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Background: The relationship of mean heart rate (MHR) with 30-day mortality in ischemic stroke patients with atrial fibrillation in the intensive care unit (ICU) remains unknown. This study aimed to investigate the association between MHR within 24 h of admission to the ICU and 30-day mortality among patients with atrial fibrillation and ischemic stroke. Methods: This retrospective cohort study used data on US adults from the Medical Information Mart for Intensive Care-IV (MIMIC-IV, version 1.0) database. Patients with ischemic stroke who had atrial fibrillation for and first time in ICU admission were identified from the MIMIC-IV database. We used multivariable Cox regression models, a restricted cubic spline model, and a two-piecewise Cox regression model to show the effect of the MHR within 24 h of ICU admission on 30-day mortality. Results: A total of 1403 patients with ischemic stroke and atrial fibrillation (mean [SD] age, 75.9 [11.4] years; mean [SD] heart rate, 83.8[16.1] bpm; 743 [53.0%] females) were included. A total of 212 (15.1%) patients died within 30 days after ICU admission. When MHR was assessed in tertials according to the 25th and 50th percentiles, the risk of 30-day mortality was higher in participants in group 1 (< 72 bpm; adjusted hazard ratio, 1.23; 95% CI, 0.79-1.91) and group 3 (≥82 bpm; adjusted hazard ratio, 1.77; 95% CI, 1.23-2.57) compared with those in group 2 (72-82 bpm). Consistently in the threshold analysis, for every 1-bpm increase in MHR, there was a 2.4% increase in 30-day mortality (adjusted HR, 1.024; 95% CI, 1.01-1.039) in those with MHR above 80 bpm. Based on these results, there was a J-shaped association between MHR and 30-day mortality in ischemic stroke patients with atrial fibrillation admitted to the ICU, with an inflection point at 80 bpm of MHR. Conclusion: In this retrospective cohort study, MHR within 24 h of admission was associated with 30-day mortality (nonlinear, J-shaped association) in patients with ischemic stroke and atrial fibrillation in the ICU, with an inflection point at about 80 bpm and a minimal risk observed at 72 to 81 bpm of MHR. This association was worthy of further investigation. If further confirmed, this association may provide a theoretical basis for formulating the target strategy of heart rate therapy for these patients.
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OBJECTIVE: Increasing evidence has shown that skeletal muscle damage plays a role in neuromyelitis optica spectrum disorder (NMOSD). The objective of this study was to compare the serum creatine kinase (sCK) levels in NMOSD patients with different clinical statuses. METHODS: In the observational study, levels of sCK were measured during the acute and stable phases for patients with NMOSD and healthy controls (HCs). RESULTS: We enrolled 168 patients with NMOSD (female:male ratio, 153:15; age: 43.9 ± 13.1 years) in the acute phase, and blood samples were collected from 85 of the patients with NMOSD during both acute and stable phases to determine the sCK levels. The mean log sCK levels of the patients with NMOSD in the acute phase were higher (4.51 ± 1.17, n = 85) than those of the patients with NMOSD in the stable phase (3.85 ± 0.81, n = 85, p = 0.000). Furthermore, the log sCK levels of the patients with NMOSD in the stable phase were lower than those of the HCs (4.31 ± 0.39, n = 200, p = 0.000). In patients with sCK levels within the normal limits, these differences were also observed (p < 0.05). In the multivariable linear regression model performed for the patients with NMOSD in the acute phase, it suggested that a higher estimated glomerular filtration rate (p = 0.026), patients with the core clinical characteristics of optic neuritis (p = 0.005), and serum anti-SSA positivity (p = 0.019) predicted lower log sCK levels. CONCLUSIONS: Muscle damage occurs in patients with NMOSD and is aggravated during the acute phase.