Implanted Cardiac Defibrillator and Pacemaker Lead Function in Patient With Cardiac Amyloidosis | oneAMYLOIDOSISvoice
Abstract & Posters

Implanted Cardiac Defibrillator and Pacemaker Lead Function in Patient With Cardiac Amyloidosis

key information

source: Journal of the American College of Cardiology

year: 2017

authors: Isata Sesay, Jordana Kron, Jayanthi Koneru, Keyur Shah

summary/abstract:

Introduction: 

Cardiac amyloidosis (CA) results from myocardial infiltration of amyloid proteins that leads to restrictive cardiomyopathy, heart failure, and conduction abnormalities. Low QRS voltage on surface electrocardiography is characteristic of CA, raising concern for poor R-wave sensing and elevated pacing and defibrillation thresholds in CA patients with Implantable Cardioverter Defibrillator (ICD) or pacemaker. We sought to characterize the performance of implanted pacemaker and ICD leads among a cohort of patients with cardiac amyloidosis.

Methods: 

We performed a retrospective analysis of 13 CA patients with ICD and pacemaker at Virginia Commonwealth University. Lead sensing, impedance, and capture threshold parameters were collected at implant and scheduled follow-up in 6-8 weeks and every 6 months thereafter. Mean follow-up was 17 months. Significant changes in lead parameters were defined as a 50% reduction in sensed electrograms, > 50 ohms change in pacing impedance, and > 2-fold increase in chronic pacing threshold.

Results: 

Nine patients had dual-chamber ICD, two had biventricular ICD, one had single right ventricle lead ICD, one had a pacemaker. The mean LV ejection fraction was 38 ± 14%. We observed significant changes in lead impedance in 2 patients. However, they did not require lead revision for evidence of lead failure.

There were no significant changes in capture threshold or sensed amplitude of electrograms from implantation to follow-up period.

100% of patients who met criteria for low voltage on EKG (n=5), had a trend towards decreased R-wave sensing.

While not significant, we observed a decrease in RV sensing overtime in 6 patients; R waves decreased by an average of 30% in all 6 patients.

Three patients (23%) had R waves < 5 mV at implantation despite extensive mapping of the RV septum. However, defibrillation testing was not performed due to concern for inability to terminate ventricular fibrillation.

Conclusions: 

We observed significant changes in lead impedance and a trend towards decreased R-wave sensing amplitude at follow-up. This could have important implications for ventricular arrhythmia detection by ICDs or pacemakers in these patients.

organization: Virginia Commonwealth University, USA

DOI: 10.1016/S0735-1097(17)33900-1

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