Admission ECG-derived resting heart rate and in-hospital mortality after acute stroke: a multicenter retrospective cohort study

Background Early triage after acute stroke requires markers that are immediately available and clinically interpretable. The prognostic value of a single admission electrocardiogram (ECG)-derived resting heart rate (RHR), especially by atrial fibrillation (AF) status, remains insufficiently described. Methods We conducted a multicenter retrospective cohort study of adults hospitalized with ischemic stroke, hemorrhagic stroke, or transient ischemic attack at five tertiary hospitals in Palestine between January 2018 and January 2025. The exposure was the first available 12-lead ECG-derived RHR recorded at rest. The primary outcome was in-hospital all-cause mortality. Multivariable logistic regression adjusted for age, sex, hypertension, diabetes mellitus, ischemic heart disease, smoking, prior stroke, AF, and stroke subtype. Results The analytical cohort included 2,247 index hospitalizations (mean age 68.4 ± 13.6 years; 57.3% male), and 177 deaths occurred during hospitalization (7.9%). AF was present in 315 admissions (14.0%). Each 10-beats/min increase in admission RHR was associated with 12% higher odds of in-hospital death (adjusted odds ratio 1.12, 95% confidence interval 1.06–1.20; p < 0.001). Descriptively, mortality was higher with RHR ≥ 76 beats/min than with lower RHR (10.9% vs. 4.8%). In rhythm-stratified descriptive analyses, this separation was clearer without AF (9.0% vs. 3.6%; crude odds ratio 2.65, 95% confidence interval 1.78–3.96) than with AF (20.0% vs. 15.0%; crude odds ratio 1.42, 95% confidence interval 0.77–2.61). Conclusion Admission ECG-derived RHR was associated with all-cause in-hospital mortality in this multicenter acute-stroke cohort. Because standardized stroke-severity measures, exact ECG timing, heart-rate-modifying medications, and cause-specific mortality were not uniformly available, this association should be interpreted as pragmatic early risk information rather than evidence that RHR is an independent causal determinant or therapeutic target.