What is the etiology of watershed infarction associated with aortic dissection surgery?

Etiology of Watershed Infarction Associated with Aortic Dissection Surgery

Watershed infarctions during aortic dissection surgery primarily result from hemodynamic compromise and embolic phenomena, with hypoperfusion being the dominant mechanism.

Primary Mechanisms

Hemodynamic Factors

• Prolonged periods of hypoperfusion during cardiopulmonary bypass can exacerbate brain low-flow in areas with pre-existing stenotic brain vessels, creating watershed infarcts in terminal vascular territories 1
• Watershed areas represent junctions between different arterial territories, making them particularly vulnerable to ischemia during periods of reduced perfusion pressure 2
• Aggressive blood pressure management during aortic dissection treatment can contribute to cerebral hypoperfusion - patients who suffered hypoperfusion brain injuries had significantly greater reductions in mean arterial pressure (ΔMAP 49 mm Hg vs 15 mm Hg) compared to patients without cerebrovascular injury 3
• Internal carotid artery stenosis ≥70% is strongly associated with watershed infarction (OR 11.7,95% CI 1.8-76.8) during cardiac surgery 4

Embolic Phenomena

• Atheroemboli dislodged from the descending thoracic aorta during device manipulation are a major cause of stroke and watershed infarcts, occurring in 2.5-8% of patients undergoing thoracic endovascular procedures 2
• Pre-existing atherosclerotic disease increases the risk of atheroemboli during endovascular manipulation 2
• Aortic arch atheroma is associated with embolic infarcts (OR 3.4,95% CI 1.0-12.0) during cardiac surgery 4
• Embolic phenomena can occur from thrombus formation on the dissection flap or from manipulation of the aorta during surgical repair 1

Risk Factors and Predisposing Conditions

Anatomical and Procedural Factors

• Increased aortic tortuosity in the proximal landing zone is associated with higher risk of endoleak and subsequent embolic complications 2
• Complex surgical procedures carry higher risk of neurological complications, with stroke rates of up to 3.1% in patients undergoing combined coronary and mitral valve surgery 1
• Manipulation of the aortic arch during endovascular procedures increases the risk of embolization to the cerebral circulation 2
• Prolonged cross-clamp times (>2 hours) increase the risk of neurological complications, particularly in patients with impaired ventricular function 1

Patient-Specific Factors

• Pre-existing cerebrovascular disease, particularly carotid stenosis, significantly increases the risk of watershed infarction during aortic surgery 4, 5
• Hypertension, found in 85% of patients with ruptured aneurysms, contributes to increased wall stress and potential for dissection, especially during winter months when blood pressure tends to be higher 6
• Old subcortical infarcts are associated with increased risk of embolic infarcts (OR 5.5,95% CI 1.1-26.6) during cardiac surgery 4
• Higher aortic valve gradient increases risk of embolic infarct (OR 1.3 per 5 mm Hg increase, 95% CI 1.09-1.6) 4

Pathophysiological Mechanisms

Cerebral Autoregulation Impairment

• Perioperative blood pressure alterations, especially hypotension, can aggravate lesions caused by microembolism by impairing the clearing of emboli 1
• Systemic inflammatory response syndrome (SIRS) triggered by cardiopulmonary bypass can impair cerebral autoregulation, making the brain more vulnerable to hypoperfusion 1
• Watershed areas are particularly vulnerable to hypoperfusion due to their location at the junction between major arterial territories 5

Vascular Compromise

• Direct extension of the dissection into the arch vessels can compromise cerebral blood flow, leading to watershed infarcts 1, 7
• Malperfusion of arch vessels may result in stroke due to hemodynamic compromise 7
• False lumen expansion can compress the true lumen, reducing blood flow to branch vessels including cerebral arteries 1

Clinical Presentation and Outcomes

• Neurologic symptoms occur in approximately 17% of patients with aortic dissection, with ischemic stroke present in 53% of those with neurologic manifestations 1
• Watershed infarcts may present with specific neurological deficits depending on the affected territory, including motor weakness 5
• Cerebrovascular injury in acute aortic dissection is associated with significantly higher mortality (54% vs 6%) 3
• Neurological complications may be transient in up to 50% of cases, and as many as one-third of patients with neurological symptoms present without complaints of chest pain 1

Prevention Strategies

• Less aggressive approach to lowering blood pressure in acute aortic dissection may reduce the risk of cerebral hypoperfusion and subsequent watershed infarction 3
• Identification of high-risk anatomical features before intervention allows for more careful procedural planning 2
• Preservation of critical branch vessels during endovascular procedures is essential to maintain adequate cerebral perfusion 2
• Close monitoring for signs of cerebral ischemia in the perioperative period is essential, especially in high-risk patients 2