Cardioembolic stroke secondary to paroxysmal atrial fibrillation in a patient with systemic lupus erythematosus

Introduction

This report describes the case of a systemic lupus erythematosus (SLE) patient with no active inflammation presenting with ischemic stroke, and the work-up for the underlying stroke mechanism.

Case report

A 59-year-old Chinese woman presented with acute onset of obscuration of the right visual field. She was diagnosed with SLE in 2008 when she presented with joint pains and vasculitic skin lesions, and tested positive for serum antinuclear, ribonucleoprotein, and Ro antibodies. She was maintained on chloroquine 150 mg once daily. At the time of this presentation, she did not present active SLE clinically. There is no family history of SLE, stroke, or atrial fibrillation (AF).

A neurological examination revealed a right homonymous superior visual field defect. Eye and skin examinations were normal, with no signs of chloroquine toxicity present . During her four-day hospitalization, repeated clinical observations and electrocardiography showed the patient was in sinus rhythm. She was started on amlodipine 5 mg once daily for newly diagnosed hypertension.

A brain magnetic resonance imaging (MRI) showed acute left occipital lobe infarction with normal anterior and posterior intracranial cerebral arteries. Erythrocyte sedimentation rate was mildly elevated at 55 mm/h. Hemogram, electrolyte, thyroid function, serum C-reactive protein, C3, C4, lupus anticoagulant, and anticardiolipin levels were normal. Anti-double stranded DNA was positive at 259 IU. Transthoracic echocardiography showed normal left ventricular ejection fraction (59%), cardiac chambers and valves. Holter monitoring for 24 h revealed paroxysmal atrial fibrillation (pAF). The patient reported palpitations corresponding to AF episodes.

The clinical diagnosis was occipital infarction of cardioembolic etiology secondary to pAF. She was treated with therapeutic anticoagulation, and prescribed warfarin for secondary stroke prevention. A review two months post-stroke showed complete resolution of any visual field defect.

Discussion

SLE is a known cause of ischemic stroke, accounting for 3.5% of ischemic strokes in patients under 45. ¹ The prevalence of stroke is high among SLE patients, reported at 5.7% in a cohort of 3649 SLE patients. ² The risk of stroke is higher in SLE patients compared to healthy controls is indicated by a Taiwanese study, ³ with an adjusted hazards ratio of 1.88 (95% CI 1.08–3.27) over five years. The average age of onset of SLE-associated stroke is 35 years and its prevalence increases with age. Most SLE-associated strokes occur within five years of diagnosis, and during active inflammation. ⁴ The risk of stroke in SLE is attributed to vasculitis, hypercoagulability, increased atherogenic potential, as well as cardioembolism from endocarditis, valvular abnormalities, and arrhythmias. ²

SLE predisposes to cardiac arrhythmias, including atrial fibrillation, with postulated mechanisms of periarteritis, myocarditis, and fibrotic infiltration.^5,6 It is not possible to determine whether the pAF condition in this case was related to SLE beyond doubt. There could also have been a co-occurrence of pAF and SLE. Although not of concern in this patient, it should be noted that chloroquine-induced cardiotoxicity has been implicated in the development of cardiac arrhythmias, although other studies suggest it has potential antiarrhythmic effects.^5,7

Conclusions

This 59-year-old patient with newly-diagnosed hypertension presented with occipital infarction three years after being diagnosed with SLE. There was no evidence of active inflammation at the time the stroke was presented. SLE-associated stroke may not always be due to vasculitis or hypercoagulability. In this patient, stroke etiology was ascertained as cardioembolism secondary to pAF, which was only detected on Holter monitoring. In patients with SLE, it is important to consider pAF as a possible cause of ischemic stroke.