Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Endovascular Treatment of Acute Stroke and Occlusive Cerebrovascular Disease
Clinical Pearls
-
Stroke has been one of the leading causes of mortality and serious long-term disability. Timely treatment of patients with acute ischemic stroke can drastically change the outcomes. Endovascular treatment has become an important treatment modality for acute ischemic strokes.
-
Noninvasive imaging prior to endovascular treatment provides the means to identify patients who are amenable to endovascular treatment and who would have the greatest benefit. Although the Alberta Stroke Programme Early CT Score can identify patients who are likely to have a poor functional outcome, perfusion studies can discern viable tissue from infarct core that can select patients who are ideal for endovascular intervention.
-
Endovascular techniques for treatment of acute ischemic stroke involve aspiration with a large bore catheter (also known as A Direct Aspiration First Pass Technique [ADAPT] if used as first pass), the use of a stent retriever device to engage the clot and retrieve it, or the use of these techniques in combination (also known as Solumbra or combined aspiration and stent retriever [CASPER]) when a stent retriever device is withdrawn while using aspiration. The comparative safety and effectiveness of each technique is the focus of the multicenter randomized controlled trial, the COMPASS (COMParison of ASpiration vs Stent) Trial: a Direct Aspiration First Pass Technique, which has closed and is currently undergoing analysis.
-
Ischemic stroke secondary to underlying intracranial atherosclerotic disease (ICAD) has a high probability of recurrence. The largest randomized controlled trial, Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis (SAMMPRIS), failed to show the benefit of percutaneous transluminal angioplasty and stenting over medical management alone. Nevertheless, patients who are refractory to medical management may benefit from endovascular treatment of ICAD using submaximal angioplasty alone.
-
Symptomatic carotid disease needs prompt treatment to prevent the recurrence of stroke. Large multicenter randomized controlled trials have shown carotid artery stenting to be equivalent to carotid endarterectomy for treatment of symptomatic carotid disease. Further trials are under way to compare the two treatment modalities in asymptomatic patients.
Introduction
Cerebral metabolism is highly active and requires 20% of the body's oxygen while representing only 2% of a person's total body weight. This suggests that the brain is highly vulnerable to hypoxia and hypoperfusion. Ischemic changes and infarcts evolve within minutes of low blood flow. Cerebral blood flow comprises nearly 18% of cardiac output to generate 50 mL/100 g of brain tissue per minute. At nearly one-fifth of the normal flow, membrane pumps fail and the typical electrochemical gradient is lost, leading to neuronal and glial cell death.
Understanding the relationship between cerebral blood flow and cerebral blood volume plays a critical role in understanding how and when to intervene in acute stroke treatment. The cerebral vasculature has a unique way of autoregulation that reflects the brain's intrinsic ability to maintain its flow. Pressure-flow relationships help surgeons understand the dynamics among severity, location, and clinical presentation of acute versus chronic occlusions as well as the flow dynamics and collateral circulations in situations of chronic low flow states.
Epidemiology
According to the Heart Disease and Stroke Statistics—2016 Update from the American Heart Association, more than 6.5 million people in the United States have a history of stroke. This number continues to rise as the annual incidence of stroke in the United States is reported to be about 795,000 cases. Of these, 87% are known to be ischemic in nature. About 1 in every 20 deaths in the United States in 2013 was attributed to stroke, with an average of stroke-related death every 4 minutes. Additionally, stroke has been one of the leading causes of serious long-term disability, and stroke-related costs are estimated to rise to $184.1 billion by 2030. Active efforts to develop and use the latest imaging modalities to promptly identify stroke patients and provide them with timely treatment are especially important, knowing that this can drastically change the outcomes.
Pathophysiology
Atherosclerotic Disease
Low-density lipoprotein (LDL) and overall triglyceride and cholesterol levels have been shown to play a significant role in atherosclerotic disease. The initial plaque (the fatty streak) caused by elevated LDL tends to accumulate as macrophages engulf more cholesterol leading to progressive inflammation. As LDL becomes highly oxidized, it tends to become incorporated into the subendothelial layers of blood vessels, especially larger high velocity vessels including the carotid and vertebral arteries. This inflammatory cycle and smooth muscle hyperplasia causes further narrowing of the vessels ( Fig. 23.1 ). Segments that incorporate significant tortuosity and flow variation allow for plaque accumulation. Furthermore, resultant injury to the intimal layer from this accumulation causes platelet aggregation and thrombus formation.
In a scenario with progressive buildup of the plaque and smooth muscle hyperplasia, the lumen decreases in size as the arterial wall begins to dilate. This continues to occur to compensate for the flow until smooth muscle and collagen reach their compensatory maximum. This atherosclerotic plaque causes progressive stenosis and eventually can result in complete occlusion. During this process, there is an elevated risk of ischemic events from a thromboembolus.
Similar processes occur in the intracranial vessels, causing flow limitations in distal vasculature. Symptoms occur when autoregulation is outpaced. Occlusive disease leads to (1) hypoperfusion, (2) occlusion at the site of stenosis secondary to plaque rupture causing acute thrombus formation or progressive growth of the plaque resulting in chronic occlusion, (3) thromboembolism distal to the stenotic segment, and (4) occlusion of small perforators near a plaque causing distal strokes.
Embolus and Arterial Dissections
Acute occlusion in the cerebral vasculature can commonly occur secondary to an embolus from a proximal site of thrombosis. Usual suspects are atrial fibrillation or atherosclerotic disease in the proximal vasculature including the aorta, carotid, or vertebral arteries as described earlier. In case of atrial fibrillation, the stasis of flow in the atrial chambers of the heart can promote thrombus formation along the endocardial walls. Small clots eventually break off and travel to the carotid branches due to their straight path and high flow from the aorta.
Dissection of the arterial wall, or a tear in the intimal layer, is another commonly encountered mechanism for acute ischemic stroke. Causes may be trauma, iatrogenic injury, or even a spontaneous occurrence without definitive etiology. The result is a false lumen preventing the normal flow of blood distal to the injury. The parent vessel narrows or can occlude as the blood flows under the intimal flap. This compromises intracranial blood flow and leads to acute stroke.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here