Page 73 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Cardiac dysfunction and cerebral perfusion in patients with aSAH
Introduction
Cerebral perfusion can be affected shortly after aneurysmal subarachnoid hemorrhage (aSAH).1 Cardiac dysfunction, consisting of echocardiographic wall motion abnormalities (WMAs), ECG changes and positive troponins suggestive of myocardial damage, may also occur after aSAH. The WMAs are independently associated with poor outcome after aSAH.2 The pathophysiology behind this finding is unclear. To investigate whether the increased risk of poor functional outcome in patients with cardiac dysfunction2 is explained by lower cerebral perfusion, a first step is to identify whether a relationship between cardiac function and cerebral perfusion exists. Therefore the aim of this study was to investigate the relationship between cardiac dysfunction and cerebral perfusion in patients with aSAH.
Methods
Design
Patients were retrieved from a prospectively collected series of aSAH patients who
were admitted to the University Medical Center Utrecht between 2005 and 2008
and participated in the SEASAH (Serial Echocardiography After SubArachnoid 5 Hemorrhage) study.2 Patients enrolled in the SEASAH study had to be admitted
within 72 hours after ictus and underwent echocardiography and blood testing within
24 hours after admission. As part of routine care in our institution all patients with
aSAH undergo non-contrast CT (NCCT), CT perfusion (CTP) and CT-angiography
(CTA) on admission, unless contrast contraindications exist. The SEASAH study was
approved by the national and local hospital medical ethics committees. Informed
consent was obtained from the patient or next of kin.
Echocardiography and troponin release
Transthoracic echocardiography was performed within 24 hours after admission. Two cardiologists, unaware of clinical and cerebral perfusion data, independently assessed the presence or absence of WMAs according to American Society of Echocardiography standards.3 More details on the scoring of WMAs are published earlier.2 For assessment of troponin release, the upper limits of normal as defined by the local laboratory were used as reference. Patients were dichotomized in “cardiac dysfunction” (with WMAs or positive troponins) or “no cardiac dysfunction” (no WMAs and negative troponins).
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