Prognostic Value of Elevated Cardiac Troponin I After Aneurysmal Subarachnoid Hemorrhage

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.

Insular cortex Hounsfield units predict postoperative neurocardiogenic injury in patients with aneurysmal subarachnoid hemorrhage

“…A plethora of antecedent studies expounded upon the correlation between troponin with myocardial impairment following a stroke. 14,16,[42][43][44] Additionally, some researchers have alluded to the concurrence of IC impairment due to stroke with elevated troponin concentrations. 45,46 Scheitz, J.F.…”

“…[11][12][13] Furthermore, pertinent preoperative relevant cardiovascular biomarkers such as cardiac troponin I have exhibited connection with unfavorable postoperative outcomes. 11,12,[14][15][16] Antecedent research has illuminated the indispensable role of the insular cortex (IC) within the central automatic network in regulating of the cardiovascular system. 17,18 To be specific, IC stimulation triggers activation of the sympathetic nervous system, engendering manifestations such as tachycardia and heightened catecholamine release, factors that may precipitate myocardial necrosis.…”

“…Notably, these complications, particularly neurocardiogenic injury (NCI), have demonstrated associations with DCI and adverse outcomes 11–13 . Furthermore, pertinent preoperative relevant cardiovascular biomarkers such as cardiac troponin I have exhibited connection with unfavorable postoperative outcomes 11,12,14–16 …”

Timing of operation for poor‐grade aneurysmal subarachnoid hemorrhage: Relationship with delayed cerebral ischemia and poor prognosis

“…We analyzed the data from patients who participated in the LongTEAM trial. The methods of this trial have been described previously 15 . In short, patients were included in the trial if they had a definite aSAH within the previous 30 days.…”

“…The methods of this trial have been described previously. 15 In short, patients were included in the trial if they had a definite aSAH within the previous 30 days. Most patients were in good clinical condition at admission and had anterior circulation aneurysms.…”