An aneurysmal subarachnoid hemorrhage (SAH) is a serious neurological condition that can trigger severe morbidity and mortality. The incidence ranges from 6 to 28 per 10,000 subjects. SAH is associated with severe neurological deficits and complications [1]. Early detection and intervention improve the clinical outcomes and reduce the risks for long-term disability and mortality [2].

Several pathophysiological changes occur in the brain and other organs (including the heart) after rupture of an intracranial aneurysm [2,3]. The term ‘neurogenic stunned myocardium’ refers to a condition characterized by transient heart dysfunction. The mechanism remains poorly understood, but electrocardiographic (ECG) abnormalities are commonly observed in patients with aneurysmal SAHs; these yield valuable insights into the associated cardiac changes [4]. In patients with acute SAHs, the common ECG abnormalities include ST-segment elevation or depression, T wave changes (negative or positive deep T waves), U waves, a prolonged QT interval (QTc), and P wave abnormalities [2,[5], [6], [7]]. Ibrahim et al. [8] hypothesized that such ECG changes might be associated with angiographic vasospasm secondary to SAH. Huang et al. [9] considered that nonspecific ST segment or T wave changes and a prolonged QTc were independently associated with greater in-hospital mortality of SAH patients. Although many scholars have described ECG changes in SAH patients, the associated epidemiological, physiological, and prognostic features require further study [3].

Our study tested the hypothesis that, in patients with non-traumatic aneurysmal SAHs, the presence of ECG abnormalities upon admission to emergency departments (EDs) is associated with more severe neurological conditions, leading to unfavorable clinical outcomes and increased mortality.