A patient in their 70s with a history of nonischemic cardiomyopathy and biventricular pacemaker presented to the emergency department with 2 days of intermittent chest pain, which had become constant for 4 hours and associated with diaphoresis and shortness of breath. Vital signs were normal, and a 12-lead electrocardiogram (ECG) was obtained (Figure). Two hours later the patient had an episode of polymorphic ventricular tachycardia.
Questions: Are there any clinical or ECG indications for cardiac catheterization laboratory activation, and what angiographic findings does the ECG predict?
The ECG shows atrial-sensed biventricular pacing with a premature ventricular contraction. Although the pacing is biventricular (which usually has a near-normal QRS duration), the structure is that of right ventricular pacing, with a wide and negative QRS complex throughout the precordium. With such a QRS complex, all leads should have secondary ST-T segment changes discordant to (in the opposite direction of) the QRS complex. But here there is subtle concordant ST-segment elevation in lead III only, with reciprocal concordant ST-segment depression in leads I and aVL. While this does not meet the modified Sgarbossa criteria of 1 mm of concordant ST-segment elevation, it is accompanied by an ST-segment in lead V1 higher than lead V2 and mild concordant ST-segment depression in leads V2 through V6. This represents the Aslanger pattern in a paced rhythm, which identifies inferior occlusion myocardial infarction (OMI) with concomitant critical stenoses. In addition, this was followed by polymorphic ventricular tachycardia, which in the context of ischemic symptoms is a sign of electrical instability from OMI. The patient, therefore, had both clinical and ECG indications for cardiac catheterization laboratory activation, despite not meeting ST-elevation MI (STEMI) criteria.