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Relationship Between Cardiac Dysfunction and Cerebral Perfusion in Patients with Aneurysmal Subarachnoid Hemorrhage
Charlotte H P Cremers1,2, Ivo A C van der Bilt3, Irene C van der Schaaf4
1Department 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.
Insights
Cardiac dysfunction after aneurysmal subarachnoid hemorrhage (aSAH) is linked to poorer outcomes. This study found that aSAH patients with cardiac dysfunction exhibit reduced cerebral blood flow and impaired perfusion.
Area of Science:
- Neurology
- Cardiology
- Radiology
Background:
- Cardiac dysfunction is a known complication following aneurysmal subarachnoid hemorrhage (aSAH).
- The underlying pathophysiological mechanisms linking cardiac dysfunction to poor outcomes in aSAH remain incompletely understood.
- Investigating the relationship between cardiac function and cerebral perfusion is crucial for understanding aSAH pathophysiology.
Purpose of the Study:
- To investigate the relationship between cardiac function and cerebral perfusion in patients diagnosed with aSAH.
- To determine if cardiac dysfunction in aSAH patients is associated with altered cerebral blood flow (CBF) and time-to-peak (TTP).
Main Methods:
- A cohort of 72 aSAH patients admitted within 72 hours of ictus were studied.
- Echocardiography and CT perfusion imaging were performed within 24 hours of admission.
- Cardiac dysfunction was defined by myocardial wall motion abnormalities or positive troponin levels. Cerebral perfusion parameters (CBF and TTP) were analyzed in relation to cardiac function.
Main Results:
- Patients with cardiac dysfunction (n=35) showed significantly decreased minimal cerebral blood flow (15.83 mL/100 g/min) compared to those without (n=37; 18.59 mL/100 g/min).
- Maximal time-to-peak was prolonged in patients with cardiac dysfunction (26.94 s) versus those without (23.10 s).
- Mean global cerebral blood flow was reduced, and mean global time-to-peak was increased in aSAH patients with cardiac dysfunction.
Conclusions:
- aSAH patients experiencing cardiac dysfunction demonstrate diminished focal and global cerebral perfusion.
- Further research is warranted to elucidate whether this association is due to a direct cardiac effect on cerebral circulation or secondary factors like hypercatecholaminemia or hypometabolism.
Introduction:
Cardiac 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.
Methods:
We 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).
Results:
In 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).
Conclusion:
aSAH 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.
