Neurocardiogenic syncope may be caused by enhanced sympathetic activity evoking a vasodepressor-cardioinhibitory reflex. Heart rate variability (HRV) methods can be used to assess the modulation of sympathetic and parasympathetic activity. To determine whether HRV measurements are related to the outcome of head-up tilt testing (HUT), we studied 29 syncopal patients aged 7-19 y. After 30 min supine, patients were tilted to 80 degrees for 30 min or until syncope occurred. Sequential beats free from ectopy were analyzed. Time domain indices included SD (SDNN), root mean square successive differences (RMSSD), percent exceeding 50 ms (pNN50). An autoregressive model was used to calculate power spectra. Low frequency power (LFP, 0.05-0.15 Hz), high frequency power (HFP, 0.15-0.40 Hz), and total power (TP, 0.01-0.40 Hz) were compared before and after tilt. Data were obtained supine before tilt (baseline), within 5 min after HUT (early), 5-10 min after HUT (mid), and 15 min after HUT or presyncope (late). Seventeen patients fainted (HUT+), and 12 patients did not (HUT-). Variability indices were different for HUT- and HUT+ at baseline: SDNN was 123 +/- 17 versus 78 +/- 6, RMSSD was 127 +/- 23 versus 64 +/- 6 ms, pNN50 was 51 +/- 6 versus 31 +/- 4, respectively. Spectral data demonstrated decreased HFP and TP in HUT+ (834 +/- 133 and 2855 +/- 420 ms2) versus HUT- (3433 +/- 840 and 7062 +/- 1500). With tilt, SDNN, RMSSD, and pNN50 decreased proportionately in HUT- and HUT+. However, sympathovagal balance, measured by the ratio LFP/HFP and by normalized LFP, was markedly increased in HUT+ (2.2 +/- 0.7 and 0.43 +/- 0.03) compared with HUT- (0.8 +/- 0.2 and 0.31 +/- 0.02) at baseline and differences increased with tilt. With syncope, sympathetic activity decreased, and parasympathetic activity increased. Decreased RR variability with decreased parasympathetic activity and increased indices of sympathovagal balance before HUT predict a positive tilt test in children referred for evaluation of neurocardiogenic syncope.
Four hundred twenty consecutive patients with symptomatic slow/fast atrioventricular nodal reentry tachycardia had attempted slow pathway radiofrequency ablation. All patients had successful slow pathway ablation and no inducible tachycardia after ablation using the standard right-sided approach except for three patients. The three unsuccessful patients had inducible slow/fast atrioventricular nodal tachycardia after attempted right-sided posterior and inferoposterior anatomic ablative techniques and with slow pathway potential electrogram guidance. Lesions were also delivered linearly in the triangle of Koch and within the coronary sinus ostium. A transseptal puncture was performed and slow pathway ablation was obtained in each of these patients. Ablation was performed from the septal mitral valve annulus, anterior to the os of the coronary sinus and inferior to the His-bundle catheter with elimination of slow pathway conduction. Prior to the ablation, two of the three patients exhibited initiation of tachycardia with a double fast/slow antegrade response, and all three patients had long AH intervals (mean 378 ms) during slow pathway conduction. These electrophysiological findings may be consistent with a large area of slow pathway conduction that may include the left atrial septum not approachable by conventional right-sided ablative techniques. Slow pathway ablation to eliminate atrioventricular nodal reentry tachycardia at times may require a left atrial/transseptal approach when conventional right-sided techniques are ineffective.
Bilateral electrical stimulation of the subthalamic nucleus is being used with increasing frequency as a treatment for severe Parkinson disease (PD). Implantable cardiac defibrillators improve survival in certain high-risk patients with coronary artery disease and ventricular arrhythmias. Because of concern about possible interaction between these devices, deep brain stimulation (DBS) systems are routinely disconnected before defibrillators are implanted in patients with PD and arrhythmia. The authors report on a patient with bilateral subthalamic stimulators who underwent successful placement of an implantable defibrillator. Testing of the devices over a wide range of settings revealed no interaction. The patient subsequently underwent multiple episodes of cardioversion when the ventricular lead became dislodged. There was no evidence of adverse neurological effects, and interrogation of the DBS devices after cardioversion revealed no changes in stimulus parameters. The outcome in this case indicates that DBS systems may be safely retained in selected patients who require implantable cardiac defibrillators.
Of 209 patients with heart failure treated with combined cardiac resynchronization therapy and implantable cardioverter-defibrillator therapy, appropriate cardioverter-defibrillator shocks occurred at 34-month follow-up in 22 of 121 patients (18%) on statins and in 30 of 88 patients (34%) not on statins (P = .009). Deaths occurred in 3 of 121 patients (2%) on statins and in 9 of 88 patients (10%) not on statins (P = .017). Stepwise Cox regression analysis showed that significant independent prognostic factors for appropriate shocks were use of statins (risk ratio = 0.46), smoking (risk ratio = 3.5), and diabetes (risk ratio = 0.34). Significant independent prognostic factors for the time to mortality were use of statins (risk ratio = 0.05), use of digoxin (risk ratio = 4.2), systemic hypertension (risk ratio = 14.2), diabetes (risk ratio = 4.3), and left ventricular ejection fraction (risk ratio = 1.1).
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