• 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
  • The ventricular integrated HFLP map of each patient


    The ventricular integrated HFLP map of each patient, from the 187-ch SAVP-ECG, was defined by the increasing gray scale and was superimposed on one spatial distribution map according the site of MI as shown in Fig. 3. The center of the integrated HFLP map of each patient was superimposed on one distribution map according the site of MI as shown in Fig. 4. The integrated HFLP maps (represented by gray scale) and the centers of HFLPs (shown as red squares) were clearly distributed from B-3 to B-6 (middle anterior chest wall) in patients with anterior MI, and in patients with lateral MI from C-2 to D-4 (left middle anterior chest wall). In patients with inferior MI, there were 2 peaks with C-1 to C-2 (upper anterior chest wall), and with C-10 to F-10 (low anterior left lateral chest wall). In patients with both anterior and inferior MI, the distribution of the integrated HFLP maps and the centers was a summation of the anterior and inferior MI patterns. This was also the case in patients with both anterior and lateral MI and in those with both inferior and lateral MI. The body surface projection of the site of integrated HFLP map recorded by 187-ch SAVP-ECG in correlation with the site of MI is shown in Fig. 5. The site of integrated HFLPs was focused on a relatively small area at the anterior chest wall in patients with anterior MI, and on an area at the anterior lateral chest wall in patients with lateral MI. However, in patients with inferior MI, the site of integrated HFLPs was scattered over the lower anterior left lateral chest wall, with the second area at the upper anterior chest wall.
    Conflict of interest
    Case report A 27-year-old man presented to the cardiology department of our hospital with syncope. He had no family history of cardiac sudden death. Syncope had repeatedly occurred, particularly during bathing or on a hot day, for 1 year. Baseline electrocardiogram (ECG) revealed no abnormality and organic CP-673451 cost disease. The Holter recording indicated signs of neither a ventricular event nor any bradycardia. During the head-up tilt (HUT) test, blood pressure decreased by 39mm Hg (from 123/78 to 84/48mm Hg) 15min after tilting. Although the heart rate also decreased abruptly from 85 to 59/min after 21min, no pause (>2.0s) was detected. Syncope or presyncope did not occur during the test (Fig. 1). No bradycardia/tachycardia (including ventricular arrhythmia) was induced by programmed electrical stimulation during the electrophysiological study. The sinus node recovery time was 1180ms. In addition, no bradycardia/pause was noted during the carotid sinus massage maneuver. Therefore, an implantable loop recorder (ILR; Reveal Dx 9528, Medtronic Inc.) was implanted for further examination. After 2 months, the patient had syncope during bathing at midnight. He was rescued from drowning in the bathtub by his family. Subsequently, he completely recovered consciousness and did not have any sequelae. Sinus arrest and a maximum ventricular pause of 10.2s were documented with ILR during this syncopal attack (Fig. 2). He was treated with permanent pacemaker implantation (ALTRUA 60 S606, Boston Scientific) and received no other medical treatment. A permanent pacemaker was programmed to the DDD at a rate of 60–120ppm and an AV delay of 250ms. Syncope did not recur, even during bathing or on a hot day, for 14 months after permanent pacemaker implantation.
    Discussion A neurally mediated syncope (NMS) is triggered by the autonomic nervous system. Because of RR prolongation during a syncopal attack followed by mild heart rate acceleration, the autonomic nervous system was suggested to play an important role in the case of syncope in this patient. The decreasing CP-673451 cost blood pressure supported the diagnosis of mild vasodepressor NMS. Moreover, the abrupt drop in heart rate (from 85 to 59/min) without a pause and symptoms at the end of the HUT test suggested a cardioinhibitory NMS. Finally, the sinus arrest with a long ventricular pause during spontaneous syncope was documented directly by ILR. It was suggested that, as NMS is a cardiovascular response, it should play a role in the mechanism underlying severe sinus arrest, as shown during the HUT test. Therefore, a permanent pacemaker was implanted, without other medical treatment, to prevent syncope and, consequently, drowning during bathing. The changes in blood pressure and heart rate while taking a bath are generally quite complicated. It has been reported that the autonomic nervous activity while bathing significantly affects heart rate [1].