תוצאת חיפוש

Serotonin Re-Uptake Inhibitors as Primary Therapy for Carotid Sinus Hypersensitivity

Amos Katz, Angel Kantor, Alexander Battler

Cardiology Dept., Soroka Medical Center and Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheba

Carotid sinus syndrome is a well-recognized cause of unexplained syncope in older patients, and may lead to significant morbidity due to trauma from falls. Dual chamber pacing has been shown to be effective in relieving symptoms due to bradycardia, but not due to vasodepressor response. We report an 84-year-old man with recurrent syncope due to carotid sinus hypersensitivity. He was treated only with a serotonin re-uptake inhibitor and was symptom-free after 3 weeks of therapy. He has remained symptom-free for the past year.

Autonomic Dysregulation in Post-Traumatic Stress Disorder: Power Spectral Analysis of Heart Rate Variability

Hagit Cohen, Uri Loewenthal, Mike A. Matar, Hanoch Miodownik, Zeev Kaplan, Yair Cassuto, Moshe Kotler

Mental Health Center, Israel Ministry of Health; Anxiety and Stress Research Unit, Faculty of Health Sciences; Dept. of Life-Sciences, Ben-Gurion University of the Negev, Beer Sheba

Spectral analysis of heart rate variability (HRV) has been shown to be a reliable noninvasive test for quantitative assessment of cardiovascular autonomic regulatory response, providing a dynamic map of sympathetic and parasympathetic interaction. In a prior study exploring the state of hyperarousal that characterizes the post traumatic stress disorder (PTSD) syndrome, we presented standardized heart rate analyses in 9 patients at rest, which demonstrated clear-cut evidence of a baseline autonomic hyperarousal state.

To examine the dynamics of this hyperarousal state, standardized heart rate analysis was carried out in 9 PTSD patients, compared to a matched control group of 9 normal volunteers. 20-minute ECG recordings in response to a trauma-related cue, as opposed to the resting state, were analyzed. The patients were asked to recount the presumed triggering traumatic event, and the control subjects recounted a significant stressful negative life event.

Whereas the control subjects demonstrated significant autonomic responses to the stressogenic stimulus of recounting major stressful experiences, the patients demonstrated almost no autonomic response to the recounting of the triggering stressful event. The patients demonstrated a degree of autonomic dysregulation at rest comparable to that seen in the control subjects' reaction to the stress model.

The lack of response to the stress model applied in the study appears to imply that PTSD patients experience so great a degree of autonomic hyperactivation at rest, that they are unable to marshal a further stress response to the recounting of the triggering trauma, as compared to control subjects. A subsequent study of the effect of medication on these parameters showed that they are normalized by use of selective serotonin re-uptake inhibitors (SSRI's).

Neither the clinical implications of these findings, nor their physiological mechanisms are clear at present. We presume that they reflect a central effect, as the peripheral automatic effects of SSRI's are relatively negligible.