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Ventricular septal motion and left ventriclular dimensions during abnormal ventricular activation
Insights
Right ventricular pacing alters septal motion and reduces left ventricular dimensions, with patterns varying by pacing site and rate. These changes mimic left bundle branch block, depending on activation sequence.
Area of Science:
- Cardiology
- Echocardiography
- Electrophysiology
Background:
- Ventricular activation sequence influences cardiac mechanics.
- Understanding abnormal septal motion is crucial for diagnosing conduction abnormalities.
Purpose of the Study:
- To investigate the impact of abnormal ventricular activation on ventricular septal motion, left ventricular endocardial motion, and dimensions.
- To compare pacing-induced septal motion patterns with spontaneous left bundle branch block.
Main Methods:
- Echocardiography was used in 12 patients with normal baseline motion.
- Incremental right ventricular pacing was performed at apical, outflow, and inflow regions.
- Ventricular septal motion, endocardial motion, and dimensions were analyzed at various pacing rates.
Main Results:
- Three distinct patterns of abnormal ventricular septal motion (Types I, II, III) were observed, dependent on pacing site.
- Right ventricular apical pacing predominantly induced Type I, while outflow and inflow pacing favored Type II.
- Left ventricular dimensions decreased with pacing rate, independent of pacing site.
Conclusions:
- Ventricular septal motion abnormalities during right ventricular pacing are sequence-dependent.
- Pacing from outflow/inflow sites mimics spontaneous left bundle branch block, unlike apical pacing.
- Left ventricular dimensional changes correlate with pacing rate, not location.
Abstract:
To determine the effect of abnormal ventricular activation on ventricular septal motion, left ventricular endocardial motion and left ventricular dimensions, 12 patients with normal motion were studied with echocardiography during incremental pacing of the right ventricular apex, outflow and inflow regions. Three types of abnormal ventricular septal motion were seen: The type I pattern was characterized by an early rapid preejection posterior ventricular septal motion followed by another posterior systolic motion that lasted throughout ejection, both of which were associated with septal thickening. In the type II pattern an early rapid preejection posterior ventricular septal motion was followed by an anterior ejection motion; the latter was not accompanied by septal thickening. The type III pattern consisted of an early preejection posterior ventricular septal motion followed by a mid and late systolic posterior motion: the latter motion extended through diastole. During right ventricular apical pacing, 8 of 11 patients showed a type 1 pattern, 1 a type II pattern and 2 a normal septal motion. During right ventricular outflow pacing,seven of nine patients showed a type II pattern, one a type III pattern and one a type I pattern. During right ventricular inflow pacing, eight of nine patients showed a type II pattern and one a type III pattern. At faster pacing rates patterns of types I and III changed to a type II pattern (five patients). End-diastolic dimensions decreased significantly during incremental right ventricular pacing when compared with those during sinus rhythm. End-systolic dimensions decreased significantly only during right ventricular apical and outflow pacing at maximal rates. In the seven patients who had pacing from all three sites, the decrease in left ventricular dimensions did not significantly differ when the three pacing sites were compared. These findings suggest that (1) abnormal ventricular septal motion during right ventricular pacing (induced left bundle branch block patterns) is dependent on the sequence of ventricular activation; (2) ventricular septal motion during right ventricular outflow and inflow pacing is similar to that seen in spontaneous left bundle branch block, whereas the pattern of septal motion during right ventricular apical pacing is different from that of spontaneous left bundle branch block; and (3) changes in left ventricular dimension are dependent on ventricular pacing rate but independent of pacing site.