Can a large vessel infarct cause damage to watershed areas?

From the Guidelines

Yes, a large vessel infarct can cause damage to watershed areas. Watershed areas, also called border zone regions, are located at the junction between two major cerebral arterial territories and receive dual blood supply from the distal branches of these arteries. When a large vessel occlusion occurs, such as in the middle cerebral artery or internal carotid artery, the resulting drop in perfusion pressure affects not only the primary territory of that vessel but can also compromise blood flow to watershed regions. This happens because watershed areas already receive relatively less blood flow under normal conditions, making them vulnerable to hypoperfusion when a proximal vessel is occluded. The mechanism involves both hemodynamic compromise from the blocked large vessel and potential microemboli that can travel to these border zones. Some key points to consider include:

• Watershed infarcts can occur due to hypoperfusion in patients with significant arterial stenosis in cervicocephalic arteries, as noted in the study 1.
• The Stenting versus Aggressive Medical Therapy for Intracranial Arterial Stenosis (SAMMPRIS) trial showed that aggressive medical treatment alone can reduce stroke recurrence in patients with large-artery intracranial atherosclerosis 1.
• Patients with severe carotid stenosis or occlusion are particularly susceptible to watershed infarcts when cerebral perfusion pressure drops.
• The presence of both territorial and watershed infarcts may indicate a proximal large vessel occlusion requiring urgent intervention.
• Aggressive medical treatment, including control of other risk factors and lifestyle changes, can play a beneficial role in secondary stroke prevention, as seen in the SAMMPRIS trial 1.

From the Research

Large Vessel Infarct and Watershed Damage

• A large vessel infarct can cause damage to watershed areas, as evidenced by studies that have investigated the relationship between large vessel occlusion and watershed infarcts 2, 3, 4, 5, 6.
• Watershed infarcts are ischemic lesions that occur in characteristic locations at the junction between two main arterial territories, and are thought to be caused by decreased perfusion in the distal regions of the vascular territories 3.
• Research has shown that large vessel occlusion, such as internal carotid artery occlusion, can lead to watershed infarcts, particularly in patients with mild symptoms 2.
• The pathogenesis of watershed infarcts is thought to be related to hemodynamic changes in blood flow, with studies demonstrating that altering hemodynamic conditions can induce watershed infarcts in animal models 4.
• In patients with internal carotid artery disease, watershed infarcts can occur in both cortical and internal watershed areas, with evidence suggesting that hemodynamic compromise plays a key role in the development of internal watershed infarcts 5.
• Etiologic subtypes of watershed infarcts have been identified, with internal watershed infarcts often attributed to large-artery atherosclerosis, and external watershed infarcts thought to be caused by embolism 6.

Mechanisms of Watershed Infarction

• Hemodynamic mechanisms, such as decreased perfusion pressure, are thought to play a key role in the development of watershed infarcts, particularly in internal watershed areas 5.
• Embolic mechanisms, such as artery-to-artery embolism, may also contribute to the development of watershed infarcts, particularly in external watershed areas 6.
• The relationship between cortical watershed infarction and hemodynamic compromise is complex, with evidence suggesting that both hemodynamic and embolic mechanisms may play a role 5.

Clinical Implications

• The identification of watershed infarcts on imaging studies, such as MRI, can be an important prognostic factor in patients with large vessel occlusion, with studies suggesting that watershed infarcts may be a key sign for predicting neurological deterioration 2.
• Understanding the mechanisms of watershed infarction can inform treatment strategies, with hemodynamic and embolic mechanisms potentially requiring different therapeutic approaches 5, 6.