Posterior circulation stroke: an easily overlooked complication of catheter ablation of atrial fibrillation

Abstract

Catheter ablation of atrial fibrillation (AF) has established itself as a safe and proven rhythm control strategy for selected patients with AF over the past decade. Thromboembolic complications of catheter ablation are becoming rare in anticoagulated patients with a risk of stroke reported as 0.3%. A particular challenge is posed by clinical presentation due to ischaemic stroke involving the posterior circulation following catheter ablation because of its substantial differences from the carotid territory stroke, making the timely diagnosis and treatment very difficult. It is crucial to keep an index of clinical suspicion in patients presenting with neurological deficits related to vertebrobasilar circulation following ablation. We describe the case of a man who presented with dizziness and palpitations after radiofrequency catheter ablation of AF. He was found to be in AF with a rapid ventricular response. His dizziness was initially attributed to the cardiac dysrhythmia. As his symptoms continued despite heart rate control, he underwent further investigations and was eventually diagnosed with a posterior circulation stroke resulting in left cerebellar infarction. He was treated with antiplatelet therapy and improved significantly over the following few days. We review and present an up-to-date brief literature review on the complications of catheter ablation of AF and describe pathophysiology, clinical features, diagnosis and treatment options for posterior circulation stroke after AF ablation. This case aims to raise awareness among clinicians about posterior circulation stroke after AF ablation.

Background

Atrial fibrillation (AF) is globally recognised as the most common cardiac arrhythmia, associated with hospitalisations, heart failure and embolic events.¹ Catheter ablation is an established strategy for rhythm control in patients with symptomatic AF that may offer a nearly fourfold higher probability of freedom from AF compared with the medical therapy alone.² The complication rates from ablation are consistently improving in the western world as the operators are getting better training, more experience and the procedural techniques and equipment are further refined.³ Most of the complications due to the catheter ablation are local, involving the heart itself; however, despite continuation of seamless anticoagulant therapy, there remains a risk of thromboembolism. Ischaemic stroke is a rare complication of AF ablation in optimally anticoagulated patients affecting approximately 0.3% of patients⁴ and can be difficult to diagnose, especially, when it involves the posterior circulation of the brain.

Case presentation

This 50-year-old man presented to the emergency department with dizziness and palpitations leading an episode of collapse without loss of consciousness. He was known to have a history of dilated cardiomyopathy and AF, for which he had a radiofrequency ablation (RFA) on the previous day. His usual medications included lansoprazole, ramipril, spironolactone, bisoprolol, digoxin, furosemide and edoxaban for anticoagulation. He had uninterrupted anticoagulation therapy throughout this period without missing any doses. On examination, he was found to have an irregularly irregular pulse with a rate of 140 bpm. Blood pressure, respiratory rate and oxygen saturations were all normal. His heart sounds were normal and chest was clear to auscultation. He was alert and oriented. There was no facial droop or limb weakness. Speech was normal.

Routine blood tests, including full blood count, renal functions, thyroid function test, electrolytes including potassium, magnesium and phosphate, were all found to be within a normal range. Cardiac troponin T was elevated 45 ng/mL (normal range 5–14 ng/mL). ECG showed AF with a rapid ventricular response (figure 1).

Figure 1.

Twelve-lead ECG showing an irregularly irregular narrow complex tachycardia with no identifiable P waves. The ventricular rate is approximately 140 bpm and the cardiac axis is normal. These findings are in keeping with atrial fibrillation with a fast ventricular response.

On initial assessment, his dizziness was considered to be secondary to AF with a rapid ventricular response. Troponin rise was considered to be secondary to the arrhythmia, as well. He was given further bisoprolol 2.5 mg orally for rate control and was transferred to a bed with cardiac monitoring on the acute medical unit. After the treatment with bisoprolol for 24 hours, his heart rate improved to 70 bpm, although he remained in AF and symptoms of palpitations settled. However his dizziness continued.

The patient was reassessed by the medical team at this point and clinical history was revisited. He described his dizziness as ‘spinning movement’ more marked with movement and standing up, associated with unsteadiness and nausea. There was no earache, discharge or tinnitus. Neurological examination revealed a Glasgow coma scale score 15/15, with no focal motor or sensory deficit with normal speech. He had nystagmus to the left side along a broad-based ataxia. No other cerebellar signs were present. The National Institute of Health Stroke Scale (NIHSS) score was 1.

Investigations

An urgent CT scan of the brain was performed that showed no abnormality. Subsequent MRI scan of the brain confirmed an acute infarct in the left cerebellar hemisphere (figures 2–4).

Figure 2.

MR scan of the brain, diffusion-weighted image, reveals a diffusion defect in the left cerebellar hemisphere, in keeping with an acute infarct (arrow).

Figure 3.

MR scan of the brain, apparent diffusion coefficient image, shows an abnormality in the left cerebellar hemisphere, consistent with infarct (arrow).

Figure 4.

MR scan of the brain (T2 image) reveals hyperintensity in the left cerebellar hemisphere (arrow).

Treatment

He was reviewed by the stroke team, edoxaban was withheld and he was started on aspirin 300 mg once daily as per stroke physician’s advice. He was transferred to stroke unit for further management. The patient made an excellent functional recovery and was discharged home within a week. Anticoagulation with edoxaban was recommenced 2 weeks after the event.

Outcome and follow-up

The patient made an excellent functional recovery and was discharged from the hospital after a week. He has had no recurrence of his symptoms since discharge.

Discussion

Catheter ablation is a well-recognised, safe and widely available treatment for drug-refractory AF. It is even argued as a first-line treatment strategy for selected patient groups, particularly in younger and otherwise healthy individuals.⁵ The conventional RFA uses heat energy to produce multiple, continguous, transmural lesions to eliminate the endocardial substrate responsible for triggering and perpetuating the arrhythmia. Cryoballoon ablation (CBA) is an alternative to the RFA and uses cryoenegry instead of heat.⁶ The application of single circular freeze with CBA can achieve pulmonary vein isolation that is often sufficient to produce durable lesions leading to the resolution of AF.⁶

The main complications of catheter ablation involve the heart and vascular access, and occur in approximately 2% cases.⁷ These include cardiac perforation leading to tamponade, pericardial effusion, pulmonary vein stenosis, atrio-oesophageal fistula, valve damage and femoral pseudoaneurysm. Pulmonary complications, for example, diaphragmatic paralysis, pneumothorax and haemothorax are uncommon. Embolic stroke is a rare but potentially serious complication of catheter ablation of AF in anticoagulated patients, affecting 0.3% of all cases.⁴ Despite optimal anticoagulant therapy, endocardial disruption produced by ablation can serve as a nidus for thrombus formation that may subsequently dislodge and embolise.⁸ Most of the resulting strokes present within 24 hours of the catheter ablation procedure. Increasing age (≥60 years), dilated left atrial size (≥45 mm), reduced left atrial appendage velocity (≤40 mm/s) and E/E’ ≥10 are associated with increased risk of stroke post AF ablation.⁹ The majority of embolic strokes involve the anterior circulation (carotid territory) and only one-fifth affect the posterior circulation (vertebrobasilar territory). The anterior circulation stroke presentations conform to the widely identifiable patterns involving facial droop, dysphasia and hemiparesis; this makes the early recognition easy with a quick link-up to hyperacute stroke pathways resulting in timely imaging and treatment. However, the clinical features of posterior circulation stroke are related to the brainstem and cerebellum and may vary significantly from those in anterior circulation stroke.¹⁰ These features include visual disturbance, incoordination, unsteadiness, dysarthria, dysphagia, vertigo, drowsiness and cranial nerve palsies; and often do not fit into commonly used stroke scoring tools, for example, FAST (face, arm, speech test) and National Institute of Health Stroke Scale (NIHSS).^{11 12}

NIHSS is also heavily weighted towards anterior circulation stroke and symptoms of posterior circulation stroke are not reliably assessed by using NIHSS.¹² The extended NIHSS (e-NIHSS) adds points for truncal ataxia, cranial nerve dysfunction and nystagmus and offers a more reliable assessment.¹³ Similarly, transient ischaemic attacks (TIA) involving the vertebrobasilar circulation that sometimes precede a posterior circulation stroke do not usually conform to the standard TIA definitions.¹⁴ Lack of recognition of clinical features of acute posterior circulation stroke may delay access to imaging and intravenous thrombolytic therapy, hence adversely affecting clinical outcomes.¹⁵ Interestingly, there is a higher incidence of subclinical AF and atrial flutter in patients with posterior circulation stroke of unknown aetiology.¹⁶ In their study on embolic stroke of undetermined source, Makimoto and colleagues found the incidence of subclinical AF to be more than twice in patients with posterior circulation stroke compared with those with anterior circulation stroke (35% vs 15%). Therefore, clinicians should look more carefully for subclinical AF in this patient cohort because it has implications for further therapeutic decisions. Distinguishing dizziness and vertigo due to posterior circulation stroke from vestibular disorders can be a real challenge. A careful history regarding the timing and trigger of these symptoms combined with bedside clinical tools including Dix-Hallpike manoeuvre, assessment of eye movements and hearing, and neurological examination can help in making the diagnosis.¹⁷

A CT scan of the brain can be used as the initial screening test and can help to rule our intracerebral haemorrhage. Nonetheless, it carries a lower sensitivity to pick up posterior circulation ischaemia or infarction. CT angiography may demonstrate a posterior circulation embolus or vascular abnormality.¹⁸ Magnetic resonance imaging particularly with diffusion weighted sequences can reliably confirm the location of the ischaemic lesion. Once diagnosed, patients with posterior circulation stroke must be assessed for their eligibility for intravenous thrombolysis depending on the time of onset and the degree of neurological deficit. There is an emerging role for endovascular therapy and clot retrieval for those with no improvements with intravenous thrombolysis.¹⁸ Due to paucity of specific data, it is difficult to ascertain whether anticoagulation should be continued in patients with AF who develop an acute stroke following ablation. In a head-to-head comparison between aspirin and warfarin for the treatment of acute ischaemic stroke in patients with AF, those on anticoagulation had a higher incidence (although statistically non-significant) of intracranial haemorrhage (0.7% vs 0.3%).¹⁹ Hence, many researchers believe that the continuation of anticoagulation in patients with AF with ischaemic stroke may increase the risk of haemorrhagic transformation of the infarct.²⁰ High-dose aspirin (300 mg) once daily for 2 weeks is recommended by the UK guideline following which patients can be restarted on anticoagulation alone, unless there is another indication to continue on long-term aspirin.²¹ An analysis of three randomised controlled trials comparing anticoagulation versus antiplatelet therapy in patients with AF who had an acute stroke found modest benefit in reducing stroke recurrence and improved functional outcomes with aspirin use. The authors favoured the administration of aspirin in acute stroke followed by an early initiation of anticoagulation therapy, typically within a couple of days of stroke.²² These studies illustrate the controversy regarding the optimal strategy for ischaemic stroke in atrial fibrillation requiring further research in general as well as in the specific scenario of post-AF ablation stroke.

Catheter ablation is becoming a widely used procedure to restore sinus rhythm in patients with AF. Posterior circulation stroke is a rare complication of AF ablation in anticoagulated patients and offers a unique diagnostic and treatment challenge due to its clinical features being substantially different from the other common stroke presentations. Clinicians should be aware of this significant, although rare complication of catheter ablation and should have an index of suspicion when dealing with neurological symptoms postablation in order to offer timely diagnosis and treatment.

Learning points.

• Catheter ablation is an established rhythm control strategy for selected patients with atrial fibrillation (AF).

• Embolic stroke is a rare complication of catheter ablation of AF in optimally anticoagulated patients.

• Diagnosing posterior circulation stroke may be challenging as it may present with clinical features substantially different from other forms of stroke.

• Timely recognition and treatment of posterior circulation stroke in this patient cohort is the key to improve clinical outcomes.