ABSTRACT
Objective: To investigate the correlation between serum parathyroid hormone (PTH) levels and in-hospital major adverse cardiovascular events (MACE) in patients with acute ST-segment elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI), and establish a risk prediction model based on parameters such as PTH for in-hospital MACE. Methods: This observational retrospective study consecutively enrolled 340 patients who underwent primary PCI for STEMI between January 2016 and December 2020, divided into a MACE group (n=92) and a control group (n=248). The least absolute shrinkage and selection operator (LASSO) and logistic regression analyses were used to determine the risk factors for MACE after primary PCI. The rms package in R-studio statistical software was used to construct a nomogram, to detect the line chart C-index, and to draw a calibration curve. The decision curve analysis (DCA) method was used to evaluate the clinical application value and net benefit. Results: Correlation analysis revealed that PTH level positively correlated with the occurrence of in-hospital MACE. Receiver operating characteristic curve analyses revealed that PTH had a good predictive value for in-hospital MACE. Multivariate logistic regression analysis indicated that Killip class II-IV, and FBG were independently associated with in-hospital MACE after primary PCI. A nomogram model was constructed using the above parameters. The model C-index was 0.894 and the calibration curve indicated that the model was well calibrated. The DCA curve suggested that the nomogram model was better than TIMI score model in terms of net clinical benefit. Conclusion: Serum PTH levels in patients with STEMI are associated with in-hospital MACE after primary PCI, and the nomogram risk prediction model based on PTH demonstrated good predictive ability with obvious clinical practical value.
ABSTRACT
The present study investigated the role of parathyroid hormone (PTH) in non-ischemic cardiomyopathy (CM) and its underlying mechanism. A total of 30 Sprague-Dawley male rats were randomly divided into a control group (n=6) and an experimental group (n=24). To induce CM in the rats of the experimental group, 2 mg/kg Adriamycin (ADR) was administered intraperitoneally with 5 equal injections every third day followed by 5 weekly injections resulting in a cumulative dose of 20 mg/kg. Following establishment of the model, rats in the experimental group were subdivided into a PTH-untreated CM group that received daily normal saline subcutaneous injections for 7 days and three treated CM groups that received daily subcutaneous injections of 5, 10, or 20 µg/kg of recombinant PTH for 7 days. Rats in the control group accordingly received intraperitoneal and subcutaneous injections of normal saline. Blood sample analysis revealed that B-type natriuretic peptide (BNP), troponin T, C-reactive protein (CRP), creatinine and phosphorus concentrations were increased in the PTH-untreated CM group compared with that in the control group, whereas PTH and calcium concentrations were decreased. Administration of PTH dose-dependently decreased BNP, CRP, creatinine and phosphorus levels, and increased PTH and calcium levels. Notably, there were significant differences in PTH, BNP, troponin T, CRP, creatinine, calcium, and phosphorus levels among the rats in the five groups (P<0.01). Cardiac ultrasonography results indicated that the left ventricular ejection fraction (LVEF) was significantly decreased in rats treated with ADR compared with the rats from the control group (P<0.01). However, the LVEF gradually recovered with elevated PTH treatment doses. The overall differences of LVEF and left ventricular end-systolic volume in the five experimental groups were statistically significant (P<0.01). Furthermore, there were dose-dependent increases in LV mass and left ventricular end-diastolic volume in PTH-treated rats; however, the differences between any two groups did not reach statistical significance (P>0.05). Immunohistochemical staining and western blot analysis using an anti-PTH polyclonal antibody was performed to evaluate the protein expression levels of PTH in myocardial tissues. The mRNA expression levels of PTH and BNP were measured using reverse transcription-quantitative polymerase chain reaction. The results demonstrated that the mRNA and protein expression levels of PTH in myocardial tissues were significantly decreased in ADR-treated rats compared with the levels in the control group rats. Injection of recombinant PTH significantly increased PTH expression and reduced BNP expression in dose-dependent manners (P<0.05). These findings demonstrated that PTH can improve cardiac function in rats with ADR-induced CM, suggesting a potential therapeutic application for PTH in non-ischemic CM.
ABSTRACT
The aim of the present study was to investigate the correlation between serum parathyroid hormone (PTH) levels and coronary artery calcification (CAC) in patients without renal failure, as well as to determine independent risk factors of CAC score (CACS). A total of 157 patients who underwent coronary computed tomography angiographic examination at the 101th Hospital of the People's Liberation Army between December 2013 and February 2015 were retrospectively evaluated. The correlation between PTH levels and CACS was determined using a Pearson correlation analysis. A receiver operating characteristic (ROC) curve was drawn to determine the best cutoff PTH level for prediction of CAC. The independent association between serum PTH levels and CAC was analyzed by using a logistic regression analysis model with the response variable Be binary class. The results revealed that PTH levels in patients in the CAC group were significantly higher than those of patients in the non-calcification group. PTH levels were positively correlated with CACS (r=0.288, P<0.001). The ROC curve suggested that a PTH level of ≥31.05 pg/ml was the best cut-off point for the prediction of CAC, with a sensitivity of 80.88%, specificity of 60.67% and an area under the curve of 0.761. After including predictive factors for CAC (gender, age, smoking status, diabetes, hypertension, hyperlipidemia, body mass index, glomerular filtration rate and calcium, phosphorus, calcium-phosphorus product, magnesium, PTH, total cholesterol, low-density lipoprotein cholesterol, triglyceride, high-density lipoprotein cholesterol and C-reactive protein levels), the odds ratio of the serum PTH levels regarding the prediction of CAC was 1.050 (95% confidence interval, 1.027-1.074; P<0.001). In conclusion, the present study suggested that serum PTH levels are correlated with CAC in patients without renal failure and may thus be used as a reliable predictor of CAC.
ABSTRACT
BACKGROUND: This double-blind, randomized controlled trial aimed to investigate inhaled budesonide and oral dexamethasone compared with placebo for their prophylactic efficacy against acute mountain sickness after acute high-altitude exposure. METHODS: There were 138 healthy young male lowland residents recruited and randomly assigned to receive inhaled budesonide (200 µg, twice a day [bid]), oral dexamethasone (4 mg, bid), or placebo (46 in each group). They traveled to 3900 m altitude from 400 m by car. Medication started 1 day before high-altitude exposure and continued until the third day of exposure. Primary outcome measure was the incidence of acute mountain sickness after exposure. RESULTS: One hundred twenty-four subjects completed the study (42, 39, and 43 in the budesonide, dexamethasone, and placebo groups, respectively). Demographic characteristics were comparable among the 3 groups. After high-altitude exposure, significantly fewer participants in the budesonide (23.81%) and dexamethasone (30.77%) groups developed acute mountain sickness compared with participants receiving placebo (60.46%) (P = .0006 and P = .0071, respectively). Both the budesonide and dexamethasone groups had lower heart rate and higher pulse oxygen saturation (SpO2) than the placebo group at altitude. Only the budesonide group demonstrated less deterioration in forced vital capacity and sleep quality than the placebo group. Four subjects in the dexamethasone group reported adverse reactions. CONCLUSIONS: Both inhaled budesonide (200 µg, bid) and oral dexamethasone (4 mg, bid) were effective for the prevention of acute mountain sickness, especially its severe form, compared with placebo. Budesonide caused fewer adverse reactions than dexamethasone.
