Archives

  • 2018-07
  • 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
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • br Materials and methods br Results We observed

    2019-05-13


    Materials and methods
    Results We observed 3 patterns of response to PHP. Pattern 1, observed in 56% of patients (nos. 4, 6, 7, 8, and 9), was characterized by S–A and V–A intervals in the septal region that were identical whether HB was captured or not, along with an unchanged atrial activation sequence (Fig. 1). In these 5 patients, a local ventricular electrogram was visible on the CS recording near the AP. Pattern 2 (AP/APL in the study by Hirao et al. [1]), observed in patient nos. 1 and 5 (22% of the study sample), was characterized by a loss of HB capture associated with an increase in the S–A interval without change in the atrial activation sequence or the V–A interval near the AP due to an increase in the S–V interval (Fig. 2). Pattern 3, observed in patient nos. 2 and 3 (22% direct renin inhibitors of the study sample), was characterized by a loss of HB capture associated with an increase in the S–A interval, as in pattern 2. However, in pattern 3 patients, neither the S–V nor the V–A interval near the AP could be measured, as the ventricular electrogram was invisible on the CS recording even when ventricular sensitivity was enhanced to a maximum level of 0.1mV/cm or the CS catheter was adjusted to obtain the local ventricular electrogram (Fig. 3). These observations are summarized in Tables 1 and 2. A mixed pattern expressing retrograde conduction over an AP and over the AV direct renin inhibitors was not observed in any patients. Following the AP ablation procedure, VA conduction persisted in patient nos. 2, 4, 5, and 8. In these 4 patients, ventricular burst and premature stimulation revealed decremental retrograde conduction, consistent with the AV node.
    Discussion Retrograde conduction over a posteroseptal AP was accurately identified in 7 of the 9 patients (78%), whereas in 2 patients (22%), retrograde AP conduction was not identifiable because of the absence of a visible ventricular electrogram near the AP. CS recordings provide important information needed to locate a left-sided AP [11] and measure the V–A interval near the AP during PHP [1], since in a majority of patients, atrial and ventricular electrograms can be recorded simultaneously [12]. Since the CS is immediately adjacent to the atrial myocardium, although Pleistocene is separated from the ventricular myocardium by a layer of fat [13–16], the amplitude of the ventricular electrograms recorded from the CS is usually <50% of the atrial electrogram amplitude, and their morphological characteristics are those of far-field signals, such as a lower amplitude with a narrower electrode spacing and a low signal frequency [12]. Furthermore, as in 2 of our patients, the far-field ventricular electrograms may not be visible from the CS, especially in the left posteroseptal region, probably because it is too distant from the mitral annulus [13–15]. Shortening of the S–A interval associated with capture of the HB, as observed in patterns 2 and 3, is due to conduction over the His–Purkinje system and earlier activation of the ventricular myocardium near the AP [1–3]. This observation is more likely in patients with a left lateral or anterolateral AP located far from the site of PHP [1], although it does occur in a minority of patients with a posteroseptal AP [1]. In the present study, a shortening of the S–A interval associated with capture of the HB was observed in 44% of our patients, suggesting that this phenomenon is not rare, even in patients with a posteroseptal AP. We hypothesize that when present in a patient with a posteroseptal AP, it is the result of a variation in the distribution of a septal branch toward the posterior septum [17,18]. In these patients, capture of the HB results in earlier activation of the ventricular posteroseptal myocardium near the AP, which shortens the S–A interval (Fig. 4). Theoretically, this phenomenon may be less likely to occur in patients with a “right-sided” posteroseopal AP than a “left-sided” posteroseptal AP because (1) the PHP site is closer to the right-sided posteroseptum than the left-sided posteroseptum, and (2) at least the proximal portion of the right bundle branch had no branching structure. In the present study, APs were successfully ablated on the mitral annulus or inside the CS in 4 patients in whom pattern 2 or 3 was observed, consistent with a “left-sided” AP.