varying patterns of LV activation in spontaneous left bundle branch block) and does not necessarily indicate a poor (electrical or mechanical) contribution from LV stimulation. In this situation, it is imperative to rule out the presence of coronary venous pacing via the middle cardiac vein or even unintended placement of two leads in the RV. During biventricular pacing with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation).In patients with sinus rhythm and a relatively short PR interval, ventricular fusion with competing native conduction during biventricular pacing may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate biventricular capture. This represents a common pitfall in device follow-up. Elimination of ventricular fusion by shortening the AV delay, is often associated with clinical improvement. Anodal stimulation may complicate threshold testing and should not be misinterpreted as pacemaker malfunction.One must be cognizant of the various disturbances that can disrupt 1:1 atrial tracking and cause loss of ventricular resynchronization. (1) Upper rate response. The upper rate response of biventricular pacemakers differs from the traditional Wenckebach upper rate response of conventional antibradycardia pacemakers because heart failure patients generally do not have sinus bradycardia or AV junctional conduction delay. The programmed upper rate should be sufficiently fast to avoid loss of resynchronization in situations associated with sinus tachycardia. (2) Below the programmed upper rate. This may be caused by a variety of events (especially ventricular premature complexes and favored by the presence of first-degree AV block) that alter the timing of sensed and paced events. In such cases, atrial events become trapped into the postventricular atrial refractory period at atrial rates below the programmed upper rate in the presence of spontaneous AV conduction. Algorithms are available to restore resynchronization by automatic temporary abbreviation of the postventricular atrial refractory period.

Notes: A dedicated pacemaker Holter system facilitates recognition of the pacemaker stimulus by amplifying and displaying it in an ECG channel without any other data. Such a Holter pacemaker channel may occasionally generate electrostatic charges that produce deflections resembling pacemaker stimuli (pseudopacemaker spikes) arising from a loose ECG electrode, crushed tape, or a dirty recording head. False-positive spikes or spurious marker deflections in Holter pacemaker channels and occasional failure to detect tiny bipolar stimuli can present challenging problems in the interpretation of pacemaker function. In multiple-channel recorders, skewing of the recording heads may lead to timing errors and puzzling recordings when one of the ECG or pacemaker channels lags behind others producing asynchrony or malalignment in simultaneously recorded tracings.The interpretation of Holter recordings from contemporary complex pacemakers requires knowledge of pacemaker timing cycles and their interrelationships, a large variety of programmable parameters or functions, behavior of the nonatrial sensor or sensors in rate-adaptive systems, device-specific responses to protect the system from a variety of undesirable situations, and an appreciation of pacemaker eccentricities.There are a few prospective studies on the value of routine Holter recordings in pacemaker patients. The real value of Holter recordings lies with symptomatic patients when symptoms occur during the recording period. Correlation between symptoms and occasional abnormality of pacemaker function during Holter monitoring remains poorly characterized. The cause of the symptoms is frequently unrelated to the pacemaker system and may not be related to coexisting arrhythmias. In asymptomatic patients, Holter recordings are particularly useful to uncover a lead problem after an unrevealing thorough investigation in the pacemaker clinic.Special instrumentation was recently developed to register telemetry data from implanted pacemakers simultaneously with ambulatory electrocardiography. In this way, diagnostic marker signals and/or intracardiac electrograms transmitted from the pacemaker can be recorded continuously for 24 hours by a Holter recorder. Advanced technology involving the memory capability of pacemakers will transform the pacemaker itself into a 24-hour Holter recorder, probably in 4 to 5 years. At present, the memory for storage of intracardiac electrograms is limited from a few seconds to less than a minute according to the manufacturer, but even such mini-Holter recordings can be diagnostically important.

Notes: This report describes two patients with sustained regular left atrial tachycardias originating from multiple pulmonary veins in the absence of clinical evidence of atrial fibrillation. The tachycardias were eliminated by activation map-guided pulmonary vein isolation. Stable sustained regular pulmonary vein tachycardias unassociated with atrial fibrillation are uncommon, and they belong to the spectrum of pulmonary vein arrhythmias that include the more common paroxysmal and unstable tachycardias engendering atrial fibrillation.

Notes: This report describes the occurrence of prolonged atrial escape intervals (AEI) initiated by sensing of ventricular premature complexes (VPC) without a preceding atrial depolarization or an AV delay in two patients with DDD pacemakers with an atrial-based lower rate response. The prolonged AEIs were due to ventriculoatrial cross-talk so that atrial sensing of the far-field R wave of the VPCs occurred before detection of the R wave by the ventricular channel as a near-field signal. Early atrial sensing of the far-field R wave was promoted by a high atrial sensitivity and/or low ventricular sensitivity and was eliminated by reducing atrial sensitivity and/or increasing ventricular sensitivity. This manifestation of far-field sensing should not be interpreted as malfunction of dual chamber pacemakers with atrial-based lower rate timing. (PACE 2003; 26:2188–2191)