“…As reported previously for patients with subarachnoid hemorrhage [21], elevation of troponin I levels may, on the one hand, result from intraventricular blood and, therefore, meningeal irritation, leading to strong systemic stress-responses [22,23]. As a result, an enhanced release of catecholamines and consequently higher myocardial stress may reflect a neurocardiac dysbalance, evident also after ICH, notably in those patients with intraventricular involvement [21,22,24]. In addition, up to now, the longitudinal occurrence of troponin elevations in ICH patients was only insufficiently established and pathophysiological considerations further include an increase of intracranial pressure additionally triggering sympathetic storms [10,21,[24][25][26].…”