Conflict of Interest: No conflicts of interest to declare.
A Clinical Phenotype of Adverse Response to Biventricular Pacing: A Case Series
Article first published online: 10 JAN 2013
©2013, The Author. Journal compilation ©2013 Wiley Periodicals, Inc.
Pacing and Clinical Electrophysiology
Volume 36, Issue 4, pages 410–415, April 2013
How to Cite
LIM, H. S. (2013), A Clinical Phenotype of Adverse Response to Biventricular Pacing: A Case Series. Pacing and Clinical Electrophysiology, 36: 410–415. doi: 10.1111/pace.12067
- Issue published online: 2 APR 2013
- Article first published online: 10 JAN 2013
- Manuscript Accepted: 13 NOV 2012
- Manuscript Revised: 13 OCT 2012
- Manuscript Received: 5 AUG 2012
- cardiac resynchronization therapy;
- heart failure
Biventricular pacing is an established therapy for patients with heart failure with reduced left ventricular ejection fraction and prolonged QRS duration. However, there are few reports on the adverse effects of biventricular pacing.
Three patients who deteriorated rapidly following biventricular pacing (heart transplantation/ventricular assist device within 3 months of device implantation) were identified. The clinical, echocardiographic, and functional characteristics before and after device implantation were evaluated. The acute hemodynamic effects of biventricular pacing were assessed by cardiac catheterization.
Preimplant assessment showed biventricular dysfunction, pulmonary hypertension, and relatively narrow QRS duration. The time from device implantation to assessment was 62, 58, and 42 days. All three patients developed right bundle branch block (RBBB)-type QRS morphology, deterioration in right ventricular (RV) function, and functional capacity in association with rapid clinical decline. Acutely, biventricular pacing resulted in higher right atrial pressure, pulmonary wedge pressure, lower cardiac output, and RV stroke work in all three patients.
A phenotype of adverse response to biventricular pacing is characterized by relatively narrow QRS duration, RV dysfunction, and pulmonary hypertension. Clinical decline is rapid and associated with the development of RBBB-type morphology, worsening of pulmonary hemodynamics, and RV dysfunction with biventricular pacing.