Library

Notes: Introduction: Atrial fibrillation (AF) is associated with increased ostial pulmonary vein (PV) diameter and commonly with hypertension. We sought to investigate ostial PV anatomy in patients with and without AF with the goal of characterizing the relationship to hypertension and cardiovascular disease. Methods and Results: Ostial PV diameter was assessed by preprocedural spiral computed tomography in 100 AF patients undergoing a PV isolation procedure and in 24 age- and sex-matched non-AF control patients. Ostial diameter of 392 PVs in 100 AF patients was increased compared to 106 PVs in 24 non-AF controls (1.50 ± 0.31 vs 1.20 ± 0.31 cm, P 〈 0.001) and diameters of individual PVs were uniformly affected (r = 0.45–0.62, P 〈 0.001). Left atrial dilation was associated with a larger PV diameter (1.56 ± 0.32 vs 1.44 ± 0.29 cm, P 〈 0.01). PV diameter in AF patients with hypertension (1.55 ± 0.32 cm), particularly if associated with left ventricular hypertrophy (1.66 ± 0.37 cm), was larger compared to AF patients without hypertension (1.43 ± 0.26 cm, P 〈 0.01). PV diameter in control patients with hypertension (n = 14) was larger than in those without hypertension (n = 10, P 〈 0.01). Patients with persistent AF had larger PV diameters (1.61 ± 0.34 cm) than patients with paroxysmal AF (1.47 ± 0.30 cm, P 〈 0.01). Male gender (P 〈 0.01), history of hypertension (P 〈 0.01), and persistent AF (P 〈 0.05) were identified as independent cofactors of increased ostial PV diameter. Conclusion: PV dilation affects all PVs uniformly in AF patients. Hypertension and hypertensive heart disease in patients with and without AF are associated with PV dilation, supporting theories that impaired left ventricular diastolic function is associated with a stretch-induced PV arrhythmia mechanism.

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: 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 termination of persistent AF refractory to multiple cardioversions and antiarrhythmic therapy in a patient without structural heart disease, with a single radiofrequency application delivered in the left upper pulmonary vein. The observations and failure of repeated internal and external cardioversion suggest a rapidly firing arrhythmia focus sustaining atrial fibrillation amenable to curative pulmonary vein ablation. (PACE 2003; 26:1420–1423)