NARROW COMPLEX VENTRICULAR TACHYCARDIA

A 61-year-old male with past medical history of hypertension, hyperlipidemia and coronary artery disease presented with sustained tachycardia. His history was remarkable for ST segment elevation myocardial infarction (MI) and had a stent placed in right coronary artery (RCA) 1 month ago. He was non-compliant with antiplatelet therapy and his RCA re-occluded within 1 week causing another MI and it was emergently restented. He was discharged to a rehabilitation facility on standard post-MI therapy. During rehabilitation, he was noted to have sustained, hemodynamically-tolerated tachycardia and returned to the hospital. His electrocardiogram (ECG) showed a regular tachycardia at 173 beats/minute with a QRS duration (QRSd) of 110 msec (Fig 1), presumed to be supraventricular in origin. His rhythm failed to respond to intravenous adenosine or diltiazem and was subsequently given intravenous amiodarone, leading to conversion to sinus rhythm with a QRSd of 90 msec. The patient’s QRS complexes during tachycardia were clearly different than in sinus rhythm, with slurring of the QRS upstroke in leads I and aVL, and manifesting an abrupt transition between leads V1 and V2 that was absent on the sinus rhythm ECG (Fig 2). The patient was admitted to the coronary care unit and maintained on intravenous amiodarone. A subsequent invasive electrophysiological (EP) study was performed. With triple extrastimuli from the right ventricle outflow tract, a non-clinical rapid monomorphic ventricular tachycardia (VT) was induced. Decremental pacing converted this into the clinical tachycardia which was associated with AV dissociation, confirming the mechanism as VT. This was successfully pace-terminated. A dual-chamber implantable cardioverter-defibrillator was placed. 

Discussion:

Sustained tachycardia is classically divided into narrow- or wide-complex tachycardia based upon a QRSd of 120 msec. Wide-complex tachycardias may be ventricular or supraventricular tachycardia (SVT) with aberrancy (with numerous published algorithms to assist in this differentiation). However, narrow-complex tachycardia utilize the His-Purkinje system and are almost exclusively supraventricular in origin. Our patient had relatively narrow complexes during sustained VT, conceivably because his fascicular system constituted a portion of the VT circuit, leading to an initial misdiagnosis of SVT. Both his clinical history and his ECG variances from his normal QRS complexes supported a mechanism of VT, which was confirmed by EP study. Thus, in patients with coronary artery disease and new-onset tachycardia, even with relatively narrow QRS complexes, a high index of suspicion for VT should be maintained.

Conclusions:

High index of suspicious for ventricular origin of tachycardia should be kept in patients with new diagnosis of tachycardia after Coronary artery disease and ventricular tachycardia can present with relatively narrow QRSd as well.