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Ann Thorac Surg 2006;81:1644-1649
© 2006 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Transcerebral Platelet Activation After Aortic Cross-Clamp Release is Linked to Neurocognitive Decline

^a Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina
^b Department of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut, USA
^c Department of Internal Medicine (Hematology), Yale University School of Medicine, New Haven, Connecticut, USA
^d Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut, USA

Accepted for publication December 20, 2005.

^_* Address correspondence to Dr Rinder, Department of Anesthesiology, Yale University School of Medicine, 333 Cedar St, PO Box 208051, New Haven, CT 06520-8051 (Email: christine.rinder{at}yale.edu).

BACKGROUND: Neurocognitive decline after cardiac surgery requiring cardiopulmonary bypass (CPB) may be caused in part by highly prothrombotic atheroemboli to the brain; the source of these emboli is likely the ascending aorta and aortic arch. We examined transcerebral platelet activation gradients using simultaneous measurements in arterial and jugular venous blood and then compared gradients with post-CPB-associated neurocognitive injury.

METHODS: Eighty-one patients undergoing elective coronary artery bypass graft surgery requiring CPB were studied. Neurocognitive function was measured preoperatively and again at 6 weeks postoperatively. Paired arterial and jugular venous blood samples were drawn before surgery, immediately before and after aortic cross-clamp removal (an event previously linked to embolic showers), and at the end of the operation. Transcerebral platelet activation gradients (venous minus arterial values) were compared in patients with and without cognitive deficit.

RESULTS: Immediately after aortic cross-clamp removal, there was a significant increase in the transcerebral platelet activation gradient (increased % P-selectin-positive platelets during transcerebral passage) in the subset of patients who subsequently developed post-CPB cognitive deficit; this platelet activation gradient did not occur in patients without cognitive injury. In contrast, there was no transcerebral gradient of platelet activation in CPB patients as an entirety, nor was there a gradient at all other time points in the patient subset who went on to have cognitive deficit develop. This fleeting gradient of transcerebral platelet activation after cross-clamp removal was also significantly correlated with the overall change in cognitive injury score.

CONCLUSIONS: Transient intracerebral platelet activation after removal of the aortic cross-clamp is associated with post-CPB neurocognitive injury.

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