The Etiology and Secondary Prevention of a Stroke Patient after Successful Catheter Ablation

Case Presentation

Austin J Clin Neurol 2021; 8(1): 1143.

The Etiology and Secondary Prevention of a Stroke Patient after Successful Catheter Ablation

Zhao J*

Department of Neurology, China

*Corresponding author: Jing Zhao, Department of Neurology, Xinsong Road 170, Shanghai, China

Received: January 25, 2021; Accepted: February 22, 2021; Published: March 01, 2021

Abstract

Ischemic Stroke (IS) is one of the leading diseases of mortality and disability worldwide. The rational administration of anticoagulant or antiplatelet drugs is of great importance to prevent stroke recurrence. Here we report an IS patient with a medical history of Catheter Ablation (CA) of Atrial Fibrillation (AF), who had a single vessel scattered lesions in the head Magnetic Resonance Imaging (MRI) scan, which indicated a remarkable correlation with morphology of atherosclerotic artery and artery embolism, while no AF recurrence was detected. At last, we focused on the possible criminal artery and found vulnerable plaques from apparent positive remodeling demonstrated by High-Resolution Vessel Wall MRI (HRVW-MRI). We provided a secondary prevention with the statin and antiplatelet therapy to reduce the risk of bleeding caused by anticoagulation and asked him to follow up Holter every three months. Along with this case report, we describe the imageology, review of literature and treatment outcomes in regard to CA of AF and discuss the prevention of IS.

Keywords: Ischemic stroke; Catheter ablation; Atrial fibrillation; HRVW-MRI

Case Presentation

A 72-year-old man woke up with left side numbness and weakness, slight alalia and the angle of his mouth deviated to right side. The patient arrived at our emergency department one hour later, as his left limb numbness disappeared, muscle strength and speech returned to normal. The neurologic examination demonstrated that left nasolabial groove was slightly shallower and left Babinski sign was positive, while the muscle strength and muscular tension of limbs were normal. Computed Tomography (CT) showed the residual left temporooccipital encephalomalacia. The National Institutes of Health Stroke Scale (NIHSS) score was 1. The patient reported a history of hypertension and atherosclerosis, with blood pressure controlled around 140-150/80-90mmHg. He also had a history of cerebral infarction 4 years ago when AF was found. CA of AF was performed 2 years ago and oral administration of aspirin was given after surgery. The patient didn’t feel palpitation and the every threemonth checking Holter showed no AF rhythm. A few weeks before this onset, the patient took bisoprolol by himself, and his lowest heart rate was 40bpm with occasional dizziness. The admission diagnosis is cerebral infarction (OCSP: PACI); grade hypertension; personal history of CA of AF (CHA2DS2-VASc score of 4). Aspirin and statins was given while thrombolytic therapy wasn’t performed due to the low NHISS score and awaken stroke.

After admission, laboratory tests (fasting plasma glucose, plasma glucose of two hours after meal, glycated hemoglobin, blood lipids, homocysteine, autoimmune antibodies, etc.) were almost normal. Holter showed some atrial premature beats, and no AF rhythm was caught. Echocardiography (EEG) showed a slightly enlarged left atrium (41mm) and a slightly thickened interventricular septum (12mm). The head Magnetic Resonance Imaging (MRI) showed some scattered diffuse limited lesions in the cortical and subcortical areas around the right central sulcus (Figure 1A-1D). The head and neck Computed Tomography Angiography (CTA) showed a suspicious stenosis in M2 segment of right Middle Cerebral Artery (MCA), which was the criminal artery comprised of precentral artery, artery of central sulcus and artery of postcentral sulcus, as well as a moderate non-criminal stenosis in M1 segment of left MCA (Figure 1E).

Citation: Zhao J. The Etiology and Secondary Prevention of a Stroke Patient after Successful Catheter Ablation. Austin J Clin Neurol 2021; 8(1): 1143.