Troponin and non-traumatic subarachnoid haemorrhage

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.