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
  • 2024-05
  • 2024-06
  • 2024-07
  • 2024-08
  • 2024-09
  • 2024-10
  • In summary we present a

    2019-05-07

    In summary, we present a rare case of magnesium sulfate-induced fetal bradyarrhythmia caused by prolongation of the refractory period of the atrioventricular node in the case of blocked premature atrial contractions. Clinicians should consider fetal bradyarrhythmia when the baseline fetal heart rate drops to <100bpm after magnesium sulfate administration.
    Conflict of interest
    Financial support
    Introduction Action potential duration (APD) alternans is a well-recognized phenomenon that occurs at rapid rates of stimulation and after an abrupt shortening of the cardiac cycle [1–8]. When the rate of stimulation is constant, the short nobiletin during alternans is followed by a longer diastolic interval and the long action potential is followed by a shorter diastolic interval. These differences in diastolic interval may be responsible for the occurrence and maintenance of APD alternans. Alternation in APD may result in alternation of the refractory period, which may become the basis of arrhythmias. The demonstration of ventricular APD alternans has been confined to experimental animal models [1,8–13], with the phenomenon being documented in only a few humans [14,15]. We sought to determine whether an increase in heart rate could induce APD alternans during clinical electrophysiologic study.
    Methods
    Results RV MAPD alternans was observed (Figs. 1–3) during RV pacing in 3 of the 45 patients. These 3 patients were among the oldest (77, 75, and 71 years) in the study group, and 2 of the 3 patients were women. Patient 1 (77-year-old woman) showed MAPD alternans at pacing CLs of 350 and 300ms (Fig. 1). Patient 2 (75-year-old man) showed MAPD alternans at a CL of 350ms (Fig. 2). The pacing CL was not decreased in this patient because of marked MAPD alternans at this CL. Patient 3 (71-year-old woman) showed MAPD alternans at pacing CLs of 350, 300, and 275ms (Fig. 3). QRS duration did not alternate at the pacing CLs at which MAPD alternans was observed in these 3 patients.
    Discussion We observed ventricular action potential alternans in 3 of 45 patients (6.7%) during rapid ventricular pacing. MAPD alternans in these 3 patients was observed at the beginning of pacing and lasted for approximately 5s, and the duration of MAPD alternans increased at the shorter pacing CL in patients 1 and 3. MAPD alternans for a short time (<10 beats) was observed in some other patients, but we did not consider these patients as MAPD-alternans positive. Occurrence of APD alternans has been well documented at rapid rates of stimulation and after abrupt shortening of the cardiac cycle in in-vitro and in-vivo animal studies [1–13]. Sutton et al. reported action potential alternans from the left ventricular epicardium before bypass surgery in 3 of 36 patients (8.3%) undergoing routine cardiac surgery [14]. We reported action potential alternans in the RV outflow tract in a patient with asymptomatic Brugada syndrome at a pacing CL of 400ms [15]. QRS wave and ST-T wave alternans were not observed when RV MAP alternans was recorded in the present study. Sutton et al. speculated that alternans is localized to small areas and, as such, by virtue of the recording technique, has been underestimated in the patient population as a whole [14]. The localized nature of this phenomenon and/or small change in the APD may explain the absence of any evidence of alternans on routine electrocardiography during atrial or ventricular pacing and suggests that clinical electrocardiography may not detect this potentially pre-arrhythmic condition in clinical settings.
    Conclusion
    Conflict of interest
    Case report A 60-year-old woman was referred to us because of sinus bradycardia with recurrent syncope. The electrocardiogram (ECG) recorded at presentation (Fig. 1) showed mild sinus bradycardia with varying P–P intervals and a pattern of grouped beating. Gradual shortening of the P–P interval over 3 beats followed by a long pause, which was less than twice the shortest P–P interval, suggested second-degree type 1 sinoatrial (SA) block. In addition, the PR interval was prolonged in the beats after the pause (shown by an asterisk). A prolonged PR interval after pauses was also consistently seen in the other recorded ECGs. J-point elevation was also noted in the right precordial leads; however, the T wave was upright in V2, making this a type-II Brugada ECG pattern and likely a normal variant. An electrophysiological study was performed, during which complete atrioventricular (AV) block was seen to occur after a pause following a spontaneous premature atrial complex (Fig. 2). Intracardiac recording of the His bundle electrogram showed that the AV block occurred below the His bundle (Fig. 3). The patient was implanted with a permanent pacemaker.