Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part I

Abstract

Cardiac resynchronization therapy (CRT) has added a new dimension to the electrocardiographic evaluation of pacemaker function. During left ventricular (LV) pacing from the posterior or posterolateral coronary vein, a correctly positioned lead V1 registers a tall R wave and there is right axis deviation in the frontal plane with few exceptions. During simultaneous biventricular stimulation from the right ventricular (RV) apex and LV site in the coronary venous system, the QRS complex is often positive (dominant) in lead V1 and the frontal plane QRS axis usually points to the right superior quadrant and occasionally the left superior quadrant. The reported incidence of a dominant R wave in lead V1 during simultaneous biventricular pacing (RV apex) varies from 50% to almost 100% for reasons that are not clear. During simultaneous biventricular pacing from the posterior or posterolateral coronary vein 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).
A negative paced QRS complex in lead V1 during simultaneous biventricular pacing with the RV lead at the apex can be caused by incorrect placement of the lead V1 electrode (too high on the chest), lack of LV capture, LV lead displacement, pronounced latency (true exit block), conduction delay around the LV stimulation site, ventricular fusion with the intrinsic QRS complex, coronary venous LV pacing via the middle or anterior cardiac vein, unintended placement of two leads in the RV and severe conduction abnormalities within the LV myocardium. Most of these situations can cause a QS complex in lead V1 which should be interpreted (excluding fusion) as reflecting RV preponderance in the depolarization process. Barring the above causes, a negative complex in lead V1 is unusual and it probably reflects a different activation of a heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation). The latter is basically a diagnosis of exclusion. With a non-dominant R wave in lead V1, programming the V-V interval with LV preceding RV may bring out a diagnostic dominant R wave in lead V1 representing the contribution of LV stimulation to the overall depolarization process. In this situation the emergence of a dominant R wave confirms the diagnosis of prolonged LV latency (exit delay) or an LV intramyocardial conduction abnormality near the LV pacing site but it rules out the various causes of LV lead malfunction or misplacement.
(Cardiol J 2011; 18, 5: 476–486)