Relationship between the lymphocyte to C­reactive protein ratio and coronary artery disease severity.

Coronary atherosclerosis is a chronic systemic inflammatory disease. Laboratory parameters such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and systemic immune inflammation index (SII) have been used to assess inflammation degree and coronary artery disease (CAD) severity. The lymphocyte-to-C-reactive protein ratio (LCR) is a new SII. However, its relationship with CAD development and severity is unclear. A total of 1,107 patients (479 in control group, 628 in CAD group) underwent coronary angiography. The routine and biochemical indices of the venous blood of patients were assessed before coronary angiography. LCR, SII, NLR and PLR were calculated and statistical analyses were performed. Propensity score matching (PSM) and a logistic regression model were used to analyze the relationship between LCR and CAD. After the PSM, 384 pairs of patients with or without CAD were successfully matched. After the median binary classification of all indicators, uni- and multivariate logistic regression analyses showed that platelet count was an independent risk factor and LCR was an independent protective factor. Using the same method, in the coronary heart disease severity group, 212 pairs were successfully matched and NLR and PLR were independent risk factors, while LCR was an independent protective factor. In conclusion, LCR is an independent protective factor against CAD development and severity.

Slow-Reflow and Prognosis in Patients with High Parathyroid Hormone Levels Undergoing Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction.

We aimed to evaluate the correlation among serum parathyroid hormone (PTH) and slow-reflow during primary percutaneous coronary intervention (PCI) and prognosis in patients with ST-segment elevation myocardial infarction (STEMI). A total of 262 patients were enrolled and divided into a slow-reflow group (n = 61) and a control group (n = 201). PTH was an independent risk factor for slow-reflow (P < 0.05), and the regression model had good discrimination and calibration. ROC curve analysis showed that PTH (≥ 63.65 pg/ml) had a predictive value for slow-reflow (P < 0.001). During the 1-year follow-up, the patients were divided into a PTH-h group (≥ 63.65 pg/ml, n = 100) and a PTH-l group (< 63.65 pg/ml, n = 162). Readmission for HF was independently associated with PTH levels (P < 0.05). KM survival analysis suggested that PTH-h had a predictive value for MACEs, especially for readmission for HF (P < 0.05). PTH levels were associated with slow-reflow during PCI and MACEs during follow-up in patients with STEMI.

PTH Predicts the in-Hospital MACE After Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction.

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.

Correlation Between GDF11 Serum Levels, Severity of Coronary Artery Lesions, and the Prognosis of Patients with ST-segment Elevation Myocardial Infarction.

We aimed to explore the correlation among serum GDF11, the severity of coronary artery lesions, and the prognosis of patients with ST-segment elevation myocardial infarction (STEMI). A total of 367 patients were enrolled and divided into control (n = 172) and STEMI (n = 195) groups. Serum GDF11 (P < 0.001) was an independent predictor of STEMI and was negatively correlated with SYNTAX score (P < 0.05). ROC curve analysis showed that serum GDF11 could screen patients for major adverse cardiovascular events (MACEs). KM curve analysis showed that patients with lower concentration of GDF11 had a higher incidence of MACEs, and Cox proportional hazards regression analysis showed that the serum GDF11 (P < 0.001) was an independent predictor of MACEs. Serum GDF11 was negatively correlated with the severity of coronary lesions and was also an independent prognostic indicator of MACEs in patients with STEMI.

Preoperative lymphocyte to C-reactive protein ratio: A new prognostic indicator of post-primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction.

BACKGROUND: The lymphocyte-to-C-reactive protein ratio (LCR) is a novel inflammatory biomarker for many diseases. This study aimed to examine the association between LCR and major adverse cardiovascular events (MACEs) in patients with ST-segment elevation myocardial infarction (STEMI) who were undergoing percutaneous coronary intervention. METHODS: A total of 382 patients with STEMI were included in this study; these patients were enrolled from January 2014 to January 2016 at a single center, and the LCR was calculated for each patient. During the in-hospital and long-term follow-up period, MACEs included cardiovascular death, new-onset non-fatal myocardial infarction, heart failure, malignant arrhythmias, revascularization in unstable angina, and new-onset atrial fibrillation. Using receiver operating characteristic curves, we assessed the predictive impact for MACEs using a combination of six inflammatory markers in patients with STEMI and focused on LCR to elucidate its prognostic value. Univariate and multivariate Cox proportional hazard models were used to define the factors associated with MACEs. RESULTS: Among the assessed variables, preoperative LCR showed the highest accuracy in predicting hospitalized (AUC:0.71) and long-term follow-up(AUC:0.602) MACEs in patients with STEMI. Decreased preoperative LCR was significantly associated with the Gensini score (P < 0.05) and no-reflow (P < 0.05). Multivariate Cox analysis showed that a high preoperative LCR (cutoff threshold = 112.4) was an independent protective factor for hospitalized MACEs in patients with STEMI (hazard ratio, 0.409; 95 % confidence interval, 0.283-0.590; P < 0.001). A high preoperative LCR (cutoff threshold = 106.3) was an independent protective factor for long-term follow-up MACEs in patients with STEMI (hazard ratio, 0.552; 95 % confidence interval, 0.369-0.740; P < 0.001). CONCLUSION: Preoperative LCR is a novel and valuable prognostic marker to determine the occurrence of MACEs in hospitals and long-term follow-up after primary percutaneous coronary intervention in patients with STEMI.

GDF11 Is a Novel Protective Factor Against Vascular Calcification.

ABSTRACT: Vascular calcification (VC) occurs via an active cell-mediated process, which involves osteogenic differentiation, apoptosis, and phenotypic transformation of vascular smooth muscle cells (VSMCs). As a member of the transforming growth factor-ß family, growth differentiation factor 11 (GDF11) can inhibit apoptosis and osteogenic differentiation and maintain the stability of atherosclerotic plaques. In this study, coronary artery calcium score (CACS) of participants with GDF11 measurements was measured using computed tomography angiography and was scored according to the Agatston score. ß-glycerophosphate (10 mM), dexamethasone (100 nM), and l -ascorbic acid (50 µg/mL) [osteogenic medium (OM)] were used to induce calcification of human aortic smooth muscle cells. We found that CACS was negatively correlated with serum GDF11 levels in patients and GDF11 was a strong predictor of elevated CACS (OR = 0.967, 95% CI: 0.945-0.991; P = 0.006), followed by age (OR = 1.151, 95% CI: 1.029-1.286; P = 0.014), triglycerides (OR = 4.743, 95% CI: 1.170-19.236; P = 0.029), C-reactive protein (OR = 1.230, 95% CI: 1.010-1.498; P = 0.04), and hypertension (OR = 7.264, 95% CI: 1.099-48.002; P = 0.04). Furthermore, exogenous GDF11 inhibited OM-induced calcification by inhibiting osteogenic differentiation, the phenotypic transformation and apoptosis of human aortic smooth muscle cells. Our study demonstrates that GDF11 plays a crucial role in reducing vascular calcification and serves as a potential intervention target to vascular calcification.

Effect of parathyroid hormone on cardiac function in rats with cardiomyopathy.

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.

Analysis of High-altitude Syndrome and the Underlying Gene Polymorphisms Associated with Acute Mountain Sickness after a Rapid Ascent to High-altitude.

To investigated the objective indicators and potential genotypes for acute mountain sickness (AMS). 176 male subjects were evaluated for symptoms scores and physiological parameters at 3700 m. EPAS1 gene polymorphisms were explored and verified effects of potential genotypes on pulmonary function by inhaled budesonide. The incidence of AMS was 53.98% (95/176). The individuals who suffered from headache with anxiety and greater changes in heart rate (HR), the forced vital capacity (FVC), and mean flow velocity of basilar artery (Vm-BA), all of which were likely to develop AMS. The rs4953348 polymorphism of EPAS1 gene had a significant correlation with the SaO2 level and AMS, and a significant difference in the AG and GG genotype distribution between the AMS and non-AMS groups. The spirometric parameters were significantly lower, but HR (P = 0.036) and Vm-BA (P = 0.042) significantly higher in the AMS subjects with the G allele than those with the A allele. In summary, changes in HR (≥82 beats/min), FVC (≤4.2 Lt) and Vm-BA (≥43 cm/s) levels may serve as predictors for diagnosing AMS accompanied by high-altitude syndrome. The A allele of rs4953348 is a protective factor for AMS through HR and Vm-BA compensation, while the G allele may contribute to hypoxic pulmonary hypertension in AMS.

Correlation between serum parathyroid hormone levels and coronary artery calcification in patients without renal failure.

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.

Short-term high-altitude pre-exposure improves neurobehavioral ability.

This study aims to evaluate the effect of the duration of high-altitude (HA) pre-exposure on human neurobehavioral parameters including mood states and cognitive performance at HA. One hundred and eleven healthy individuals (ranging in age from 18 to 35 years) were recruited to participate in this study. They were divided into two groups: a 4-day short-term HA pre-exposure group (n=57) and a 3-month long-term HA pre-exposure group (n=54). All participants lived in the area at 400 m altitude above sea level before pre-exposure to HA. They were then transported to 3700 m plateau for either a 4-day or a 3-month HA pre-exposure, and finally delivered to 4400 m plateau. On the last day of pre-exposure at 3700 m and on the 10th day at 4400 m, neurobehavioral parameters of the participants in the two groups were evaluated. At the end of pre-exposure and on the 10th day of HA exposure, participants in the short-term group had significantly lower negative mood states, better cognitive performance with higher sensorimotor, attention, and psychomotor abilities, and less acute mountain sickness in comparison with the participants in the long-term pre-exposure group. Our field study with large samples showed that in comparison with 3-month long-term pre-exposure, 4-day short-term HA pre-exposure at 3700 m has a better effect in improving human neurobehavioral parameters including mood states and cognitive performance and reducing acute mountain sickness when exposed to a HA at 4400 m.

Left ventricular function during acute high-altitude exposure in a large group of healthy young Chinese men.

OBJECTIVE: The purpose of this study was to observe left ventricular function during acute high-altitude exposure in a large group of healthy young males. METHODS: A prospective trial was conducted in Szechwan and Tibet from June to August, 2012. By Doppler echocardiography, left ventricular function was examined in 139 healthy young Chinese men at sea level; within 24 hours after arrival in Lhasa, Tibet, at 3700 m; and on day 7 following an ascent to Yangbajing at 4400 m after 7 days of acclimatization at 3700 m. The resting oxygen saturation (SaO2), heart rate (HR) and blood pressure (BP) were also measured at the above mentioned three time points. RESULTS: Within 24 hours of arrival at 3700 m, the HR, ejection fraction (EF), fractional shortening (FS), stroke volume (SV), cardiac output (CO), and left ventricular (LV) Tei index were significantly increased, but the LV end-systolic dimension (ESD), end-systolic volume (ESV), SaO2, E/A ratio, and ejection time (ET) were significantly decreased compared to the baseline levels in all subjects. On day 7 at 4400 m, the SV and CO were significantly decreased; the EF and FS Tei were not decreased compared with the values at 3700 m; the HR was further elevated; and the SaO2, ESV, ESD, and ET were further reduced. Additionally, the E/A ratio was significantly increased on day 7 but was still lower than it was at low altitude. CONCLUSION: Upon acute high-altitude exposure, left ventricular systolic function was elevated with increased stroke volume, but diastolic function was decreased in healthy young males. With higher altitude exposure and prolonged acclimatization, the left ventricular systolic function was preserved with reduced stroke volume and improved diastolic function.

Inhaled budesonide and oral dexamethasone prevent acute mountain sickness.

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.