• Charlotte H P Cremers, Ivo A C van der Bilt, Irene C van der Schaaf, Mervyn D I Vergouwen, Jan Willem Dankbaar, Maarten J Cramer, Arthur A M Wilde, Gabriel J E Rinkel, and Birgitta K Velthuis.
• Department of Neurology and Neurosurgery, Room G03.232, Brain Center Rudolf Magnus, University Medical Center Utrecht, PO Box 85500, 3508 GA, Utrecht, The Netherlands. c.h.p.Cremers-2@umcutrecht.nl.
• Neurocrit Care. 2016 Apr 1; 24 (2): 202-6.

IntroductionCardiac dysfunction may occur after aneurysmal subarachnoid hemorrhage (aSAH). Although it is associated with poor outcome, the pathophysiological mechanism of this association remains unclear. We investigated the relationship between cardiac function and cerebral perfusion in patients with aSAH.MethodsWe studied 72 aSAH patients admitted within 72 h after ictus with echocardiography and cerebral CT perfusion within 24 h after admission. Cardiac dysfunction was defined as myocardial wall motion abnormalities or positive troponin. In patients with and without cardiac dysfunction, we calculated the mean perfusion [cerebral blood flow (CBF) and time-to-peak (TTP)] in standard regions of interest and calculated differences with 95% confidence intervals (95% CI).ResultsIn 35 patients with cardiac dysfunction minimal CBF was 15.83 mL/100 g/min compared to 18.59 in 37 without (difference of means -2.76; 95% CI -5.43 to -0.09). Maximal TTP was 26.94 s for patients with and 23.10 s for patients without cardiac dysfunction (difference of means 3.84; 95% CI 1.63-6.05). Mean global CBF was 21.71 mL/100 g/min for patients with cardiac dysfunction and 24.67 mL/100 g/min for patients without cardiac dysfunction (-2.96; 95% CI -6.19 to 0.27). Mean global TTP was 25.27 s for patients with cardiac dysfunction and 21.26 for patients without cardiac dysfunction (4.01; 95% CI 1.95-6.07).ConclusionaSAH patients with cardiac dysfunction have decreased focal and global cerebral perfusion. Further studies should evaluate whether this relation is explained by a direct effect of cardiac dysfunction on cerebral circulation or by an external determinant, such as a hypercatecholaminergic or hypometabolic state, influencing both cardiac function and cerebral perfusion.

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