A Sensitive Dissection
Profound Bradycardia Complicating Carotid Dissection
A 49-year-old woman with a history of hypertension and vasovagal syncope presented to the emergency department with abrupt onset of left-sided hemiplegia and slurred speech. The clinical diagnosis of acute stroke was supported by radiographic evidence of an acute right middle cerebral artery infarct, involving the posterolateral right frontal lobe on computed tomography and magnetic resonance angiography imaging of her head (Figure 1). At the time, a carotid dissection was not evident, although it was apparent on magnetic resonance imaging scan performed 3 days later. At the time of presentation, a carotid bruit was not present. The patient received intravenous tissue plasminogen activator (tPA) as short-term treatment for her stroke. During infusion of tPA, the patient lost consciousness during an associated 18-second sinus pause (Figure 2). The infusion was immediately discontinued. When the patient was given atropine, sinus rhythm with ventricular bigeminy spontaneously returned at a rate of 80 bpm. The episode was not associated with neck movements or pressure to the carotid sinus and manual carotid sinus massage was not performed. The patient had 5 additional episodes of sinus arrest lasting between 10 and 20 seconds over the next 4 days that were conservatively managed. The patient’s neurological status improved gradually and she regained near normal strength and sensation of her left upper and lower limbs, but she had a persistent left sided facial droop.
A 12-lead ECG on admission demonstrated sinus rhythm at a rate of 79 bpm with normal PR and QTc intervals. Her serum potassium, calcium, magnesium, and thyroid-stimulating hormone levels were normal. An echocardiogram with a bubble study did not demonstrate a patent foramen ovale or any evidence of structural heart disease. A computed tomography arteriogram 2 months later demonstrated a patent carotid bulb and a proximally occluded right internal carotid artery (Figure 3). There were pseudoaneurysms of the left vertebral and internal carotid artery consistent with fibromuscular dysplasia. Incidentally, she developed a vasovagal response with nausea and presyncope during femoral artery cannulation in preparation for the computed tomography scan.
The differential diagnosis of arrhythmia that the patient experienced includes carotid sinus dysfunction, intrinsic sinus node dysfunction, the cardioinhibitory form of vasovagal syncope or its carotid sinus hypersensitivity variant, and insular mediated arrhythmia after stroke.1 Arrhythmias and electrocardiographic changes are not uncommon in patients with acute intracranial vascular events due to neurohormonal changes, although the patient did not exhibit the electrocardiographic changes commonly observed, such as QT prolongation, depressed ST segments, and flat or inverted T waves.1 The patient did not have a history of bradycardia before this hospitalization, making isolated sinus node dysfunction a highly unlikely explanation for her presentation. The observed gradual slowing of the heart rate and a previous history of vasovagal syncope suggested a reflex rather than intrinsic sinus node disease. Carotid sinus hypersensitivity is defined as a sinus pause >3 seconds with a decrease in systolic blood pressure of at least 50 mm Hg during carotid sinus massage.2 Bradycardia due to carotid hypersensitivity from secondary causes has been observed during angioplasty of the carotid artery for atherosclerotic disease.3
In the present case, the mechanical pressure to an already sensitive carotid sinus from thrombus secondary to a dissection of the internal carotid artery was postulated to be the mechanism of episodic sinus arrest in this patient who was prone to vasovagal syncope. Although the episodes of sinus pauses and bradycardia were hemodynamically significant, a conservative approach was adopted and the bradycardia resolved. This improvement is most likely secondary to reduction of the pressure from the organizing thrombus in the carotid sinus, thus alleviating the state of transient carotid sinus hypersensitivity.
Management of carotid dissection is typically conservative, with intravenous heparin and subsequent warfarin administration. The working diagnosis of the neurology team was ischemic stroke when the tPA was administered because the dissection was not apparent on the initial magnetic resonance angiography. There is limited experience with use of thrombolytic therapy in this context.4 The use of tPA arguably may have been beneficial to the patient despite the transient arrhythmias noted. Further exploration of the role of thrombolytics is needed to guide future management of dissection.
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Zipes D, Libby P, Bonow RO, Braunwald E. Braundwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 7th Ed. Philadelphia, Pa: Saunders; 2004.
Derex L, Nighohossian N, Turjman F, Hermier M, Honnorat J, Neuschwander P, Froment JC, and Trouillas P. Intravenous tPA in acute ischemic stroke related to internal carotid artery dissection. Neurology. 2000; 215–2161.