Cerebrovascular Injuries Are Commonly Found in Acute Type B Aortic Dissections and Are Associated With Blood Pressure Derangements and Poor Outcome
Al Adas Z, Miller D, Weaver M, Shepard A, Nypaver TJ, Nour K, Balraj P, and Kabbani L. Cerebrovascular injuries are commonly found in acute type b aortic dissections and are associated with blood pressure derangements and poor outcome. J Vasc Surg 2017; 66(2):E28-E28.
J Vasc Surg
Objectives 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 All patients presenting to a tertiary medical center with an ATBAD between January 2003 and October 2012 were retrospectively reviewed. All CVIs were adjudicated by a vascular neurologist and assigned a probable etiology. The initial intensity of anti-impulse therapy was defined as the difference in mean arterial pressure (MAP) from presentation to subsequent admission to the intensive care unit. Data analysis was conducted on SPSS 22.0 software (IBM, Armonk, NY).
Results A total of 112 patients (64% males) were identified. Average age was 61 years, and 59% were African American. Twenty patients required operative intervention (14 thoracic endovascular aortic repairs [TEVARs] and 6 open). CVI occurred in 13 patients (11.6%): 9 hypoperfusion (6 diffuse hypoxic brain injuries, 3 watershed infarcts), 2 procedure-related (both TEVARs), 1 intracranial hemorrhage upon presentation, and 1 probable embolic stroke upon presentation. CVI patients with and without hypoperfusion had demographics and comorbidities comparable to the non-CVI patients. CVI was associated with operative intervention (54% of CVI patients had an intervention vs 13% of non-CVI patients; P = .002). Thirty-day mortality was significantly higher in CVI patients (54% vs 6%; P < . 001). MAP upon presentation to the emergency department, however, was higher in hypoperfusion patients than in the non-CVI patients (142 vs 120 mm Hg; P = .034). These same patients had a significantly greater reduction in MAP than those who did not have a CVI (49 vs 15 mm Hg, respectively; P < . 001). A decline in MAP by at least 30% was significantly associated with a hypoperfusion CVI ( P = .001).
Conclusions CVI in ATBAD is more frequent than previously reported and increases the mortality of this entity. The most common etiologies are related to cerebral hypoperfusion. Higher MAP on presentation and more rapid decline in MAP are associated risk factors for hypoperfusion CVI. A less aggressive approach to lowering MAP warrants further study in an attempt to reduce CVI in ATBAD.