Cerebrovascular injuries found in acute type B aortic dissections are associated with blood pressure derangements and poor outcome.

OBJECTIVE

Cerebrovascular injury (CVI) is a recognized but underappreciated complication of acute type B aortic dissection (ATBAD). This study was performed to determine risk factors for CVI associated with ATBAD and, in particular, the possible contributory role of aggressive anti-impulse therapy.

METHODS

A retrospective review of all patients presenting to a tertiary medical center with an ATBAD between January 2003 and October 2012 was conducted. All CVIs were adjudicated by a vascular neurologist and assigned a probable cause. The initial intensity of anti-impulse therapy was defined as the difference in mean arterial pressure (ΔMAP) from presentation to subsequent admission to the intensive care unit.

RESULTS

A total of 112 patients were identified. The average age was 61 years; 64% were male, and 59% were African American. Twenty patients required operative intervention (14 thoracic endovascular aortic repairs and 6 open). CVI occurred in 13 patients (11.6%): 9 were hypoperfusion related (6 diffuse hypoxic brain injuries and 3 watershed infarcts), 2 were procedure related (both thoracic endovascular aortic repairs), 1 was an intracranial hemorrhage on presentation, and 1 was a probable embolic stroke on presentation. CVI patients had demographics and comorbidities comparable to those of the non-CVI patients. CVI was associated with operative intervention (54% vs 13%; P = .002). Thirty-day mortality was significantly higher in CVI patients (54% vs 6%; P < .001). Patients who suffered a hypoperfusion brain injury had a higher MAP on presentation to the emergency department (142 mm Hg vs 120 mm Hg; P = .034) and a significantly greater reduction in MAP (ΔMAP 49 mm Hg vs 15 mm Hg; P < .001) by the time they reached the intensive care unit compared with the non-CVI patients.

CONCLUSIONS

In our series, CVI in ATBAD is more frequent than previously reported and is associated with increased mortality. The most common causes are related to cerebral hypoperfusion. Higher MAP on presentation and greater decline in MAP are associated risk factors for hypoperfusion-related CVI. A less aggressive approach to lowering MAP in ATBAD warrants further study in an attempt to reduce CVI in ATBAD.