High frame rate speckle tracking echocardiography to visualize the mechanical activation sequence of the left ventricle

Background Cardiac arrhythmias are a known cause of morbidity and mortality, with catheter ablation being an effective treatment. In order to detect the focal source or the re-entrant circuit of the arrhythmia, i.e. the ablation target, current practice includes performing an electrophysiological study. This technique is invasive, with increased patient related risk and variable success rate. Conversely, echocardiography could be used to determine the correct ablation target. High frame rate (HFR) ultrasound has a temporal resolution adequately high to detect the onset of myocardial deformation and could assist the accurate localisation of the arrhythmia source. Purpose To test whether HFR speckle tracking echocardiography (STE) can be used to create cardiac mechanical activation maps. Methods 18 healthy volunteers (HV) (age 30±6y; 69 %males) and 12 heart failure patients treated with cardiac resynchronisation therapy (CRT) (age 69±10y; 75 %males) were included. All participants were scanned with a research HFR ultrasound scanner (∼849fps) and the 3 standard apical views were acquired. Patients were scanned with CRT on and after turning CRT off, in order to allow intrinsic ventricular conduction. Data from one CRT patient were acquired by temporarily altering the pacing pole of the CRT LV lead. All patients had a left bundle branch block (LBBB) pattern of native activation on the surface ECG. For each view, a manually placed contour was tracked during the cardiac cycle by a custom-made 2D HFR STE algorithm; the contours were divided in a standard 16 segment model and segmental strain rate (SR) curves were computed and used to measure the temporal distance between electrical and mechanical activation (i.e. distance between the beginning of QRS and the first positive to negative zero crossing in the SR curve). Finally, an activation map for each subject was created by placing the extracted timings in the middle of the corresponding segment of a bull’s-eye plot and interpolating values between them. Results Tracking was feasible in 94% of the segments; SR curves showed a physiological pattern (Fig. 1A). For the HV, mechanical activation started from mid anteroseptal (72%) or mid inferoseptal (28%) segment at 23±5ms, spreading to basal posterolateral segment at 49±8ms from the start of QRS, in all but one case, where activation ended at basal inferoseptal segment (Fig. 1B). During CRT off, septal wall was activated 31±9ms and lateral wall 74±20ms after the beginning of QRS (p<0.01) (Fig. 1C), whereas during CRT on, septal wall was activated 41±11ms and lateral wall 38±7ms after the beginning of QRS (p=0.3) (Fig. 1D). Changing the pacing pole of the LV lead in one CRT patient also changed the start of mechanical activation in the lateral wall (Fig. 2). Conclusion Our findings comply with left ventricular activation as described in the literature and show that HFR STE could be a useful tool in defining the ablation target for arrhythmia treatment.