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LOW AMPLITUDE VAGUS NERVE STIMULATION AFFECTS HEART RATE AND NEUROHORMONES IN HUMANS
A16.E154 JACC March 9, 2010 Volume 55, issue 10A
CARDIAC FUNCTION AND HEART FAILURE LOW AMPLITUDE VAGUS NERVE STIMULATION AFFECTS HEART RATE AND NEUROHORMONES IN HUMANS ACC Oral Contributions Georgia World Congress Center, Room B408 Monday, March 15, 2010, 5:15 p.m.-5:30 p.m.
Session Title: Novel Electrical Stimulation Therapies in Heart Failure Abstract Category: Myocardial Function/Heart Failure--Clinical Nonpharmacological Treatment Presentation Number: 0913-06 Authors: Katherine Fan, Raymond Yee, Lorna Gula, Cathy Bentley, Avram Scheiner, Sum Lam, Macrina Wong, Maria Parke, Ruth Nicholson Klepfer, Allan Skanes, Grantham Hospital, Aberdeen, Hong Kong, London Health Sciences Center University Hospital, London, ON, Canada Background: Direct Vagus Nerve Stimulation (VNS) has shown promising results as a heart failure (HF) therapy. Amplitudes used clinically for VNS typically result in laryngeal vibration (LVib). We conducted an acute study to evaluate the cardiac and systemic effects of VNS in the internal jugular vein (IJV) at amplitudes that produce LVib. Methods: Thirty subjects indicated for an electrophysiology study were enrolled. A decapolar catheter was placed in the IJV. VNS (20Hz, 500μs) was delivered at various locations and amplitudes (1.9±1.6mA) for 15-20s. Catheters were placed in the right atrium and ventricle, and 12 lead ECG was collected. Medians of the first and last 5s of intervals during normal sinus rhythm (NSR) and VNS were compared. In a subset of patients (n=11), serum catecholamines were measured before and after 10 minutes of VNS and compared. Results: There is a small but statistically significant reduction in heart rate in the first 5s of VNS compared to NSR (Table 1). There was no effect on cardiac intervals in the last 5s of VNS, suggesting this effect is transient. No significant change in catecholamines due to VNS were observed across all subjects. However, there was a decrease in venous norepinephrine during VNS in subjects with HF (n=4) (-75±74 pg/mL) that was significantly different than the response in non-HF subjects (N=7) (9±51 pg/mL, p=0.035). Conclusions: We conclude that transvenous low amplitude VNS effects efferent cardiac fibers and exerts systemic neurohormonal effects in heart failure.
CARDIAC FUNCTION AND HEART FAILURE LOW AMPLITUDE VAGUS NERVE STIMULATION AFFECTS HEART RATE AND NEUROHORMONES IN HUMANS ACC Oral Contributions Georgia World Congress Center, Room B408 Monday, March 15, 2010, 5:15 p.m.-5:30 p.m.
Session Title: Novel Electrical Stimulation Therapies in Heart Failure Abstract Category: Myocardial Function/Heart Failure--Clinical Nonpharmacological Treatment Presentation Number: 0913-06 Authors: Katherine Fan, Raymond Yee, Lorna Gula, Cathy Bentley, Avram Scheiner, Sum Lam, Macrina Wong, Maria Parke, Ruth Nicholson Klepfer, Allan Skanes, Grantham Hospital, Aberdeen, Hong Kong, London Health Sciences Center University Hospital, London, ON, Canada Background: Direct Vagus Nerve Stimulation (VNS) has shown promising results as a heart failure (HF) therapy. Amplitudes used clinically for VNS typically result in laryngeal vibration (LVib). We conducted an acute study to evaluate the cardiac and systemic effects of VNS in the internal jugular vein (IJV) at amplitudes that produce LVib. Methods: Thirty subjects indicated for an electrophysiology study were enrolled. A decapolar catheter was placed in the IJV. VNS (20Hz, 500μs) was delivered at various locations and amplitudes (1.9±1.6mA) for 15-20s. Catheters were placed in the right atrium and ventricle, and 12 lead ECG was collected. Medians of the first and last 5s of intervals during normal sinus rhythm (NSR) and VNS were compared. In a subset of patients (n=11), serum catecholamines were measured before and after 10 minutes of VNS and compared. Results: There is a small but statistically significant reduction in heart rate in the first 5s of VNS compared to NSR (Table 1). There was no effect on cardiac intervals in the last 5s of VNS, suggesting this effect is transient. No significant change in catecholamines due to VNS were observed across all subjects. However, there was a decrease in venous norepinephrine during VNS in subjects with HF (n=4) (-75±74 pg/mL) that was significantly different than the response in non-HF subjects (N=7) (9±51 pg/mL, p=0.035). Conclusions: We conclude that transvenous low amplitude VNS effects efferent cardiac fibers and exerts systemic neurohormonal effects in heart failure.