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Joy Amundson, NP Mohamed H. Hamdan, MD, MBA, FHRS Division of Cardiology, University of Wisconsin School of Medicine and Public Health, Madison mhamdan@medicine.wisc.edu
This work was supported by funds provided from the Dr. Herman and Aileen Tuchman Chair in Clinical Cardiology.
The authors reported no potential conflict of interest relevant to this article.
First, several investigators have reportedtransient increases in vagal tone and syncope following PE consistent with a vasovagal-like response.7,18 Therefore, it is possible that the reduction in preload associated with PE triggered a Bezold-Jarisch-like reflex leading to syncope. The patient’s history of vasovagal syncope was certainly indicative of increased susceptibility to reflex-mediated events, thus supporting our hypothesis.
Second, our patient had a cluster of events following surgery compared to the one to 2 events she experienced per year prior to surgery. The increased incidence of events would be an unusual progression of her syncope in the absence of clear triggers, again rendering our hypothesis more plausible.
The patient was admitted to our hospital and started on a higher dose of enoxaparin (60 mg twice daily). She was subsequently discharged home on rivaroxaban 15 mg twice daily and midodrine 2.5 mg twice daily in addition to the medications she was already taking. At her 6-week follow-up visit, she reported no recurrences.
THE TAKEAWAY
This case demonstrates that non-massive PE can present as vasovagal syncope. Recognizing that PE could lead to reflex-mediated syncope in the absence of massive emboli, it is important to rule it out in the evaluation of patients with vasovagal syncope when risk factors for PE are present.