Case Presentation: A middle-aged female with hypertension, hyperlipidemia, and squamous cell cancer of oropharynx, presented to us for with syncope.In the six months prior to presentation, patient had had two admissions to the hospital for transient bradycardia leading to unresponsiveness. She had required brief round of CPR the first time, and IV epinephrine and intubation the second time. Work up at the time included echocardiogram with a new reduction in left ventricular ejection fraction (LVEF) to 25%, left heart catheterization with non-obstructive coronary artery disease, an unremarkable MRI brain, and a CTA head and neck (H&N) which showed 50% narrowing of left internal carotid artery. At the time her syncope was considered due to Takotsubo’s cardiomyopathy. She was started on metoprolol 25 mg BID and discharged with close cardiology follow up. Outpatient cardiac stress MRI had shown recovery of LVEF to 45%. In the week before presentation to us, her metoprolol had been switched to carvedilol for BP ranging in 200s/110s. Pertinent vitals on presentation: BP 86/52, HR 32. Initial cardiac rhythm is not known. Patient went unresponsive and pulseless requiring one dose of IV epinephrine which improved BP to 177/84 and HR to 68. Mentation improved to baseline. EKG showed sinus bradycardia with intermittent junctional escape complexes. Troponin negative. CT head was unremarkable. CTA H&N showed a 3.2 x 2.6 cm soft tissue mass at the level of carotid bifurcation. Beta-blockers were stopped. Cardiology, electrophysiology, and neurology were consulted. Review of neck imaging from as early as 1 year before presentation showed a lower neck mass, a known met from her oropharyngeal cancer encasing the carotid artery. Doppler’s showed 50-69% stenosis of left internal carotid artery. Patient remained in sinus bradycardia on telemetry. It was decided to implant a permanent pacemaker (PPM) for persistent SA node and AV node dysfunction and cardioinhibitory/vasodepressor syncope from compression of the carotid bulb from metastatic tumor. After placement of PPM, patient had two more presentations to the ED for presyncope, but no episodes of unresponsiveness. Patient had unfortunately reached her lifetime limit of radiation dosage and could not get any more radiation to the metastatic tumor around the carotid bulb. Vascular surgery was consulted but patient was deemed not to be a candidate for denervation of carotid sinus given history of radiation to the region. A regional block was considered but deferred at the time as patient continued to improve.
Discussion: Carotid sinus syndrome/syncope (CSS) is a form of reflex syncope secondary to pathological activation of carotid baroreceptors. CSS is a rare cause of syncope with 35-40 cases/million/year. It is a disease of the elderly male with the highest prevalence in age > 70 years and a male to female ratio of 4:1 (1). In our patient’s case carotid sinus massage, which is diagnostic for CSS, was not done due to the presence of left internal carotid stenosis and the diagnosis was made clinically. Our patient did not fit the usual demographics of this disease and her disease was related to extrinsic compression of the carotid body.
Conclusions: This report presents an uncommon and challenging case of syncope in a patient outside the usual demographics for the disease. It highlights the importance of keeping unusual differentials in mind when dealing with syncope in patients w/ metastatic cancer.