• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • br Discussion A previous report demonstrated an adenosine se


    Discussion A previous report demonstrated an adenosine-sensitive reentrant AT not involving an AV nodal pathway in the vicinity of the apex of Koch\'s triangle, which could be ablated at the earliest atrial activation site in the right supero-septal region [3]. Otomo et al. reported a “left-variant” form of an adenosine-sensitive AT due to focal reentry involving the leftward AV nodal transitional area originating from the LCC [4]. In this case, the adenosine-sensitive AT could be induced by an atrial extrastimulus and burst pacing. However, the induced AT did not include an inverse relationship between the coupling interval of the atrial extrastimulus and the post-pacing interval of AT initiation, and in addition, spontaneous AT self-termination could be observed under an ISP infusion. Thus, we speculated that triggered activity may buy 4EGI-1 be the mechanism of this arrhythmia, although it presented some confounding characteristics consistent with a reentrant mechanism. A previous report has supported triggered activity as a mechanism of this type of AT [5]. Previous reports also showed that an AT of this type could be ablated from the NCC, possibly because of its proximity to the right superoseptum [1,6,7]. In this case, RF energy delivered from the NCC temporarily terminated the AT with a variable cycle length, and may have been located in close proximity to the AT focus in that area. As an anatomical consideration, the right atrial myocardium behind the NCC extends from the His-bundle region to a superior site of the tendon of Todaro, which is slightly anterior to the interatrial septum [8]. This AT is likely to have originated from the mitral annulus–aorta junction (M–Ao junction) [4]. The MA–Ao junction can be the source of a left antero-septal AT [9]. The curtain-like structure of the MA–Ao junction separates the left ventricular (LV) outflow tract from the LV inflow tract, which supports the NCC, posterior buy 4EGI-1 of the LCC, and anterior leaflet of the mitral valve. The remnants of the developmental specialized conduction system in this area can be the underlying AT substrate [4], and can give rise to triggered activity under the influence of catecholamines [4,10]. Furthermore, the action potentials from this musculature have AV nodal-type characteristics [4]. These unique properties can be characterized by their responsiveness to adenosine. In this case, the adenosine-sensitive non-reentrant AT could be successfully ablated from the antero-septal region of the left atrium. The right atrial supero-septal area and NCC were activated early simultaneously, and were successful sites with transient AT termination, but both areas were slightly distant from the final successful ablation site. Because the atrial septal region contains non-uniform complex multiple tissue structures, such as the compact atrioventricular node, transitional tissue, and the bundle with left and right extensions, the conduction properties around the septal area have not been fully characterized. The findings in this case imply a representation by the AT of a close linkage of conduction between the supero-septal right atrium and antero-septal left atrium. Furthermore, the rapid conduction property in the direction of the antero-septal right atrium, possibly enhanced by ISP, may preferentially facilitate bridging between both areas. Previous reports support the assumption that this kind of dominant property could be present even in patients with AT from the MA–Ao junction and/or atrioventricular nodal reentrant tachycardia [4,11]. In addition, RF energy applied at the NCC on the other end of the MA–Ao junction, which is directly connected to the AT focus, may exert a partial suppressive effect on the MA–Ao junction itself.
    Conflict of interest
    Introduction In the perinatal field, magnesium sulfate therapy is likely to remain a common management strategy for eclampsia, preeclampsia, and preterm labor [1–4]. Its mechanism of action is unclear, but more than one mechanism is likely to be involved [5,6]. It is well known that magnesium sulfate decreases the baseline and variability of fetal heart rate [2–4,7–9]. Studies have reported a substantial decrease of 2–15bpm in the baseline fetal heart rate, but there has been no report of a decrease in the baseline fetal heart rate to <100bpm after magnesium sulfate administration [2–4]. Here, we describe a rare case of fetal bradyarrhythmia following magnesium sulfate administration.