65 research outputs found

    Demonstration of a Posterior Atrial Input to the Atrioventricular Node During Sustained Anterograde Slow Pathway Conduction

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    AbstractObjectives. This study sought to demonstrate electrophysiologic evidence for the existence of different anatomic atrial input sites of fast and slow conduction pathways in patients with dual atrioventricular (AV) node physiology.Background. Although a separate posterior exit site exists for a retrograde slow AV node pathway, it remains unresolved whether a separate atrial input site into the AV node actually exists in patients with dual anterograde AV node pathway physiology.Methods. In 10 patients with dual AV node pathway physiology, atrial pacing at three chosen drive cycle lengths (DCL1, DCL2 and DCL3) was performed at an anterior site (A) just above the His bundle recording site and at a posterior atrial site (P) just below the coronary sinus ostium. DCL3 was chosen as the one cycle length that resulted in a long AH interval consistent with slow pathway conduction. The stimulus to His bundle conduction times (SH) at both sites (SHPand SHA, respectively) and their differences (ΔSH = SHP− SHA) at each of the three drive cycle lengths were analyzed.Results. The mean ± SD ΔSH values for DCL1 and DCL2 measured 9 ± 16 and 8 ± 18 ms, respectively, and the mean ΔSH value at DCL3 measured −34 ± 24 ms, which was significantly different from the mean ΔSH values at DCL1 and DCL2 (both p < 0.05).Conclusions. The significant change in the ΔSH (SHP− SHA) value during slow pathway conduction could be accounted for by a corresponding shift of anterograde input from an anterior to a posterior entry site to the AV node. These findings support the notion that a separate anterograde entry site of the slow pathway does exist in patients with dual AV node pathway physiology

    Clinical significance of ventricular fibrillation-flutter induced by ventricular programmed stimulation

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    Two hundred twenty-four patients underwent ventricular programmed stimulation (VPS) without prior documentation of the clinical occurrence of sustained ventricular tachycardia (VT) or ventricular fibrillation-flutter (VF). Indications for VPS were: palpitations or nonsustained VT during ambulatory monitoring (85 patients), syncope or presyncope (137 patients), and a family history of sudden death (two patients). Sustained VF requiring transthoracic defibrillation was initiated by VPS in 18 patients (8.0%). Four patients were treated for inducible VF with antiarrhythmic agents directed by electropharmacologic testing; five patients were treated empirically; nine patients received no therapy. No patient has had a cardiac arrest or sudden death during a follow-up period of 25.2 +/- 13.8 months (mean +/- standard deviation). VF was initiated by two ventricular extrastimuli in three patients and by three extrastimuli in 15 patients. The incidence of VF was similar in patients with and without previous symptoms (8.8% vs 6.9%) or heart disease (7.1% vs 9.6%). It was significantly higher when VPS at three ventricular sites with a current of 5 mA (pulse width 2 msec) was compared to programmed stimulation at two ventricular sites with a current twice diastolic threshold (pulse width 2 msec) (15.2% vs 3.0%, p &lt; 0.05). VF initiated by VPS in patients without prior VT or VF appears to be a nonspecific finding. Antiarrhythmic therapy for VF may not be necessary in these patients.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25695/1/0000249.pd
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