Continuously severely elevated cardiac troponin-T levels in sepsis patients increased 28-day mortality (HR 1.52; 95% CI 1.27-1.82; p<0.001) and new-onset atrial fibrillation by day 7.
Cohort (n=4,556)
Do continuously elevated cTnT trajectories increase the risk of 28-day mortality and new-onset atrial fibrillation in ICU patients with sepsis?
Persistent mild or severe elevations in cTnT over 72 hours in sepsis patients are independently associated with increased 28-day mortality, with new-onset atrial fibrillation acting as a key mediator.
Estimación del efecto: HR 1.52 (95% CI 1.27-1.82)
valor p: p=<0.001
BACKGROUND Elevated levels of cardiac troponin-T (cTnT) are frequently seen in patients with sepsis, yet the connection between cTnT levels and the prognosis remains debated. Many evaluations of cTnT in sepsis patients tend to focus on static and isolated measurements, failing to capture the dynamic progression that unfolds throughout the course of the disease. This study employed latent class mixed models (LCMM) to explore cTnT fluctuations and their impact on sepsis outcomes. OBJECTIVES Our study aimed to explore the associations between the trajectory of the cTnT and prognosis through the MIMIC IV database. METHODS A retrospective cohort study was conducted using data from the Medical Information Mart for Intensive Care-IV (MIMIC-IV). Patients were randomly divided into development and validation cohorts at a 7:3 ratio. LCMM were used to categorize distinct patterns of cTnT changes over 72 h in ICU patients. We used the Cox proportional model and Fine-Gray subdistribution hazard model to assess the impact of cTnT trajectory-based classification on outcomes. A mediation effect model was constructed to analyze whether there was a mediating effect of new-onset atrial fibrillation (NOAF) on the relationship between cTnT trajectory and 28-day mortality. RESULTS In the retrospective cohort study, a total of 4556 patients from the MIMIC IV database were randomly divided into a development cohort (n = 3189) and a validation cohort (n = 1367). We identified five cTnT trajectories with distinct characteristics. Compared to the class with normal cTnT, continuously mildly elevated cTnT levels were associated with a higher risk of mortality within 28 days(HR = 1.24; 95 %CI 1.07-1.44; p = 0.003). Continuously severely elevated cTnT levels increased both the 28-day mortality rate(HR = 1.52; 95 %CI 1.27-1.82; p < 0.001) and the occurrence of NOAF by day 7(HR = 1.45; 95 %CI 1.07-1.99; p = 0.016). Notably, NOAF partially mediated the relationship between cTnT trajectory and 28-day mortality (5.9 %) . These associations were similar in external validation. Discrimination among classes was good, with mean posterior class membership probability (MPCMP) ranging from 72.2 % to 92.8 %. Similar additional risk for these classes was evident in the validation cohort, continuously severely elevated cTnT levels in the external validation cohort was associated with the risks of development of NOAF by day 7 (HR = 1.60; 95 %CI 1.20-2.13; p < 0.001) and 28-day mortality (HR = 1.47; 95 %CI 1.12-1.93; p = 0.005) CONCLUSION: Persistent mild or severe elevations in cTnT are independently linked to increased 28-day mortality, emphasizing the need for vigilant cTnT monitoring. For patients with persistently high cTnT, NOAF serves as a key mediator of mortality risk. Proactive detection and management of NOAF may improve survival in these patients. Prioritize early identification and treatment of NOAF in this at-risk population.
Gu et al. (Sat,) conducted a cohort in sepsis (n=4,556). Continuously severely elevated cTnT levels vs. Normal cTnT levels was evaluated on 28-day mortality (HR 1.52, 95% CI 1.27-1.82, p=<0.001). Continuously severely elevated cardiac troponin-T levels in sepsis patients increased 28-day mortality (HR 1.52; 95% CI 1.27-1.82; p<0.001) and new-onset atrial fibrillation by day 7.