Page 77 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Cardiac dysfunction and cerebral perfusion in patients with aSAH Table 2: Perfusion values (with 95% confidence intervals)
Cardiac dysfunction (n=35)
No cardiac dysfunction (n=37)
All
WMAs and positive troponins (n=11)
WMAs only (n=5)
Positive troponins only (n=19)
Focal perfusion
Minimal CBF (mL/100g/min)
Maximal TTP (s)
Global perfusion
Mean CBF (mL/100g/min)
Mean TTP (s)
15.83 16.13 17.14 15.32 (14.17-17.49) (12.22-20.03) (10.16-24.11) (13.30-17.34)
26.94 28.39 24.81 26.66 (25.56-28.32) (26.10-30.67) (20.14-29.48) (24.60-28.72)
21.71 22.47 23.03 20.93 (19.87-23.55) (18.05-26.88) (15.63-30.42) (18.72-23.13)
25.27 26.56 22.98 25.12 (23.97-26.56) (24.71-28.42) (18.23-27.73) (23.14-27.10)
18.59 (16.47-20.72)
23.10 (21.34-24.85)
24.67 (21.99-27.35)
21.26 (19.63-22.88)
n = number; WMAs = wall motion abnormalities; CBF
= cerebral blood flow; TTP = time-to-peak.
Early vasospasm was seen in only two patients (2.8%) on admission CTA. One
patient had severe (>50%) arterial narrowing of the right MCA bifurcation in the
presence of a MCA aneurysm, substantial SAH and a large intracerebral hematoma.
The lowest perfusion values were also seen in the right MCA territory. The other
patient had more diffuse bilateral moderate (25-50%) narrowing of both MCA and 5 ACA in the presence of an anterior communicating artery aneurysm. In this patient
lowest perfusion values were seen in the right thalamus and the right PCA territory. Both patients with early vasospasm were in the subgroup with cardiac dysfunction, one had increased troponins and one patient had WMAs. Excluding these two patients did not change the results.
Discussion
The results of our study show that aSAH patients with cardiac dysfunction have an impaired cerebral perfusion, both on a focal and global level.
Cardiac complications following central nervous system events such as ischemic or hemorrhagic stroke, brain tumors and even emotional stress have been described extensively.5-6 In recent years there has been increasing interest in this “heart-brain axis” and its clinical implications. Early onset cardiac and cerebral dysfunction are both related to poor outcome after aSAH.2,7 Understanding the pathophysiology
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