Abstract
Object: Patients with aneurysmal subarachnoid hemorrhage (aSAH) have an increased incidence of cardiac events and short-term unfavorable neurological outcomes during the acute phase of bleeding. We studied whether troponin I elevation after ictus can predict future major adverse cardiac events (MACEs) and long-term neurological outcomes after 2 years.Methods: Consecutive aSAH patients within 3 days of bleeding were eligible for review from a prospective observational cohort (ClinicalTrials.gov Identifier: NCT04785976). Potential predictors of future MACEs and unfavorable long-term neurological outcomes were calculated by Cox and logistic regression analyses. Additional Kaplan–Meier curves were performed.Results: A total of 213 patients were enrolled with an average follow-up duration of 34.3 months. Individuals were divided into two groups: elevated cTnI group and unelevated cTnI group. By the last available follow-up, 20 patients had died, with an overall all-cause mortality rate of 9.4% and an annual all-cause mortality rate of 3.8%. Patients with elevated cTnI had a significantly higher risk of future MACEs (10.6 vs. 2.1%, p = 0.024, and 95% CI: 1.256–23.875) and unfavorable neurological outcomes at discharge, 3-month, 1-, 2-years, and last follow-up (p = 0.001, p < 0.001, p = 0.001, p < 0.001, and p < 0.001, respectively). In the Cox analysis for future MACE, elevated cTnI was the only independent predictor (HR = 5.980; 95% CI: 1.428–25.407, and p = 0.014). In the multivariable logistic analysis for unfavorable neurological outcomes, peak cTnI was significant (OR = 2.951; 95% CI: 1.376–6.323; p = 0.005). Kaplan–Meier analysis indicated that the elevated cTnI was correlated with future MACE (log-rank test, p = 0.007) and subsequent death (log-rank test, p = 0.004).Conclusion: cTnI elevation after aSAH could predict future MACEs and unfavorable neurological outcomes.
Highlights
The brain-heart connection loses balance after stroke [1]
Patients with elevated cardiac troponin I (cTnI) had a significantly higher risk of future major adverse cardiac events (MACEs) (10.6 vs. 2.1%, p = 0.024, and 95% confidence intervals (CI): 1.256–23.875) and unfavorable neurological outcomes at discharge, 3-month, 1, 2-years, and last follow-up (p = 0.001, p < 0.001, p = 0.001, p < 0.001, and p < 0.001, respectively)
In the Cox analysis for future MACE, elevated cTnI was the only independent predictor (HR = 5.980; 95% CI: 1.428–25.407, and p = 0.014)
Summary
The brain-heart connection loses balance after stroke [1]. Cardiac complication has been shown to frequently occur in the emergency aneurysmal subarachnoid hemorrhage (aSAH) [2,3,4]. A series of previous studies have shown that circulating cardiac biomarkers, including creatine phosphokinase isoenzyme-MB (CK-MB), troponin, brain natriuretic peptide (BNP), and N-terminal pro-B-type natriuretic peptide (NT-proBNP), are associated with delayed cerebral ischemia (DCI), short-term unfavorable neurological outcomes, and in-hospital mortality at the acute phase after aSAH [5,6,7,8]. Among the cardiac biomarkers listed above, the incremental level of cardiac troponin I (cTnI) on admission was reported in 21–68% of emergency aSAH patients [6, 9], and the cardiac troponin has been shown to reach high sensitivity and specificity in the identification of cardiac abnormalities indicating subsequent major adverse cardiac events (MACEs) at the acute phase of aSAH, though conflicting results have been reported [2, 3, 10,11,12]. We aimed to explore whether the admission cTnI of emergency aSAH patient at the acute phase could predict future MACEs and long-term unfavorable neurological outcomes
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
