Clin Res Cardiol 100, Suppl 1, April 2011

P404 - Transvenous Phrenic Nerve Stimulation to Treat Central Sleep Apnea in a Heart Failure Population: An Early Experience
 
O. Oldenburg1, D. Michalkiewicz2, D. Czarnecka3, B. Bart4, A. Hasan5, T. Bitter1, K.-J. Gutleben1, W. T. Abraham5, D. Horstkotte1, P. Ponikowski6
 
1Kardiologische Klinik, Herz- und Diabeteszentrum NRW, Ruhr-Universität Bochum, Bad Oeynhausen; 2Central Military Institute, Warsaw, Polen; 3Jagiellonian University, Krakow, Polen; 4Hennepin County Medical Center, Minneapolis, Minnesota, USA; 5Ohio State University, Columbus, Ohio, USA; 64th Military Hospital, Wroclaw, Polen;
 
Introduction: Central Sleep Apnea (CSA) is strongly associated with heart failure (HF) with a prevalence approaching 40% in this patient population. There is growing evidence that CSA contributes to the progression of HF and an increase in morbidity and mortality. There is evidence that CSA also decreases time to first appropriate defibrillator shock in HF patients carrying defibrillators. Treatment today focuses on mask-based therapies requiring patient acceptance and compliance. Stimulation of the phrenic nerve is a new therapeutic option to overcome the cycle of sleep apnea and recurrent episodes of hypoxia. We evaluated whether  unilateral stimulation of the phrenic nerve may restore natural breathing patterns and reduce hypopneas/apneas in pts with CSA and present updated data from the yet completed feasibility trial.
Methods: Sixteen male HF patients (age: 56.6 ±11.7 years, NYHA I-III, LVEF: 30.2± 12%) with predominantly CSA sleep disordered breathing (>50% of apneas in CSA pattern) by prior testing were studied. Twenty-five percent of patients had a concomitant device. The patients underwent temporary implantation of a transvenous lead in either the left pericardiophrenic vein or the brachiocephalic vein. Patients were studied with both a control and treatment period. In all 16 patients, the phrenic nerve was successfully stimulated during periods of CSA.
Results: Overall apnea/hypopnea index (AHI) decreased from 47.2±11.5 to 24.4±15 (p=0.002).  Central apnea index decreased from 25.1±13.8 to 3.0±4.0 (p<0.001).  Oxygen desaturation index (ODI 4%) decreased from 30.8±10.7 to 15.6±12.1 (p=0.002). Patients tolerated therapy well and mean arousals decreased from 32/hr to 16.4/hr (p=0.001) There was also a decrease in mean heart rate (bpm) from 73.3 to 71.1 (p=0.0316) suggesting a therapy-associated acute reduction in sympathetic activation. No adverse events or reports of patient discomfort and no significant changes in obstructive apneas or hypopneas were observed.
Conclusions: In this feasibility study, acute phrenic nerve stimulation significantly improved AHI and oxygenation.  This may lead to a novel treatment approach for CSA in HF.
 
Clin Res Cardiol 100, Suppl 1, April 2011
Zitierung mit Vortrags- oder Posternummer s.o.
DOI 10.1007/s00392-011-1100-y

http://www.abstractserver.de/dgk2011/ft/abstracts/P404.htm