Relation of the Atrial Input Sites to the Dual Atrioventricular Nodal Pathways:

Dual AV Nodal Pathways. Introduction : The usually accepted definition of the dual pathway electrophysiology requires the presence of conduction curves with a discontinuity ("Jump"). However, AV nodal reentrant tachycardia has been ohserved in patients with "smooth" conduction curves, whereas discontinuity of the conduction curve does not guarantee induction of stable reentry. We hypothesize that the duality of AV nodal conduction can be revealed by careful choice of stimulation sites during the generation of AV nodal conduction curves.
Methods and Results : In 21 rabbit heart atrial-AV nodal preparations, programmed electrical stimulation with S1-S2-S3 pacing protocol was applied eitber posteriorly at the crista terminalis input site (CrT) or anteriorly at the lower interatrial septum input site (IAS), or (in 8 preparations with surgically divided input sites) at both. We found tbat in intact preparations with "smooth" conduction curves, pacing at long coupling intervals produced shorter AV nodal conductiim times from the IAS (56 ± 9.8 msec vs 69 ± I 0.1 msec; P < 0.01). At short coupling intervals, in contrast, shorter conduction times were obtained from the CrT (173 ± 21.8 msec vs 188 ± 22.8 msec; P < 0.01). This resulted in a characteristic crossing of the superimposed IAS and CrT conduction curves. After division of the inputs, the IAS site had rapid conduction to the His bundle but a longer refractory period, whereas the CrT site bad long conduction times and sborter refractory periods. Wavefronts entering the AV node from these two inputs can summate, resulting in improved conduction.
Conclusion : Pacing protocols designed to accentuate tbe asymmetry between tbe AV nodal inputs can belp to reveal tbe functional difference between tbe dual pathways and thus to better assess the properties of AV nodal conduction.     

Head-up Tilt Testing Predicts Syncope During Ventricular Tachycardia in Implantable Cardioverter Defibrillator Patients

Implantable cardioverter defibrillator (ICD) programming is usually based on results of supine electrophysiological (EP) testing. However, EP testing does not provide any information about tolerance to ICD therapy in the upright posture. We hypothesized that in addition to the arrhythmia duration and ventricular tachycardia (VT) cycle length, cerebral perfusion may play a role in determining tolerance to tiered ICD therapy. Transcranial Doppler (TCD) and cerebral venous oxygen saturation (rCVOS) are relatively new noninvasive techniques that may be used to assess dynamic changes in cerebral blood flow and metabolism during VT. Sixteen patients with pace-terminable VT and ICDs underwent supine (S) and upright tilt (HUT) ICD testing in conjunction with TCD and rCVOS monitoring. ICDs were programmed to deliver antitachycardia pacing, cardioversion, and defibrillation for VT, in the ascending order of aggressivity. Despite no significant differences in the induced VT cycle length (320 ± 100 msec, S, vs 330 ± 90 msec, HUT) and VT duration (14.6 ± 6.7 sec, S, vs 17 ± 9.2 sec, HUT), cerebral perfusion was more significantly impared during HUT (21 ± 10 [S] vs 29 ± 7% decrease from baseline [HUT], P < 0.001), and rCVOS decreased from baseline (5 ± 6 [S] vs 10 ± 6 [HUT] %, P < 0.001). Five of 16 patients experienced syncope during HUT and none during supine testing. At 1-year follow-up five patients who experienced syncope during HUT experienced at least one episode of syncope, whereas none not so identified did. We conclude that: (1) Supine ICD testing is insufficient to predict individual patient tolerance to ICD therapy; (2) HUT testing predicts tolerance to ICD therapy; and (3) noninvasive neuromonitoring techniques are useful for assessment of cerebral blood flow and metabolism during ICD testing.     

Is Defibrillation Testing Safe?

Determination of defibrillation thresholds (DFTs) and implantable cardioverter defibrillalur (ICD) testing requires repeated inductions of ventricular fibrillation (VF) and defibrillation attempts using known energy outputs. Little is known about the individual and cumulative effects of repetitive brief episodes of VF and hypoperfusion on cerebral function. The potential clinical utility of quantitative electroencephalographic (QEEG) monitoring during intraoperative ICD testing, by using processed 19-channel EEG (0.5–35 Hz bandwidth), was examined in ten anesthetized patients, five males and five females (mean age 62 ± 10 years), who underwent ICD implantation and testing. Ischemic QEEG patterns were defined as those with a 3 standard deviation increase (P < 0.01) in absolute delta (1.5–3.5 Hz) power persisting for ≥ 2.5 minutes. The majority (80%) of the VF episodes (70) were accompanied by QEEG "slowing" (doubling of the pre-VF low frequency delta waves amplitude). All the patients (5/5) experiencing > 6 VF episodes showed a statistically significant increase in the low frequency amplitude. In contrast, this EEG abnormality was apparent in only one of five patients experiencing < 6 VF episodes. These results suggest a cumulative QEEG depression associated with ICD testing. QEEG may provide an objective means for establishing an individualized upper safe limit of DFT testing and the total number of induced VF episodes.     

Report of the NASPE Policy Conference on Antibradycardia Pacemaker Follow-Up: Effectiveness, Needs, and Resources

On May 4–5, 1993, a policy conference was held in San Diego, California, under the sponsorship of the North American Society of Pacing and Electrophysiology (NASPE) to identify the fundamental goals of antibradycardia pacemaker follow-up, evaluate the effectiveness with which it achieves those goals, and formulate specific recommendations as to how it can be made more effective. The conference addressed clinical, administrative, and educational objectives, focusing on existing and potential resources for follow-up testing and the appropriate frequency of their application. The training of physicians and associated professionals engaged in follow-up also was addressed, as were regulatory and reimbursement issues. This report summarizes the conclusions and recommendations arrived at during the conference and subsequently approved by the NASPE Board of Trustees.     

Implanted Automatic Defibrillators: Effects of Drugs and Pacemakers

The automatic implantable cardioverter defibrillator is an effective device for prevention of sudden cardiac death. Patients who require the implantation of the device often require permanent pacing for symptomatic bradyarrhythmias and may require antiarrhythmic drug therapy. Antiarrhythmic drugs may alter the defibrillation thresholds, arrhythmia cycle length and frequency, pacing thresholds and postshock excitability. Interactions between the defibrillator and the pacemaker may result in sensing problems, leading to multiple counting and inappropriate shocks, or ventricular fibrillation nondetection, sensing or capture failure post defibrillation and pacemaker reprogramming induced by defibrillator discharge. The potential for interactions will increase as the new generation of programmable defibrillators become clinically available, combining features of permanent pacemakers, antitachycardia pacemakers and defibrillators.     

Actual Pacemaker Longevity: The Benefit of Stimulation by Automatic Capture Verification

Background: We evaluated the impact of an algorithm for automatic right ventricular (RV) stimulation compared to fixed‐output pacing (FOP) stimulation on actual pacemaker longevity over a 9‐year follow‐up. Methods: Prospective observation of 300 patients implanted with VDDR/DDDR pacemakers in 1999–2000 up to October 31, 2008. Sixty‐one patients were paced by Autocapture? pacing (ACP), 239 were paced by FOP; they were seen twice yearly at the pacemaker clinic. Factors known to affect pacemaker longevity were collected: median heart rate, %A&V paced activity, pacing output, and impedance. Patients dead before pacemaker replacement, lost to follow‐up, or who developed permanent atrial fibrillation were excluded from analysis. Results: One hundred twenty‐six of three hundred patients completed the study. Adverse clinical events due to an increased RV threshold occurred in two FOP patients compared to none among ACP. Pacemaker replacement occurred in 1/34 ACP patients versus 60/92 FOP patients (P < 0.001). ACP was the single independent predictor of pacemaker longevity at multivariable analysis (hazard ratio = 0.03, P < 0.001) either in the overall population or in the specific patients subgroups (sick sinus syndrome, atrioventricular block, and neurally mediated syncope). Conclusions: Automatic verification of stimulation is reliable at long term, and warrants superior safety in the event of pacing threshold changes. It allows a significant longevity increase compared to FOP stimulation that may heavily impact the patients’ quality of life and the cost of pacing therapy. Moreover, it is a fundamental technology in a strategy of remote patient and device monitoring, and may enable automatic device follow‐up operated by trained, nonmedical personnel. (PACE 2010; 873–881)     

Effects of Systolic Atrial Function on Plasma Renin Activity and Natriuretic Peptide Secretion after High Rate Atrial and Ventricular Pacing in Dogs

Rapid atrial rates cause electrical, structural remodeling, and neuro-humoral changes. This study compares the effects of mechanical remodeling on plasma renin activity (PRA) and atrial natriuretic peptide (ANP) secretion. Eight beagles were subjected to rapid atrial pacing (AP) at 400 beats/min for 16 days. After complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of equal duration. Left atrial systolic maximal dimension (LAmax) and left atrial appendage (LAA) peak late emptying velocity (LAA-E) were assessed by echocardiography. Blood samples were taken from the right atrium and from the peripheral vein. LAmax after AP and VP enlarged significantly (2.16 ± 0.21 cm vs 2.41 ± 0.23 cm, P = 0.002). Compared with baseline, LAA-E velocities were significantly reduced (0.65 ± 0.12 m/s vs 0.26 ± 0.16 m/s, P = 0.001) after AP only. AP caused a significant elevation of PRA in right atrial (9.28 ± 4.23 nmol/L per hour) and peripheral samples compared with baseline values (4.82 ± 2.53 nmol/L per hour, P = 0.04). ANP levels increased after AP (1117.12 ± 252.21 fmol/L) with respect to baseline values (824.37 ± 159.08 fmol/L, P = 0.001). There was no difference in PRA and ANP levels between atrial and peripheral samples. Atrial size and impaired systolic appendage function play an important role in secretion of PRA and ANP. Both neuro-humoral pathways may be therapeutic targets in the treatment of patients with AF.     

Impact of anesthetic agents on cerebrovascular physiology in children

The role of the pediatric neuroanesthetist is to provide comprehensive care to children with neurologic pathologies. The cerebral physiology is influenced by the developmental stage of the child. The understanding of the effects of anesthetic agents on the physiology of cerebral vasculature in the pediatric population has significantly increased in the past decade allowing a more rationale decision making in anesthesia management. Although no single anesthetic technique can be recommended, sound knowledge of the principles of cerebral physiology and anesthetic neuropharmacology will facilitate the care of pediatric neurosurgical patients.