Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • Fig shows an example of RNRVAS in a dual chamber

    2019-04-28

    Fig. 3 shows an example of RNRVAS in a dual-chamber pacemaker recipient with sinus node disease, with the pacemaker set in rate adaptive DDI-R mode pacing with an AV interval of 300ms and lower rate limit of 60ppm. The tracing shows sensor-driven DDIR pacing at 80bpm (V–V Sephin 1 length=750ms). Ventricular captures are conducted in a retrograde manner through the AV node, and the atrial events are sensed within the PVARP after a 220-ms VA conduction time. Rate adaptive atrial pacing is driven by a sensor at a rate of 80ppm. Since the interval between the sensed retrograde P wave within the PVARP and the next atrial paced event is only 200ms, the pacing stimulus does not capture the atrium. Ventricular pacing follows ineffective atrial pacing at the programmed AV delay of 320ms. RNRVAS continues as long as the sensor-driven rate response is >80ppm. However, after gradual slowing of sensor-driven pacing, the interval between the sensed P wave within the PVARP and the atrial paced event lengthens to >250ms, allowing successful capture of the atrium (⁎), return to intrinsic AV conduction, and then terminate without VA conduction [23]. In this case, RNRVAS was induced with rate adaptive DDI-R pacing and observed in the setting of acceleration of sensor-driven DDD or DDDR dual-chamber pacing with long AV intervals [17,19]. Another example of RNRVAS, induced by the AOP algorithm set for the prevention of AF in DDD mode, is shown in Fig. 4[3,14]. The retrograde P wave after ventricular pacing falls within the PVARP, activating the AOP algorithm. Since the interval between the sensed retrograde P wave and the next atrial paced event initiated by the AOP algorithm is very short, the atrial pacing stimulus falls in the atrial refractory period and fails to capture the atrium. Ventricular pacing after a programmed AV interval long enough for recovery of the atrial myocardium allows repetitive VA conduction and perpetuation of RNRVAS. While RNRVAS is not common, it is generally observed in the presence of VA conduction and retrograde P waves sensed within the PVARP, after ventricular pacing triggers the AOP algorithm, and when a relatively long AV interval has been programmed to limit unnecessary ventricular pacing, particularly in instances of sinus node disease.
    Clinical diagnosis of RNRVAS
    Clinical implications The potential adverse effects of RNRVAS are shown in Fig. 1 and include: (1) loss of optimal AV delay, (2) inappropriate increase in ventricular pacing, (3) trigger of atrial arrhythmias, (4) inaccurate diagnosis of AHRE, and (5) loss of optimal AV conduction by automatic switch from DDD to DDI or VVI modes. These adverse effects might increase unnecessary ventricular pacing and might affect ventricular function, especially in pacemaker recipients who present with sinus node disease and preserved AV conduction. The loss of optimal AV delay with RNRVAS causing pacemaker syndrome-like symptoms has been reported [24]. Furthermore, the repetitive occurrence of RNRVAS may cause AF (Fig. 5). In this case, the transition from sustained RNRVAS to AF was confirmed.
    Summary
    Conflict of interest
    Introduction Since the implantable cardiac pacemaker was first introduced into clinical practice, various developments have been achieved in both generator and lead systems. In particular, the pacing lead is the most important part of a pacing system, because it should be functional throughout a patient׳s life, unless unexpected problems are encountered. Therefore, a high-quality lead is required to ensure longevity, safety, stability, and good electrical performance. The first experimental studies on the transvenous endocardial screw-in lead were published in 1971 in Japan by Abe et al. [1]. Six years later, the first clinical experiences with the transvenous screw-in lead were described by Kleinert and Bisping [2]. With the introduction of the screw-in lead system, atrial pacing has become feasible, and the incidence of dislodgment was dramatically reduced [3,4]. The initial concern with the screw-in lead system was the rise in acute and subacute thresholds; however, the use of the steroid tip has overcome this problem [5,6]. Recently, right ventricular apical pacing was reported to be harmful because it impaired left ventricular function due to a dyssynchronous movement: consequently, the indications for ventricular septal pacing with screw-in leads have increased in an effort to provide a hemodynamic advantage [7,8]. Thus, the screw-in lead has become indispensable in current device implantation practice. On the other hand, the risk of cardiac perforation has been sporadically reported, which might discourage some surgeons from using the screw-in leads [9]. However, the causes of perforation might be largely attributed to the implanting technique used by the surgeon, not to the actual device. Therefore, we suggest methods for safely using the Sweet Tip™ type screw-in lead.