Triple-site pacing in patients with biventricular device-incidence of the phenomenon and cardiac resynchronization benefit

. 2004 Feb ; 10 (1) : 37-45.

Jazyk angličtina Země Nizozemsko Médium print

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/pmid14739748

BACKGROUND: In patients with biventricular pacing (BIV), triple-site pacing (TSP), i.e. standard biventricular cathodal pacing of the right and the left ventricle plus additional anodal capture of the right ventricle, is sometimes present. AIMS: To evaluate the incidence of TSP phenomenon, to examine TSP-related QRS changes, and to assess the effect of TSP on intraventricular resynchronization by means of tissue Doppler imaging (TDI). METHODS AND RESULTS: 23 patients with a first generation biventricular device (Medtronic 8040) and 16 patients with a new generation device (Medtronic 8042) were evaluated to look for the presence of TSP. TSP was found in 6 patients (26%) with the Medtronic 8040 (group I) and in 13 patients (81%) with the Medtronic 8042 device (group II). QRS duration decreased by 10 to 20 ms and QRS amplitude of leads I and aVL increased in almost all patients in group I during TSP modality. In group II, QRS morphology, duration and amplitude did not change as obviously. TDI analysis of the left ventricular (LV) basal segments showed significant shortening of the systole, together with a corresponding prolongation of the diastole, at the inferior wall of the LV, during TSP compared to standard BIV in all patients ( p < 0.01). Other LV segments did not show any change. Qualitative TDI electro-mechanical activation pattern of all LV segments improved in 22%, while it remained unchanged in 72%. CONCLUSIONS: TSP phenomenon can be identified in approximately a quarter of patients with the first-generation biventricular devices on the basis of the QRS morphology changes. In the second-generation biventricular pacemakers it can be demonstrated in the vast majority of patients. TSP may increase the effectiveness of cardiac resynchronization therapy by counteracting the regional activation delay located at the inferior wall of the LV.

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