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J Thorac Cardiovasc Surg 2009;137:1012-1019
© 2009 The American Association for Thoracic Surgery
Cardiothoracic Transplantation |
a Center for Advanced Cardiac Care, Columbia University Medical Center, New York, NY
b Department of Neurology, Columbia University Medical Center, New York, NY
c Division of Biostatistics, Columbia University Medical Center, New York, NY
d Division of Cardiology, University of Minnesota, Minneapolis, Minn
e Division of Cardiothoracic Surgery, University of Minnesota, Minneapolis, Minn
f Department of Neurology, University of Minnesota, Minneapolis, Minn
g Division of Cardiology, Georgetown University–Washington Hospital Center, Washington, DC
h Division of Cardiothoracic Surgery, Mayo Clinic, Rochester, Minn
Received for publication March 12, 2008; revisions received October 19, 2008; accepted for publication November 22, 2008. * Address for reprints: Katherine Lietz, MD, PhD, Center for Advanced Cardiac Care, Division of Cardiology, Columbia University Medical Center, PH-12 Stem Rm 134, 622W 168th St, New York, NY 10032. (Email: KL2384{at}columbia.edu).
Objective: Cerebral hyperperfusion is a life-threatening syndrome that can occur in patients with chronically hypoperfused cerebral vasculature whose normal cerebral circulation was re-established after carotid endarterectomy or angioplasty. We sought to determine whether the abrupt restoration of perfusion to the brain after left ventricular assist device (LVAD) implantation produced similar syndromes.
Methods: We studied the role of increased systemic flow after LVAD implantation on neurologic dysfunction in 69 consecutive HeartMate XVE LVAD (Thoratec, Pleasanton, Calif) recipients from October 2001 through June 2006. Neurologic dysfunction was defined as postoperative permanent or transient central change in neurologic status, including confusion, focal neurologic deficits, visual changes, seizures, or coma for more than 24 hours within 30 days after LVAD implantation.
Results: We found that 19 (27.5%) patients had neurologic dysfunction, including encephalopathy (n = 11), coma (n = 3), and other complications (n = 5). The multivariate analysis showed that an increase in cardiac index from the preoperative baseline value (relative risk, 1.33 per 25% cardiac index increase; P = .01) and a previous coronary bypass operation (relative risk, 4.53; P = .02) were the only independent predictors of neurologic dysfunction. Reduction of left ventricular assist device flow in 16 of the 19 symptomatic patients led to improvement of symptoms in 14 (87%) patients.
Conclusions: Our findings showed that normal flow might overwhelm cerebral autoregulation in patients with severe heart failure, suggesting that cerebral hyperperfusion is possible in recipients of mechanical circulatory support with neurologic dysfunction.
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