Hemodynamic challenges in traumatic subarachnoid hemorrhage complicated by cerebral vasospasm
John Papanikolaou

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, PhDJohn Papanikolaou
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Correspondence
- Corresponding author at: Biopolis, 41110 Larissa, Greece. Tel.: +30 241 068 2960; fax: +30 241 067 0838.

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John Papanikolaou
Search for articles by this author
Correspondence
- Corresponding author at: Biopolis, 41110 Larissa, Greece. Tel.: +30 241 068 2960; fax: +30 241 067 0838.

Demosthenes Makris, PhD
,,Department of Critical Care, School of Medicine, University of Thessaly, University Hospital of Larissa, Thessaly, Greece
Article Info
Publication History
Published Online: February 12, 2016Accepted: January 25, 2016; Received: January 16, 2016;
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Figure
Neuroimaging evolution in our two patients with traumatic subarachnoid hemorrhage.
We have read with great interest the recent review by Varvarousi et al
[1]
on the role of levosimendan in the clinical setting of aneurysmal subarachnoid hemorrhage (SAH). Previous work by us
[2]
and others
[3,4]
proposed depressed cardiac output (CO), mainly attributed to catecholamine-mediated myocardial dysfunction, as a critical determinant of delayed cerebral ischemia (DCI) and poor neurologic outcome. In this respect, rapid hemodynamic augmentation, with either levosimendan
[5]
or other agents
[6]
, has the potential to reverse cerebral ischemia and prevent further brain damage.
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