scholarly journals High-voltage impedance rise; mechanism and management in patients with transvenous implantable cardioverter-defibrillators: a case series

2019 ◽  
Vol 3 (4) ◽  
pp. 1-8
Author(s):  
Christopher Monkhouse ◽  
Alex Cambridge ◽  
Anthony W C Chow ◽  
Jonathan M Behar
Keyword(s):  
High Voltage ◽  
Low Voltage ◽  
Case Series ◽  
Left Ventricular ◽  
Boston Scientific ◽  
Implantable Cardioverter Defibrillators ◽  
Historical Cohort ◽  
Current Output ◽  
Gradual Rise ◽  
Cardioverter Defibrillators

Abstract Background We describe a case series of patients for a gradual rise in daily, low-voltage sub-threshold measurement (LVSM) of shock (high-voltage, HV) impedance in a group of patients with Boston Scientific implantable cardioverter-defibrillators (ICDs) and investigate the cause of the abnormality. Case summary Six patients presented with a gradual rise in HV impedance above normal range (132.5 ± 20.8 Ω). Patients were young with a mean age of 29 ± 11 years, four patients had hypertrophic cardiomyopathy, one left ventricular non-compaction, and one long QT. All lead designs were silicon body with GORE polytetrafluoroethylene (ePTFE) coated coils, and a lower true shock impedance (TSI) was seen in all cases with full output synchronized shock. We compared the rate of HV impedance rise with our historical cohort of Boston ICDs using an unpaired t-test. The change in impedance per month was significantly higher amongst our six patients when compared with our cohort of Boston Scientific ICDs (3.2 ± 1.9 Ω/month vs. 0.0008 ± 0.005 Ω/month, P < 0.001). Patients were individually investigated and management discussed in a dedicated device multi-disciplinary team meeting (MDT). Discussion There are distinct differences between TSI and LVSM. The TSI is derived from a full output shock, whilst LVSM is calculated from a small current output. These cases highlight the inaccuracies of the LVSM measurement. The gradual rise in LVSM is significantly higher than the value for TSI in these patients we propose the most likely mechanism is encapsulation fibrosis surrounding the right ventricular shock coil. Management for these patients requires vigorous testing to rule out electrical failure, and replacement maybe necessary.

Cardiac Sarcoidosis

2020 ◽  
Vol 41 (05) ◽  
pp. 626-640 ◽  
Author(s):  
David H. Birnie
Keyword(s):  
Heart Failure ◽  
Cardiac Involvement ◽  
Cardiac Sarcoidosis ◽  
Positron Emission Tomography Imaging ◽  
Left Ventricular ◽  
Implantable Cardioverter Defibrillators ◽  
Heart Failure Treatment ◽  
Positron Emission ◽  
Minimal Data ◽  
Cardioverter Defibrillators

AbstractApproximately 5% of patients with sarcoidosis will have clinically manifest cardiac involvement presenting with one or more of ventricular arrhythmias, conduction abnormalities, and heart failure. It is estimated that another 20 to 25% of pulmonary/systemic sarcoidosis patients have asymptomatic cardiac involvement (clinically silent disease). Cardiac presentations can be the first (and/or an unrecognized) manifestation of sarcoidosis in a variety of circumstances. Immunosuppression therapy (usually with corticosteroids) has been suggested for the treatment of clinically manifest cardiac sarcoidosis (CS) despite minimal data supporting it. Positron emission tomography imaging is often used to detect active disease and guide immunosuppression. Patients with clinically manifest disease often need device therapy, typically with implantable cardioverter defibrillators (ICDs). The extent of left ventricular dysfunction seems to be the most important predictor of prognosis among patients with clinically manifest CS. In the current era of earlier diagnosis, modern heart failure treatment, and use of ICD therapy, the prognosis from CS is much improved. In a recent Finnish nationwide study, 10-year cardiac survival was 92.5% in 102 patients.

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