Previous investigations demonstrated that ventricular (V) pacing causes abnormal déformation in the epicardium of the left ventricular (LV) anterior wall. We examined to what extent V pacing influenced deformation around the entire LV, using magnetic Resonance Imaging (MRI) tagging. In 2 anesthetized dogs MRI compatible pacing leads were positioned on right atrium (RA), right ventricular (RV) apex and LV base. During intervals of stopped ventilation high temporal (20 ms) and spatial resolution (5 mm distance between the parallel taglines) images were obtained in 2 sets of 8 short axis slices and a set of 9 radially oriented long axis slices. During RA pacing (normal electrical activation of LV) circumferential and longitudinal shortening started at endocardia! sites and continued towards the epicardum. During the ejection phase the amount of shortening uniformly increased at all sites around the LV, reaching values of 15 +/- 3% in m id myocardium. During RVapex and LVbase pacing initially rapid shortening occurred at the pacing site, accompanied by stretching of later activated regions, as large as 15% in midmyocardium of most remote regions (located across the chamber from the pacing site). During the ejection phase, however, early activated regions did not shorten or were even stretched, whereas late activated remote regions shortened by up to 30%. Displaying isoshortening lines on a 3D reconstruction of the LV showed rapid radial and longitudinal but slower circumferential propagation of the contraction wave, suggesting the possibility locating the site of ectopic activation by this completely non-invasive deformation measurement. The large differences in deformation within the entire LV during V pacing, also from the RV apex site, urges further studies on consequences of abnormal electrical activation of the LV during pacing protocols used clinically.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology