Introduction
Intracranial atherosclerotic disease (ICAD) is defined as atherosclerosis of the large intracranial arteries, namely the intracranial internal carotid artery (ICA), intracranial vertebral and basilar arteries, middle, anterior and posterior cerebral arteries, and their cortical branches (up to M3, A3, or P3 segments). Atherosclerotic disease of the small perforator and penetrating arteries is termed as small vessel (or small artery) disease. The term intracranial stenosis (ICS) usually denotes atherosclerotic narrowing of the main segments of the intracranial arteries involving the intracranial ICA, proximal segments of middle cerebral artery (MCA) (M1), anterior cerebral artery (ACA) (A1), posterior cerebral artery (PCA) (P1), basilar artery (BA), and the distal segment of vertebral artery (V4).
ICAD is a major cause of ischemic stroke accounting for up to 10% of strokes in the United States and as many as 30% in Asian, Hispanic, and African American communities. After one symptomatic event, the risk of recurrent stroke may be as high as 15% per year. Treatment with aspirin (or warfarin) in addition to other risk factor modification reduces the risk but the risk may still be as high as 22% at 2 years despite therapy. Multiple randomized clinical trials including SAMMPRIS (Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis) and VISSIT (The Vitesse Intracranial Stent Study for Ischemic Stroke Therapy) have evaluated the outcome after medical management alone and with percutaneous angioplasty and stenting. In spite of all efforts, management of ICAD is still challenging and optimal treatment modality is still unclear.
Pathophysiology of Strokes in Intracranial Stenosis
It is imperative to understand the pathophysiology of strokes in ICAD patients to perceive the complications associated with its treatment. ICS can produce symptoms through the following mechanisms :
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artery-to-artery emboli
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hemodynamic insufficiency
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acute thrombotic occlusion (unstable plaque)
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branch (perforator) occlusive disease
The literature tends to be unclear regarding in-depth descriptions of these pathophysiologic mechanisms in individual patients. This is particularly relevant in the case of branch occlusive disease (BOD). This entity is often mistakenly identified as small vessel disease while in reality it is ICAD that incorporates the perforator origins. The plaques in these cases have been identified on high resolution MRI to be unstable, despite a relatively smaller extent of luminal stenosis. This has potential implications in interpreting data from stenting trials. MRI in such cases shows small deep “lacunar” infarcts. The phenomenon of hypoperfusion from severe stenosis is well described and occurs as a result of exhausted cerebrovascular reserve in the affected vascular territory. Patients typically develop orthostatic or exercise/stress-related ischemic symptoms. MRI reveals multiple water-shed cortical infarcts in the affected arterial territory. Patients with ICS who have hypoperfusion symptoms have a higher recurrent stroke risk than those without. Although SAMMPRIS failed to identify these patients as benefiting from stenting, well-designed prospective single center studies have shown impressive reduction in recurrent ischemic events in such patients following extracranial–intracranial (EC–IC) bypass. Finally, one of the important causes of stroke in ICAD patients is the artery-to-artery embolism in which small emboli formed de novo because of relative stasis or plaque rupture may travel along the gradient to smaller distal territories to produce focal strokes.
All three of these pathomechanisms produce distinct stroke patterns and have different therapeutic and prognostic implications. For example, perforator related strokes are usually located in the subcortical or basal ganglia region, hypoperfusion strokes affect the water-shed areas, and artery-to-artery embolic strokes affect distal small vascular territories. Hypoperfusion related border-zone infarct was the most common pattern observed in the SAMMPRIS trial in contrast to the territorial strokes from artery-to-artery emboli seen in the WASID (Warfarin Aspirin Symptomatic Intracranial Disease) trial. Nevertheless, the stroke pattern in ICAD patients can be mixed, involving more than one pathomechanism.
Treatment
The optimal treatment protocol of ICAD is still evolving and is subject to great controversy especially after multiple randomized trials published variable results. However, the SAMMPRIS trial and its subsequent post hoc analysis studies, along with the VISSIT trial, have supported the role of medical management as the first line therapy to be instituted in all patients of ICAD with a significant risk of stroke. Surgical/endovascular management is now reserved for patients who develop recurrent transient ischemic attack (TIA) or strokes despite aggressive medical management. Although the protocol for maximal medical management is poorly defined, broadly it includes smoking cessation, antiplatelet therapy such as aspirin, clopidogrel, or dual antiplatelet therapy (DAPT), hyperlipidemia management with statins, hypertension control, and lifestyle modification with diet and activity.
Up to 12% of patients with medical management may fail therapy at 1 year, which may increase to 14%–22% at 2 years, and keep experiencing recurrent stroke/TIA symptoms. These patients are the focus of potential endovascular neurosurgical intervention. It is reiterated that based on studies to date it is advisable to prove failure of full medical therapy and, where indicated, demonstrate hemodynamic insufficiency before embarking on the endovascular path.
Endovascular Procedures
Since the 1980s, endovascular angioplasty has emerged as a successful minimally invasive treatment option for intracranial stenosis. Multiple retrospective and non-randomized studies published successful treatment with balloon angioplasty with or without stenting with a technical success rate of around 97% and complication rates ranging from 10% to 50%. The landmark SAMMPRIS trial was designed to evaluate the role of stenting in patients with severe stenosis with the Wingspan stent (Stryker Inc., Fremont, California). Interestingly, the trial concluded that intracranial stenting carried a higher 30-day and 2-year primary end-point of stroke, TIA, or death from vascular cause than best medical therapy. Similarly, the VISSIT trial enrolled 112 patients with symptomatic intracranial stenosis (70%–99%) into medical management and balloon-expandable stent group; however, the trial was prematurely halted because the interim analysis showed clear increased 30-day risk of any stroke in the stented group.
There is appreciation in the neurovascular world that there is most likely a distinct subset of patients with ICAD who may benefit from endovascular luminal restoration techniques in addition to medical therapy. This is especially relevant as technology rapidly evolves making devices much safer and more user-friendly than those used in SAMMPRIS. The high periprocedural stroke rate related to intracranial stenting in select locations in SAMMPRIS, which used a first-generation device, has led to a resurgence of interest in balloon angioplasty. The technique of submaximal angioplasty has been described in prospective studies to be feasible and safe, with periprocedural complication rates of around 5% as opposed to the nearly 15% rate in SAMMPRIS. The technique has been described using Gateway or Maverick (Boston Scientific, Fremont, California) or Mini-trek (Abbott, Abbott Park, Illinois) balloon catheters. The latter two are semi-compliant coronary balloons. The actual surgical technique involves using a standard access system with a sheath and an intermediate guide catheter. A 0.014′′ microwire is navigated across the stenosis and the balloon is navigated either as an exchange technique with a microcatheter or directly delivered over the wire. The balloon is 50%–80% undersized for the luminal diameter. Inflation is gradually performed and held at nominal pressure for up to a minute. Total flow arrest times are thus negligible and only one inflation usually suffices. The angiographic end-point that is aimed for is restoration of luminal diameter of more than 50% instead of a perfect-appearing result.
Complications with Endovascular Therapy of ICS
Although many of the prospective and retrospective individual case series have reported an acceptable complication rate, the main reason for negativisms for angioplasty and stenting from the SAMMPRIS and VISSIT trial is the higher periprocedural and 30 days event rates. It should be noted that these trials did not stratify lesions based on morphology, which probably influenced the trial results. A detailed understanding of complications of endovascular therapy is needed to advise patients. Overall, these complications can be categorized into two types:
General complications associated with cerebral angiography.
Specific complications related to angioplasty and/or stenting.
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General complications associated with cerebral angiography
These are dealt with in detail elsewhere in this book. Briefly, they mostly relate to access site hematoma, pseudoaneurysm, or contrast nephropathy ( Table 51.1 ). The important complications related to catheterization of cervicocerebral arteries are thromboembolism and spasm or dissection. These important adverse events can be catastrophic and may be caused by poor technique, challenging vessel anatomy, and underlying vasculopathy related to atherosclerosis. There was a higher than expected angiographic stroke rate in the SAMMPRIS trial. Tortuous arch anatomy with a high burden of aortic arch/carotid artery atherosclerosis, improper technique, prolonged intravascular time, inadequate preparation with antiplatelets, or anticoagulation are potential risk factors. Transradial access has been described as a means of reducing complications from catheterizing across the arch. Clot formation in the catheter with distal embolism in the catheterized vessel is a very common yet partially avoidable complication. Use of pressurized flush lines, use of periprocedural anticoagulation with heparin and/or antiplatelet agents, and proper cleaning of guidewires before reinsertion are potentially helpful toward reducing complications. Dissection is a feared complication but can be minimized with over-the-wire and proper techniques.
Table 51.1
Important complications and their preventive measures.
Type
Complication
Preventive measures
Access related
Groin hematoma
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Arterial puncture over the femoral head that allows appropriate application of manual pressure after the procedure
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Use of USG for vessel localization that avoids multiple punctures
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Appropriate use of closure devices
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Manual pressure application as indicated
Retroperitoneal hematoma
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Arterial puncture along the extraperitoneal course of femoral artery
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Arterial puncture at an angle of 45 degrees
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Arterial puncture over the femoral head that allows appropriate application of manual pressure after the procedure
Femoral artery dissection
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Arterial puncture at angle of 45 degrees
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Use of soft Glidewire after vessel puncture
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Avoidance of forceful insertion of guide sheath or catheters
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Use of longer sheaths that avoid vessel trauma from multiple insertion of catheters
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Careful insertion of sheath or catheters in presence of massive atherosclerotic or calcified femoral artery
Pseudoaneurysm
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Minimize vessel trauma during puncture by using USG
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Appropriate use of closure devices
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Manual pressure to seal the puncture site in case of bleeding
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Serial USG monitoring for vessel diameter in case of groin hematoma
Thrombosis
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Avoidance of larger guide sheath or catheters in narrowed femoral vessel
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Use of pressurized flush lines using heparinized saline
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Appropriate anticoagulation during procedure
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Avoid kinking of guide sheath
Infection
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Use of appropriate sterile precautions during procedure
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Use of prophylactic antibiotics not recommended
Renal
Contrast-induced nephropathy
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Preoperative documentation of kidney disease, previous contrast induced nephropathy
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Adequate periprocedural hydration
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Minimal possible use of intravenous contrast
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Maximum suggested contrast dose=(5 mL× body weight [kg])/baseline serum creatinine (mg/dL)
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Consider dilution of contrast during injection if kidney function is marginal and/or volumes of contrast become high
Intracranial
Vasospasm
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Use of appropriate sized catheter
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Smooth and slow navigation of catheter
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Appropriate use of balloon catheter and inflation at nominal pressure
Dissection
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Smooth and slow navigation of catheter
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Use of appropriate sized catheter
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Avoid navigation through acute kinks and tortuous vessel
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Avoid forceful navigation
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Placement of catheter tip along the curve of the vessel before contrast injection
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Avoid stiffer wires or catheters
Thrombosis and embolism
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Appropriate use of pressurized flush lines with heparinized saline
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Avoid exchange wires if possible. If necessary, wipe the wire properly before insertion of catheter over the wire
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Follow safe contrast injection techniques to avoid air embolism
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Periprocedural anticoagulation and antiplatelets
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Maximize procedural time efficiency without compromising techniques
Vessel perforation
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Use of soft wires and catheters
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Avoid forceful navigation through kinks and tortuous vessels
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Careful navigation through atherosclerotic plaques
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