Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 59, Num. 5, 2011, pp. 772-773

Neurology India, Vol. 59, No. 5, September-October, 2011, pp. 772-773

Letter to Editor

Sinus arrest: Complicating acute posterior cerebral artery stroke

Alok Mandilya¹, Narayanan Namboodiri², Sapna Erat Sreedharan¹, PN Sylaja¹

¹ Department of Neurology, Comprehensive Stroke Care Centre, Thiruvananthapuram, Kerala, India
² Department of Cardiology, Sree Chitra Thirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India
Correspondence Address: P N Sylaja, Department of Neurology, Comprehensive Stroke Care Centre, Thiruvananthapuram, Kerala India, sylajapn@hotmail.com

Date of Submission: 31-Aug-2011
Date of Decision: 01-Sep-2011
Date of Acceptance: 01-Sep-2011

Code Number: ni11234

PMID: 22019674

DOI: 10.4103/0028-3886.86564

Sir,

A 64-year-old gentleman type 2 diabetic presented with a wake up stroke after six hours of symptom onset. Neurological examination revealed conscious patient with left hemiparesis, hemisensory loss, left sided ataxia, and the National Institutes of Health Stroke Scale (NIHSS) score of 11. Computed tomography (CT) of brain done six hours of onset was suggestive of acute infarct in right posterior cerebral artery (PCA) territory sparing brain stem. CT-angiography showed occlusion of right P2 segment of PCA. Patient was started on single antiplatelet and statin. After four hours of admission in stroke unit, he suddenly developed bradycardia associated with unresponsiveness and no pulse. His electrocardiogram (ECG) showed sinus bradycardia for initial four beats followed by sinus arrest for 13 seconds which recovered to sinus rhythm with physical stimulation without any medication [Figure - 1]. A review of the telemetric tracings revealed another episode of asymptomatic sinus bradycardia that lasted for five seconds with sinus rate less than 30 beats per minute an hour prior to this event [Figure - 1]. A similar type of episode was observed in casualty during examination without any ECG documentation. His serum potassium and calcium were normal. He did not have further similar episode during his hospital stay. His subsequent continuous ECG monitoring in stroke unit did not show any rhythm disturbance. He was evaluated with 24-hour Holter monitoring which was normal without any sinus pause/paroxysmal atrial fibrillation.

The mechanisms for sinus pause to be considered in a acute stroke setting are intrinsic sinus node dysfunction, cardioinhibitory form of vasovagal syncope, or insula mediated arrhythmia. ^[1],[2],[3] Studies have shown that both the sympathetic and parasympathetic autonomic cardiovascular regulatory mechanisms are impaired in acute stroke. ^[4] The absence of any symptoms suggestive of primary sinus nodal abnormality prior to admission and a normal Holter evaluation a week later suggests that intrinsic sinus node dysfunction is unlikely. CT head did not show any evidence of insular involvement. Slowing of sinus rate immediately prior to and after the sinus pause suggest vagotonia as the likely mechanism in this patient. The clear temporal correlation suggests that acute stroke is the inciting factor for the profound vagotonia. Fortunately, the sinus pause was self limiting and patient did not have any hemodynamic consequences. Rarely, the sinus arrest can be life threatening leading on to unexplained death and may require temporary pacing. ^[1] This also highlights the importance of need of continuous ECG monitoring of acute stroke patients in stroke unit.

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