Background <p>Repetitive transcranial magnetic stimulation (rTMS) is an effective treatment for major depressive disorder (MDD) with a low incidence of adverse effects. However, bradycardia is not commonly recognized as an adverse effect of rTMS. In this case report, we present the first documented instance of a patient with MDD and premature ventricular contractions (PVCs) who developed severe bradycardia following rTMS treatment.</p> Case presentation <p>We report the case of a 46-year-old Chinese woman with a 7-year history of MDD and a 6-year history of PVCs. She had been taking paroxetine, tandospirone citrate, and metoprolol long-term without experiencing bradycardia. After initiating rTMS treatment, she developed severe bradycardia. Even after discontinuing metoprolol, the severe bradycardia persisted for several days. Notably, the severe bradycardia disappeared one day after pausing rTMS therapy. When rTMS was resumed, the bradycardia reoccurred and subsequently resolved again upon pausing the rTMS treatment.</p> Conclusion <p>The influence of rTMS on heart rate (HR) is likely mediated through the autonomic nervous system (ANS). Currently, severe arrhythmias are not widely recognized as adverse effects of rTMS. While the exact mechanisms by which rTMS affects the cardiovascular system remain unclear, this case underscores the necessity for caution when using rTMS to treat psychiatric patients with arrhythmias.</p>

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Severe bradycardia triggered by repetitive transcranial magnetic stimulation in a patient with major depressive disorder and premature ventricular contractions: a case report

  • Shuping Fang,
  • Bowen Song,
  • Xin Yang,
  • Ling Ma,
  • Zhe Li

摘要

Background

Repetitive transcranial magnetic stimulation (rTMS) is an effective treatment for major depressive disorder (MDD) with a low incidence of adverse effects. However, bradycardia is not commonly recognized as an adverse effect of rTMS. In this case report, we present the first documented instance of a patient with MDD and premature ventricular contractions (PVCs) who developed severe bradycardia following rTMS treatment.

Case presentation

We report the case of a 46-year-old Chinese woman with a 7-year history of MDD and a 6-year history of PVCs. She had been taking paroxetine, tandospirone citrate, and metoprolol long-term without experiencing bradycardia. After initiating rTMS treatment, she developed severe bradycardia. Even after discontinuing metoprolol, the severe bradycardia persisted for several days. Notably, the severe bradycardia disappeared one day after pausing rTMS therapy. When rTMS was resumed, the bradycardia reoccurred and subsequently resolved again upon pausing the rTMS treatment.

Conclusion

The influence of rTMS on heart rate (HR) is likely mediated through the autonomic nervous system (ANS). Currently, severe arrhythmias are not widely recognized as adverse effects of rTMS. While the exact mechanisms by which rTMS affects the cardiovascular system remain unclear, this case underscores the necessity for caution when using rTMS to treat psychiatric patients with arrhythmias.