Ventricular Tachycardia Induced by Biventricular Pacing in Patient with Severe Ischemic Cardiomyopathy

• Published in: Journal of cardiovascular electrophysiology Vol. 16; no. 6; pp. 655 - 658
• Main Authors: MYKYTSEY, ANDREW, MAHESHWARI, PRADEEP, DHAR, GAURAV, RAZMINIA, MANSOUR, ZHEUTLIN, TERRY, WANG, TED, KEHOE, RICHARD
• Format: Journal Article
• Language: English
• Published: 350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK Blackwell Science Inc 01.06.2005
• Subjects: Acute Disease; Aged; Cardiac Pacing, Artificial - adverse effects; cardiac resynchronization therapy; Cardiomyopathy, Dilated - physiopathology; Coronary Artery Bypass; Heart Failure - physiopathology; Heart Failure - therapy; Humans; ischemic cardiomyopathy; left ventricular pacing; Male; Myocardial Infarction - physiopathology; Myocardial Infarction - surgery; Tachycardia, Ventricular - etiology; ventricular tachycardia
• ISSN: 1045-3873; 1540-8167
• DOI: 10.1111/j.1540-8167.2005.40764.x

Introduction: Cardiac resynchronization therapy (CRT) is a new alternative which affords symptomatic improvement in two‐thirds of patients who exhibit medically refractory congestive heart failure (CHF) as well as significant prolongation of the QRS duration (>135 msec). As more experience with CRT accrues, unexpected complications of this promising therapy may become apparent. Herein, we describe a patient with severe ischemic cardiomyopathy and refractory CHF who developed incessant ventricular tachycardia (VT) after the initiation of biventricular pacing. The patient is a 75‐year‐old man who suffered an inferior myocardial infarction 6 years before presenting for CRT. He underwent a three‐vessel CABG in 1997. Subsequently, episodes of near syncopal sustained VT developed, for which he received a dual chamber ICD. In 2001 he developed refractory CHF and ECG revealed LBBB with a QRS duration of 195 msec. Shortly after the initiation of biventricular pacing, the patient developed multiple episodes of drug resistant monomorphic VT that could be terminated only transiently by ICD therapies. Ultimately, the only intervention, which proved to be effective in eliminating VT episodes, was inactivation of LV pacing. Despite subsequent therapeutic regimen of sotalol, lidocaine, tocainide, and quinidine all subsequent attempts to reactivate LV pacing resulted in prompt VT recurrence. Conclusion: This case represents a clear example of CRT induced proarrhythmia, which required inactivation of LV pacing for effective acute management. Such an intervention should be considered in CRT patients who exhibit a notable increase in drug refractory VT episodes.