13 Intracranial Atherosclerosis

13.1 Goals

13.2 Case Example

13.2.1 History of Present Illness

A 75-year-old patient complained of recurrent episodes of left-sided weakness and speech disturbance. Magnetic resonance (MR) imaging showed acute infarcts in the left cerebellar hemisphere, right pons, and left occipital lobe (▶ Fig. 13.1a, b). A basilar artery stenosis was detected on MR angiography (▶ Fig. 13.1c). Best medical treatment was initiated including dual antiplatelet treatment with acetylsalicylic acid (ASA) and clopidogrel, atorvastatin at 80 mg daily, and an optimization of antihypertensive medication. One month later, the patient experienced palpitations and was diagnosed with atrial fibrillation. The treating cardiologist performed cardioversion and replaced the dual antiplatelet treatment with rivaroxaban without any other change of medication.

Another month later, episodes of speech disturbance and perioral paresthesia occurred. These episodes were interpreted as brainstem transient ischemic attack (TIA), but MR imaging did not show any new infarcts or stenosis progression. ASA was added to rivaroxaban. A few weeks later, atrial fibrillation relapsed. The patient was readmitted and treated with amiodarone. During the course of the hospital stay, the patient experienced two more episodes of speech disturbance. This time MR imaging revealed a new pontine infarction. Since all infarcts and the TIA were in the territory of the basilar artery, it was assumed that a large artery atherosclerosis was the cause rather than atrial fibrillation. After interdisciplinary discussion with the neurologist, neuroradiologist, and cardiologist, endovascular therapy was regarded as the only treatment option left and the patient gave informed consent after careful consideration. During prepro-cedural medical work-up, a slight drop in hemoglobin was recognized. In view of the extensive postprocedural anticoagulation required, an endoscopy was performed. An angio-dysplasia was found in the colon and coagulated.

Past Medical History: hypertension, hyperlipidemia, heterozygous factor-V-Leiden mutation with previous deep vein thrombosis, impaired glucose tolerance, atrial fibrillation (CHA2DS2-VASC 5).

Past surgical history: Previous bilateral cataract surgery. Family history: Answered negative to family history of stroke.

Fig. 13.1 The patient presented with recurrent episodes of left-sided weakness and speech disturbance. Diffusion-weighted magnetic resonance (MR) imaging revealed infarcts in the left cerebellar hemisphere (a), pons and left occipital lobe (b). A high-grade basilar stenosis was found in MR angiography (c).

Fig. 13.2 Treatment and follow-up of a high-grade basilar artery stenosis, (a) A 3D rotational angiography was acquired to precisely measure the dimensions of the basilar artery and the stenosis, (b) After catheterization of the right posterior cerebral artery with a 0.014″ microwire, a 3.5- to 8-mm balloon-expandable stent was placed at the site of the stenosis (arrows indicate the proximal and distal balloon marker), (c) After stent deployment, the stenosis resolved completely, (d) Twelve-month control angiography revealed patency of the stent and no restenosis.

13.2.2 Treatment Plan

The patient was scheduled for intracranial stenting under general anesthesia. A balloon-expandable stent was uneventfully implanted (▶ Fig. 13.2a-c). After the procedure, the anticoagulation medication was changed to dabigatran at HOmg twice daily with ASA and clopidogrel for 4 weeks. Then, the medication was changed to rivaroxaban and clopidogrel.

13.2.3 Follow-up

Clinical, MRI, and angiographic follow-up was scheduled at 6 and 12 months. The patient did not experience any new ischemic symptoms. There was no evidence of new infarcts in imaging studies and no restenosis occurred (▶ Fig. 13.2d). At 12 months, the antithrombotic medication was changed to rivaroxaban and ASA.

13.3 Case Summary

The first attempt to clarify the uncertainty about the optimal antithrombotic therapy in patients with symptomatic intracranial atherosclerosis was the “Warfarin and Aspirin for Symptomatic Intracranial Stenosis (WASID)” trial.¹ The trial was terminated early since the use of warfarin was associated with an increased mortality and major bleeding risk without any benefit in terms of stroke prevention. The increased risk of major hemorrhage was largely triggered by excess international normalized ratio (INR) values and low values were associated with an increased risk of stroke. Out of range INR was not infrequent within the trial. Novel anticoagulants (NOACs) are more suitable in this aspect and have proven to be superior to warfarin in terms of safety and efficacy in patients with cardioembolic stroke. Therefore, they might play a future role in the treatment of patients with symptomatic intracranial atherosclerosis. The “Stenting versus Aggressive Medical Therapy for Intracranial Arterial Stenosis (SAMMPRIS)” trial compared stenting with aggressive medical management to aggressive medical management alone for the treatment of high-grade symptomatic intracranial stenosis.^2,3 The likelihood of a primary end-point event in the noninterventional arm of the trial was only 5.8% at 30 days and much lower than expected. Dual antiplatelet treatment with ASA and clopidogrel during the first 3 months after randomization was an essential component of medical therapy.

The superiority of dual antiplatelet treatment compared to ASA alone to prevent recurrence of cerebral ischemia without an increased risk of hemorrhage was demonstrated in the “Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack (CHANCE)” trial.⁴ A CHANCE subgroup analysis focusing on patients with intracranial atherosclerosis showed only a trend for improved outcome with dual antiplatelet therapy.⁵ This may be attributable to the very common phenomenon of “clopidogrel resistance,” which is caused by the inability to convert the prodrug clopidogrel into the active form via the CYP2C19 enzyme. An additional subgroup analysis showed that the benefit of dual antiplatelet therapy was not present in carriers of CYP2C19 loss-of-function alleles but was highly significant in noncar-riers.⁶ Ticagrelor has the same mode of action as clopidogrel but does not require enzymatic conversion. Therefore, it will likely overcome the issue of clopidogrel resistance. The safety and efficacy of ticagrelor in patients with intracranial large artery atherosclerosis has not been investigated yet.

2.What are the most important adjunctive components of medical therapy in symptomatic intracranial atherosclerosis? The medical treatment arm of the SAMMPRIS trial showed the most favorable clinical results in patients with symptomatic intracranial atherosclerosis so far.³ Therefore, medical therapy in the real-world setting should ideally be aligned to the trial guidelines. Specific risk factor targets were as follows⁷: systolic blood pressure < 140 mm Hg (< 130 mm Hg if diabetic), LDL cholesterol < 70 mg/dL, non-HDL lipoprotein < 100 mg/dL, HbAlc< 7%, smoking cessation, weight management (for initial BMI of 25-27 kg/m²: target BMK25 kg/m²; for initial BMI > 27 kg/m²

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