Page 78 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Chapter 5
of this early heart-brain dysfunction may have implications for preventing cerebral hypoperfusion after aSAH and therefore for better outcome.
The clinical impact of lower cerebral perfusion is not well understood, as it is unknown at what perfusion value thresholds patients develop cerebral ischemia in the context of aSAH. We could not study the influence of elevated intracranial pressure as a possible cause of cerebral hypoperfusion, as ICP measurements are not part of routine care in all aSAH patients in our hospital. Moderate to severe early vasospasm (≥25% arterial luminal narrowing) was only seen in 2 patients on CT angiography that was performed on admission in all patients.
The worse clinical condition in patients with cardiac dysfunction might therefore be explained by a lower cerebral perfusion caused by cardiac dysfunction, or by a systemic determinant that influences both cardiac dysfunction and cerebral perfusion, such as the hypercatecholaminergic response. Excessive release of norepinephrine from myocardial sympathetic nerve terminals may lead to denervation of both the myocytes and the nerve terminals and thereby to focal WMAs and cardiac dysfunction.8 In addition, this systemic hypercatecholaminergic response might also cause dysfunction of the cerebral autoregulation and thereby lead to perfusion deficits in the brain. Other potential mechanisms underlying early cerebral hypoperfusion after aSAH are endothelial dysfunction resulting from both the initial hypoperfusion insult as well as the pro-inflammatory, pro-thrombotic and pro-vasoconstriction properties of extravasated subarachnoid blood. Another possible explanation is a hypometabolic state, which was also found to be associated with the early cerebral hypoperfusion in a PET study in SAH patients.9
In this study we investigated whether a relationship between cardiac function and cerebral perfusion exists in patients with aSAH. We were unable to determine whether this is a causal relationship.
Further studies need to evaluate whether cerebral hypoperfusion occurring soon after aSAH is explained by cardiac dysfunction or by an external determinant, such as a hypercatecholaminergic reaction or hypometabolic state, influencing both cardiac function and cerebral perfusion. Future studies could also investigate whether treatment of cardiac dysfunction or a systemic response, improves cerebral perfusion and thereby prognosis.
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