case_images: PMC10656738_01
case_images: Cardiac MRI, four-chamber view. Depicted long- and short-axis cine images. Red arrows: thickened LV septal and apical wall (up to 20 mm); small apical pericardial effusion.
case_images: fcvm-10-1240189-g001.jpg
case_images: PMC10656738_01_fcvm-10-1240189-g001.jpg
case_images: F1
case_images: However, cardiac magnetic resonance imaging was not diagnostic but showed pathologic LV thickening of the anteroseptal and mid-anteroseptal and apical parts (Figure 1, up to 21 mm), leading to the diagnosis of non-obstructive HCM.
case_images: (A) Twelve-lead resting ECG (June 2016) (1.25 mg/d bisoprolol) before the first cardiac event depicting sinus bradycardia (45 bpm), regular conduction and repolarization, and tall T-waves. (B) Twelve-lead resting ECG (January 2018) (medication: 200 mg twice/day amiodarone, 60 mg twice/day diltiazem) with sinus rhythm and a heart rate of 50 bpm.
case_images: fcvm-10-1240189-g002.jpg
case_images: PMC10656738_01_fcvm-10-1240189-g002.jpg
case_images: F2
case_images: However, cardiac magnetic resonance imaging was not diagnostic but showed pathologic LV thickening of the anteroseptal and mid-anteroseptal and apical parts (Figure 1, up to 21 mm), leading to the diagnosis of non-obstructive HCM. The baseline ECGs showed a normal but bradycardic sinus rhythm (45 bpm; Figure 2A) and conduction at rest without any disturbances of repolarization or LV hypertrophy.
case_images: (A) Electrograms during the exercise of the dual-chamber ICD in August 2016. Sensing of a spontaneously occurring ventricular tachycardia (approximately 230 ms, 260 bpm, red arrow in the left upper panel) can be observed. Of note, initially regular atrial sensing (approximately 400 ms or 150 bpm; exercise-related) (upper two leads in the left upper panel) but further degeneration into VF (red arrow in the right upper panel) and sinus bradycardia and arrest (middle panels, red rectangle) can be seen. In the lower panel, ventricular shock (41 J) and hereafter atrial pacing (1,000 ms or 60 bpm) and ventricular sensing indicated a recurrence of regular ventricular activity. (B) Histograms corresponding to (A). Spontaneously occurring ventricular tachycardia and fibrillation (upper panel) arising from sinus tachycardia (exercise, 150 bpm) (red arrow in upper panel) can be observed. In the lower panel, a red arrow indicates the occurrence of sinus bradycardia and sinus node arrest during VF. Vertical lines indicate an ICD shock (41 J) and atrial stimulation.
case_images: fcvm-10-1240189-g003.jpg
case_images: PMC10656738_01_fcvm-10-1240189-g003.jpg
case_images: F3
case_images: However, cardiac magnetic resonance imaging was not diagnostic but showed pathologic LV thickening of the anteroseptal and mid-anteroseptal and apical parts (Figure 1, up to 21 mm), leading to the diagnosis of non-obstructive HCM. This illustrates a rare ECG registration and co-event of VF and SAN arrest or AA (Figures 3A,B).
case_images: (A) First electrograms of the dual-chamber implantable cardioverter-defibrillator (ICD) (during physical exercise, September 2017). Re-occurrence of a VF episode (red arrow in left upper panel), again induced by physical exercise. Remarkably, during persisting VT, the atrial sensing aggravated again into sinus bradycardia and finally sinus node arrest until the second ICD shock, hereafter, atrioventricular pacing (right middle and left lower panels). (B) Electrograms (September 2017). ICD sensing shows a VF at the ventricular level and atrial tachycardia that further decelerates (red arrows). Vertical lines indicate ICD shock (41 J each) to restore regular and paced rhythm and rhythm restoration but re-occurrence of VF and sinus node arrest.
case_images: fcvm-10-1240189-g004.jpg
case_images: PMC10656738_01_fcvm-10-1240189-g004.jpg
case_images: F4
case_images: However, cardiac magnetic resonance imaging was not diagnostic but showed pathologic LV thickening of the anteroseptal and mid-anteroseptal and apical parts (Figure 1, up to 21 mm), leading to the diagnosis of non-obstructive HCM. AS to sinus bradycardia followed by asystole (Figures 4A,B).