“…The appearance of pacemaker syndrome in the dual-chamber mode can be explained by recordings of left-atrial activity, e.g. by transoesophageal ECGs 38 . These show an interatrial conduction delay (IACD) in a significant number of patients, particularly if they are elderly 39 or if left-atrial dilatation is present.…”
Section: Consequences Of Ddd Pacing With Nominal Av Delaymentioning
confidence: 99%
“…40 However, IACD can postpone left-atrial activation by 130 ms or more. 38,39,41 Thus, with a programmed AV delay of 120 ms (nominal value in many dual-chamber pacemakers), left-sided AV intervals can be very short if intraventricular conduction is normal ( Fig. 4) and may even be negative ( Fig.…”
Section: Consequences Of Ddd Pacing With Nominal Av Delaymentioning
confidence: 99%
“…4) and may even be negative ( Fig. 5), 38 i.e. left-atrial activation occurs after ventricular pacing.…”
Section: Consequences Of Ddd Pacing With Nominal Av Delaymentioning
confidence: 99%
“…Thus, in this case, ventricular stimulation occurs before left-atrial activity if the AV delay is programmed to 150 ms. Only after prolongation of the AV delay to 270 ms, left-atrial activation occurs just before the ventricular pacing spike. With permission from Ismer et al38…”
Asynchronous ventricular pacing has been shown to increase the risk of development of atrial fibrillation (AF) because of various mechanisms: retrograde atrioventricular (AV) conduction with increase in atrial pressure causing acute atrial stretch and reverse flow in the pulmonary veins, mitral regurgitation, reduced coronary blood flow, adverse neuroendocrine reactions, etc. Dual-chamber pacing preserves atrioventricular synchrony. However, in randomized multicentre trials comparing VVI(R) with DDD(R) pacing, AF is only slightly less frequent in the dual-chamber mode. This is most likely due to unnecessary ventricular pacing, which is frequent in dual-chamber pacing. At nominal values, dual-chamber devices usually do not permit intrinsic AV conduction but promote delivery of the ventricular stimulus at an inappropriate time in an inappropriate place. Programming of long AV delays facilitates spontaneous AV conduction but usually cannot completely avoid unnecessary ventricular pacing and causes other problems in the dual-chamber mode. Atrial septal lead placement can improve left-sided AV synchrony and promote spontaneous AV conduction. Programming of the AAI(R) mode is superior to the dual-chamber mode but cannot be used if AV conduction is impaired intermittently or permanently. Therefore, dedicated algorithms enhancing spontaneous AV conduction in the dual-chamber mode are desirable for a large proportion of pacemaker patients.
“…The appearance of pacemaker syndrome in the dual-chamber mode can be explained by recordings of left-atrial activity, e.g. by transoesophageal ECGs 38 . These show an interatrial conduction delay (IACD) in a significant number of patients, particularly if they are elderly 39 or if left-atrial dilatation is present.…”
Section: Consequences Of Ddd Pacing With Nominal Av Delaymentioning
confidence: 99%
“…40 However, IACD can postpone left-atrial activation by 130 ms or more. 38,39,41 Thus, with a programmed AV delay of 120 ms (nominal value in many dual-chamber pacemakers), left-sided AV intervals can be very short if intraventricular conduction is normal ( Fig. 4) and may even be negative ( Fig.…”
Section: Consequences Of Ddd Pacing With Nominal Av Delaymentioning
confidence: 99%
“…4) and may even be negative ( Fig. 5), 38 i.e. left-atrial activation occurs after ventricular pacing.…”
Section: Consequences Of Ddd Pacing With Nominal Av Delaymentioning
confidence: 99%
“…Thus, in this case, ventricular stimulation occurs before left-atrial activity if the AV delay is programmed to 150 ms. Only after prolongation of the AV delay to 270 ms, left-atrial activation occurs just before the ventricular pacing spike. With permission from Ismer et al38…”
Asynchronous ventricular pacing has been shown to increase the risk of development of atrial fibrillation (AF) because of various mechanisms: retrograde atrioventricular (AV) conduction with increase in atrial pressure causing acute atrial stretch and reverse flow in the pulmonary veins, mitral regurgitation, reduced coronary blood flow, adverse neuroendocrine reactions, etc. Dual-chamber pacing preserves atrioventricular synchrony. However, in randomized multicentre trials comparing VVI(R) with DDD(R) pacing, AF is only slightly less frequent in the dual-chamber mode. This is most likely due to unnecessary ventricular pacing, which is frequent in dual-chamber pacing. At nominal values, dual-chamber devices usually do not permit intrinsic AV conduction but promote delivery of the ventricular stimulus at an inappropriate time in an inappropriate place. Programming of long AV delays facilitates spontaneous AV conduction but usually cannot completely avoid unnecessary ventricular pacing and causes other problems in the dual-chamber mode. Atrial septal lead placement can improve left-sided AV synchrony and promote spontaneous AV conduction. Programming of the AAI(R) mode is superior to the dual-chamber mode but cannot be used if AV conduction is impaired intermittently or permanently. Therefore, dedicated algorithms enhancing spontaneous AV conduction in the dual-chamber mode are desirable for a large proportion of pacemaker patients.
BackgroundR-wave synchronised atrial pacing is an effective temporary pacing therapy in infants with postoperative junctional ectopic tachycardia. In the technique currently used, adverse short or long intervals between atrial pacing and ventricular sensing (AP–VS) may be observed during routine clinical practice.ObjectivesThe aim of the study was to analyse outcomes of R-wave synchronised atrial pacing and the relationship between maximum tracking rates and AP–VS intervals.MethodsCalculated AP–VS intervals were compared with those predicted by experienced pediatric cardiologist.ResultsA maximum tracking rate (MTR) set 10 bpm higher than the heart rate (HR) may result in undesirable short AP–VS intervals (minimum 83 ms). A MTR set 20 bpm above the HR is the hemodynamically better choice (minimum 96 ms). Effects of either setting on the AP–VS interval could not be predicted by experienced observers. In our newly proposed technique the AP–VS interval approaches 95 ms for HR > 210 bpm and 130 ms for HR < 130 bpm. The progression is linear and decreases strictly (− 0.4 ms/bpm) between the two extreme levels.ConclusionsAdjusting the AP–VS interval in the currently used technique is complex and may imply unfavorable pacemaker settings. A new pacemaker design is advisable to allow direct control of the AP–VS interval.
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