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BACKGROUND: This study aimed to establish an eff ective nomogram to predict the survival of heat stroke (HS) based on risk factors. METHODS:This was a retrospective, observational multicenter cohort study. We analyzed patients diagnosed with HS, who were treated between May 1 and September 30, 2018 at 15 tertiary hospitals from 11 cities in Northern China.RESULTS: Among the 175 patients, 32 patients (18.29%) died before hospital discharge. After the univariate analysis, mechanical ventilation, initial mean arterial pressure <70 mmHg, maximum heart rate, lab results on day 1 (white blood cell count, alanine aminotransferase, creatinine), and Glasgow admission prediction score were included in multivariate analysis. Multivariate Cox regression showed that invasive ventilation, initial mean arterial pressure <70 mmHg (1 mmHg=0.133 kPa), and Glasgow admission prediction score were independent risk factors for HS. The nomogram was established for predicting 7-d and 14-d survival in the training cohort. The nomogram exhibited a concordance index (C-index) of 0.880 (95% confidence interval [95% CI] 0.831-0.930) by bootstrapping validation (B=1,000). Furthermore, the nomogram performed better when predicting 14-d survival, compared to 7-d survival. The prognostic index cut-off value was set at 2.085, according to the operating characteristic curve for overall survival prediction. The model showed good calibration ability in the internal and external validation datasets.CONCLUSION: A novel nomogram, integrated with prognostic factors, was proposed; it was highly predictive of the survival in HS patients.

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At present, the pathogenesis of sepsis-induced myocardial dysfunction (SIMD) is not completely clear and effective treatment measures are lacking. Apelin is an endogenous ligand of the angiotensin like G protein coupled receptor APJ and a cardiovascular peptide with multiple functions. Our aim is to analyze the protective effect and mechanism of Apelin/APJ system on lipopolysaccharide (LPS)-induced myocardial dysfunction. One hour before LPS treatment, apelin-13 or an APJ antagonist [Ala]-apelin-13 (F13A) was given for pre-intervention to observe the effect of apelin-13 on cardiac ultrasound, pathological changes and inflammatory factors in LPS-treated mice. Another part of the mice was treated with apelin-13 or apelin-13 combined with F13A one hour after LPS treatment. The results showed that apelin-13 injection significantly reversed the decrease of ejection fraction and the increase of inflammatory factors induced by LPS in mice. Endogenous apelin may have protective effect on SIMD induced by LPS. Exogenous administration of apelin may inhibit LPS-induced inflammation, apoptosis and increase autophagy through TLR4/ERK1/2/NF-κB pathway.

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