Introduction: Primary neurocardiogenic injury (NCI) in aneurysmal subarachnoid haemorrhage (aSAH) is believed to be mediated by an early, transient surge in catecholamines. About 30% of aSAH is complicated by symptomatic cerebral artery vasospasm (VS), resulting in regional, potentially reversible, ischaemia. Treatment is directed at increasing cerebral perfusion pressure by inducing systemic hypertension (ISH) with vasopressors such as noradrenaline which, in itself, can cause myocardial injury. The aim of our study was to assess the safety profile of ISH with noradrenaline vasoconstriction for the treatment of VS.
Methods: This is a retrospective observational service evaluation of patients suffering aSAH-associated VS treated with noradrenaline to achieve individualized mean arterial pressure (MAP) targets. Multivariable regression analysis was used to examine the association between noradrenaline dose, MAP, patient characteristics or SAH severity and troponin I (cTnI) as a biomarker of myocardial injury. Additionally,half-time of cTnI released during induced hypertension was estimated.
Results: There was no association between cTnI release in primary NCI and that in ISH (OR=1.5; p = 0.71). A statistically significant positive association between noradrenaline dose and cTnI rise and an inverse association between MAP (range 60-155 mmhg) and cTnI were found during ISH. Age, sex, WFNS and Fisher grade and fluid balance showed no association with cTnI release during ISH. Half-time of cTI after secondary rise was 3.3 days.
Conclusions: Our study shows that the NA dose, rather than achieved MAP or primary NCI, predispose the patient to myocardial injury. This is of particular importance for clinical decision-making and choice of MAP targets in the context of VS treatment. With a half-time of cTI three times longer than in acute myocardial infarction, the mechanism of injury seems to be a result of prolonged toxic effect on myocytes.
Patient Care: Informs clinical decision-making and safe choice of MAP targets in the context of vasospasm treatment
Learning Objectives: Primary neurocardiogenic injury in SAH does not predispose to further myocardial injury during induced hypertension treatment in vasospasm. Noradrenaline dose used directly correlates with release of Troponin, used here as biomarker of myocardial injury.