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Keywords

aneurysmal subarachnoid haemorrhage
non-aneurysmal
non-traumatic subarachnoid haemorrhage
cardiac troponin
cardiac markers
neurogenic cardiac dysfunction
stress cardiomyopathy

How to Cite

Stoica, R. ., Iacob, D.-G. ., & Iacob, G. . (2022). Troponin and non-traumatic subarachnoid haemorrhage: Results from a study of 243 consecutive patients. Romanian Neurosurgery, 36(2), 139–144. https://doi.org/10.33962/roneuro-2022-025

Abstract

Introduction: Subarachnoid haemorrhage (SAH) is a devastating event, with a mortality of up to 50%. Acute cardiac dysfunction is common after such an event, and it is known to have a negative impact on the outcome of these patients. Cardiac troponin release occurs frequently after SAH and represents an early biomarker for neurogenic cardiac dysfunction.

Objective: The present study aimed to evaluate the impact of a raised troponin value on the outcome of SAH patients.

Methods: This is a prospective observational study held between 2014-2017 at the University Emergency Hospital, Bucharest. Data on clinical admission status, high-sensitivity troponin I, ECG and echocardiographic evaluation results, ICU length of stay and in-hospital mortality rate. Statistical analysis was performed using non-parametrical Mann-Whitney and chi-square tests. The results were considered significant at p<0.05.

Results: A total of 335 consecutive patients with non-traumatic SAH were admitted during the study period. 92 of them were excluded and 243 were analyzed, 203 with aneurysmal SAH and 40 with non-aneurysmal, non-traumatic SAH. High-sensitivity troponin I reached its peak level 48 to 72 hours after SAH and was higher in patients with aneurysmal SAH. For all SAH patients, its median and peak values on days 1 and 2 were correlated with the ICU length of stay and inversely correlated with in-hospital length of stay. For the first 3 days, the median and maximum troponin values are higher in patients who died compared with those who survived and were discharged home (p-value < 0.001). Predictors of an elevated troponin on day 1 are loss of consciousness at ictus, a high Hunt and Hess and Fisher Scale grade, intraventricular haemorrhage and cerebral midline shift.

Conclusions: The release of cardiac troponin is a valuable marker of neurogenic cardiac dysfunction in the first 3 days after SAH. The study replicates other data in the literature and highlights the association between SAH severity, early troponin elevation and in-hospital death.

https://doi.org/10.33962/roneuro-2022-025
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