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An 89 year old woman with a history of hypertension, type 2 diabetes mellitus, and involution depression presented with a syncope of 3−5 minutes duration occurring in a sitting position without associated seizure or other neurological signs. On admission she had signs of mild dehydration, a heart rate of 80 beats/min (bpm), and a blood pressure of 140/80 mm Hg. The baseline ECG showed sinus rhythm of 87 bpm with left anterior fascicular block and left atrial abnormality. Echocardiography did not reveal any alteration that could possibly explain the syncope. Holter monitor recording revealed two runs consisting of wide complexes of variable morphology apparently consistent with a non-sustained polymorphic ventricular tachycardia (VT), a potential underlying cause of the syncope. Monomorphic premature ventricular complexes also occurred before, in between, and after the wide complex runs. The first wide complex run follows and might be assumed to be initiated by a premature ventricular complex (see fig). However, closer observation of the tracings revealed the continued presence of normal QRS complexes at the cycle length of baseline rhythm within the apparent wide complexes (marked by arrows) and an unstable baseline on the electrogram before the tachycardia events. This resulted in the recognition that the wide complexes were electrocardiographic artefacts. Other signs that indicated the artefactual nature of the tachycardia were: the occurrence of a very early sinus QRS complex at the end of the first tachycardia episode (shown by the last arrow of the second rhythm strip), and the absence of haemodynamic deterioration during the Holter monitoring.
The most likely cause of the electrocardiographic artefact was body movement. An electrocardiographic artefact can closely simulate VT, and even cardiologists not infrequently misdiagnose it as VT, resulting in unnecessary and potentially dangerous medical therapies or interventions.
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