PMC5420022_01
A: Echocardiographic appearance of this patient's left ventricular apical hypertrophy. B: Progressive electrical changes over time per surface electrocardiograms (ECGs) (N = 47). R-wave amplitude and T-wave amplitude both declined over time. Units are in mV (millimeters have been converted accordingly from each ECG's calibration). Examples of V4 complexes are displayed on the right (R-wave reduction -37%, ST -96%).
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T waves measuring 20 mm (2 mV), the pattern often seen in AHCM. Transthoracic echocardiography showed severe left ventricular apical hypertrophy (13 mm thickness of the septum and posterior walls, but 23 mm at the apex) without any apical aneurysm (Figure 1A). At this time, the ECG showed V4 R wave of 20 mm, QRS width 106 msec, no ST-segment depression, and T wave now upright (Figure 1B).
Electrogram as recorded by the device at the onset of ventricular fibrillation (VF) demonstrates failure to sense VF.
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Within 3.5 seconds the activity became highly fractionated, with segments of much lower amplitude consistently less than 3 mV (minimal <1 mV) and detection gaps of 443 msec, leading to counter resetting and failure to shock (Figure 2).
A: Electrograms prior to placing the right ventricular (RV) septal lead. B: Catheter placement is shown with a 20-pole mapping catheter in the right ventricle that has been advanced as distally as possible to approximate sensing at the apical lead and a 4-pole mapping catheter to approximate the high septal activity. The apical activity (DD1-2) is fractionated, low-amplitude signal during ventricular fibrillation (VF). However, the same activity is discrete and high-amplitude at the basilar RV septum. C: New RV septal lead with associated electrogram during induced VF with cleaner signal (red) as compared to the old lead (blue), also with activity during VF.
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B). Based on these data we placed an active-fixation sense/pace lead with an 11-mm separation (BSC RELIANCE) at the mid RV septum as noted in the posteroanterior chest radiograph image (Figure 3C).