Response to Letter Regarding Article, “A Sensitive Dissection: Profound Bradycardia Complicating Carotid Dissection”
We thank Dr Sarikaya and colleagues for their response to our image and case report on carotid dissection and profound bradycardia, and we welcome diversity of interpretation of the underlying mechanism of the observations.1 The profound progressive bradycardia observed was reminiscent of reflex bradycardia seen most often in vasovagal syncope and carotid sinus sensitivity. The patient’s history of vasovagal syncope in combination with local injury to the carotid bulb region lead us to conclude that the most likely explanation for the profound and recurrent bradycardia was a local one, but this is by no means either conclusive or exclusive. We were unable to perform carotid sinus massage in this case, which may have strengthened the mechanistic association. The insult in this case involves dissection between intima and media with hemorrhage into the arterial wall where the carotid receptors reside, with secondary thrombosis and occlusion. The very transient nature of the bradycardia suggested a brief reflex response and not an ongoing central mechanism influencing heart rate and blood pressure control, though this cannot be excluded. Clearly the insula is important in the “brain-heart” interaction and may have played a role in this case.2
With respect to the assertion by Dr Sarikaya and colleagues that they have not observed this in 136 patients, failing to observe this by no means excludes carotid hypersensitivity, given that “absence of proof is not proof of absence.” Mokri et al described syncope in 1 of 36 patients with carotid dissection, which would have been our case had the patient not presented an hour later.3 Individuals with carotid-related tumors are also well known to present with syncope and bradycardia, though they are thankfully rare.4 Furthermore, syncope in conjunction with stroke is well described,5 and cardiac monitoring is not necessarily in place early in the course of stroke to correlate with. As indicated in our discussion, the mechanism of bradycardia may have been a “carotid sinus hypersensitivity variant, and insular mediated arrhythmia after stroke.” Analogous to the incomplete understanding of the mechanism underlying vasovagal syncope, it is likely that the final explanation is both complex and multifactorial.
Dulay D, Gould PA, Leung A, Krahn A. A sensitive dissection: profound bradycardia complicating carotid dissection. Circulation. 2008; 118: e152–e153.
Onrot J, Wiley RG, Fogo A, Biaggioni I, Robertson D, and Hollister AS. Neck tumour with syncope due to paroxysmal sympathetic withdrawal. J Neurol Neurosurg Psychiatry. 1987; 50: 1063–1066.