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Objective. The purpose of this study is to compare the effects of high-intensity interval training (HIIT) versus moderate-intensity continuous training (MICT) on exercise capacity and several prognostic markers in patients with coronary artery disease (CAD) and heart failure (HF). Methods. This systematic review is registered on the INPLASY website (number: INPLASY202080112). We conducted a comprehensive search in eight databases of literature before September 13, 2019. Trials comparing HIIT and MICT in participants with CAD or HF aged 52–78 years were included. Exercise capacity (peak oxygen consumption (peak VO2)) and prognostic markers, such as the anaerobic threshold (AT), minute ventilation/carbon dioxide production (VE/VCO2) slope, left ventricular ejection fraction (LVEF), and prognostic value of the predicted VO2 max per cent (the predicted VO2 peak (%)) were examined. Results. A total of 15 studies were included comprising 664 patients, 50% of which were male, with an average age of 60.3±13.2 years. For patients with CAD, HIIT significantly improved peak VO2 values (95% CI 0.7 to 2.11) compared with MICT, but peak VO2 values in patients with HF did not seem to change. For training lasting less than eight weeks, HIIT significantly improved peak VO2 values (95% CI 0.70 to 2.10), while HIIT lasting 12 weeks or longer resulted in a modestly increased peak VO2 value (95% CI 0.31 to 5.31). High-intensity interval training significantly increased the AT when compared with MICT (95% CI 0.50 to 1.48). High-intensity interval training also caused a moderate increase in LVEF (95% CI 0.55 to 5.71) but did not have a significant effect on the VE/VCO2 slope (95% CI −2.32 to 0.98) or the predicted VO2 peak (95% CI −2.54 to 9.59) compared with MICT. Conclusions. High-intensity interval training is an effective therapy for improving peak VO2 values in patients with CAD. High-intensity interval training in the early stage (eight weeks or fewer) is superior to MICT. Finally, HIIT significantly improved prognostic markers, including the AT and LVEF in patients with CAD and HF.

Background Watching short videos is an integral part of the daily lives of young and middle-aged people. Nevertheless, the correlation between the screen time spent watching short videos at bedtime and essential hypertension in young and middle-aged people remains unclear. We aimed to explore the correlation between the screen time spent watching short videos at bedtime and essential hypertension among young and middle-aged people and construct a nomogram prediction model for assessing the probability of developing essential hypertension for these age groups. Methods This study included 4318 young and middle-aged people who underwent medical examinations at Hengshui People’s Hospital between January 2023 and September 2023. The collected data, including self-reported screen time spent watching short videos at bedtime and general information, were partitioned into a training set and a test set, with the former being divided into hypertensive and non-hypertensive groups. R programming language was used for statistical analysis and processing. Results The results of multifactorial logistic analysis showed that screen time of 0< time ≤ 1 h (95% confidence interval [CI]: 2.022–6.082, P <0.05), 2< time ≤ 3 h (95% CI: 1.538–4.665, P <0.05), 3< time ≤ 4 h (95% CI: 5.327–16.691, P <0.05), and time>4 h (95% CI: 21.382–78.15, P <0.05) were independently associated with essential hypertension among young and middle-aged people. Sex, age, screen time, occupation, high-sodium diet, physical activity, sleep, overweight or obesity, diabetes or glucose tolerance abnormality, dyslipidaemia, hyperuricaemia, and family history of hypertension were screened to construct a nomogram prediction model. The model had an area under the curve of the participant’s work characteristics of 0.934 (95% CI: 0.925–0.943), along with a preferably fitted calibration curve. After model validation using the test dataset, the area under the working characteristic curve for participants was 0.911 (95% CI: 0.895–0.928), and it was a well-fitted calibration plot. Conclusions The screen time spent watching short videos at bedtime was significantly associated with essential hypertension in young and middle-aged people, and the nomogram was a good predictor of the risk of essential hypertension among young and middle-aged people.

We sought to explore the risk factors for anxiety and depression in patients with coronary heart disease and subclinical hypothyroidism through logistic regression analysis. A retrospective analysis was conducted on 168 patients with coronary heart disease and subclinical hypothyroidism admitted to the Department of Cardiology of our hospital from February 2020 to November 2022. Patients were categorized into the control group, anxiety group, and depression group based on the Hamilton Anxiety Scale (HAMA) and Hamilton Depression Rating Scale (HAMD) scores. All participants were informed about the protocol and provided signed informed consent upon inclusion. The study examined influencing factors for anxiety and depression in patients with coronary heart disease and subclinical hypothyroidism. Collect patients’ gender, age, presence or absence of chronic diseases (including Diabetes, hypertension and hyperthyroidism), sleep quality, dietary habits, psychosocial stress, living environment, social support, education level, and blood TSH levels. The linear relationship between anxiety, depression, and each influencing factor was quantified using the Pearson correlation coefficient. Blood level of TSH and free T4 were detected by chemiluminescence immunoassay. Multiple logistic regression was applied to analyze the factors influencing anxiety and depression in these patients. Various factors were identified as significant influencers of anxiety and depression in patients with coronary heart disease and subclinical hypothyroidism. For anxiety, presence or absence of chronic diseases, sleep quality, dietary habits, psychosocial pressure, living environment, and blood TSH levels were found to be influential ( P  < 0.05). Similarly, for depression, presence or absence of chronic diseases, sleep quality, social support, quality of life, social support, education level, and blood TSH levels were identified as significant factors ( P  < 0.05). The study revealed positive correlations between presence or absence of chronic diseases, psychosocial stress, and TSH levels with anxiety symptoms in patients with coronary heart disease and subclinical hypothyroidism ( P  < 0.05). Conversely, sleep quality, dietary patterns, and living environment showed negative correlations with anxiety symptoms ( P  < 0.05).Gender and age had no correlation with anxiety levels ( P  > 0.05). Presence or absence of chronic diseases and TSH levels were positively correlated with depressive symptoms in patients with coronary heart diseaseand subclinical hypothyroidism ( P  < 0.05). On the other hand, sleep quality, social support, quality of life, and educational level were negatively correlated with anxiety symptoms ( P  < 0.05). Gender and age had no correlation with depression ( P  > 0.05). Notably, TSH levels in both the anxiety and depression groups were higher than those in the control group ( P  < 0.05), with no significant difference in free T4 levels among the groups ( P  > 0.05). The combination of chronic illness types, living habits (sleep quality, dietary habits), psychosocial pressure, living environment, and TSH levels emerged as risk factors for anxiety in patients with coronary heart disease and subclinical hypothyroidism ( P  < 0.05). Similarly, the combination of chronic illness types, sleep quality, social support, quality of life, education level, and TSH levels were identified as risk factors for depression in these patients ( P  < 0.05). This logistic regression analysis underscores the significant impact of factors such as types of chronic illness, sleep quality, social support, living environment, education level, and TSH levels on anxiety and depression symptoms in patients with coronary heart disease and subclinical hypothyroidism. These findings highlight the importance of considering these multiple risk factors collectively when devising treatment and management strategies to reduce the risk of mental health issues in this patient population.

This study aims to evaluate the role of the peri-coronary Fat Attenuation Index (FAI) and High-Risk Plaque Characteristics (HRPC) in the assessment of coronary heart disease risk. By conducting coronary CT angiography and coronary angiography on 217 patients with newly developed chest pain (excluding acute myocardial infarction), their degree of vascular stenosis, FAI, and the presence and quantity of HRPC were assessed. The study results demonstrate a correlation between FAI and HRPC, and the combined use of FAI and HRPC can more accurately predict the risk of major adverse cardiovascular events (MACE). Additionally, the study found that patients with high FAI were more prone to exhibit high-risk plaque characteristics, severe stenosis, and multiple vessel disease. After adjustment, the combination of FAI and HRPC improved the ability to identify and reclassify MACE. Furthermore, the study identified high FAI as an independent predictor of MACE in patients undergoing revascularization, while HRPC served as an independent predictor of MACE in patients not undergoing revascularization. These findings suggest the potential clinical value of FAI and HRPC in the assessment of coronary heart disease risk, particularly in patients with newly developed chest pain excluding acute myocardial infarction.

Nitric oxide (NO) is produced from endothelial cells and cardiomyocytes composing the myocardium and benefits cardiac function through both vascular-dependent and—independent effects. This study was purposed to investigate the possible adverse effect of NO focusing on the voltage-gated Na + channel in cardiomyocytes. We carried out patch-clamp experiments on rat neonatal cardiomyocytes demonstrating that NOC-18, an NO donor, significantly reduced Na + channel current in a dose-dependent manner by a long-term application for 24 h, accompanied by a reduction of Nav1.5-mRNA and the protein, and an increase of a transcription factor forkhead box protein O1 (FOXO1) in the nucleus. The effect of NOC-18 on the Na + channel was blocked by an inhibitor of thiol oxidation N -ethylmaleimide, a disulfide reducing agent disulfide 1,4-Dithioerythritol, or a FOXO1 activator paclitaxel, suggesting that NO is a negative regulator of the voltage-gated Na + channel through thiols in regulatory protein(s) for the channel transcription.

Sodium is crucial for maintaining cardiovascular health, especially in relation to heart failure. The impact of baseline serum sodium concentrations on the outcomes of newly diagnosed coronary heart disease (CHD) without heart failure remains unclear. This prospective cohort study included 681 patients who were newly diagnosed with CHD. Cox proportional hazards models and restricted cubic spline (RCS) analysis were used to assess the relationship between serum sodium concentrations and major adverse cardiovascular events. The improvement in traditional prediction models by the addition of serum sodium concentrations was assessed using changes in the C-statistic, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). During a median follow-up of 51.04 months (IQR: 40.88–53.80 months), 131 events were recorded. Multivariate Cox proportional hazards models showed that the L2 group (136–138.9 mmol/L) had the highest MACE risk. Compared to L2, the hazard ratios (HRs) and 95% confidence intervals (CIs) for the L1 (130–135.9 mmol/L), L3 (139–140.9 mmol/L), L4 (141–142.9 mmol/L), and L5 (143–147.0 mmol/L) groups were 0.31 (0.14–0.70, P  = 0.005), 0.48 (030–0.78, P  = 0.003), 0.56 (0.34–0.92, P  = 0.022), and 0.37 (0.22–0.64, P  < 0.001), respectively. Including serum sodium concentrations in the prediction model significantly improved the C-statistic from 0.647 to 0.679 ( P  = 0.022), with an NRI of 0.338 ( P  < 0.001) and an IDI of 0.026 ( P  < 0.001). RCS analysis showed a nonlinear relationship: within the 130–138 mmol/L sodium range, MACE risk gradually increased with higher sodium levels (HR 1.39, 95% CI 1.09–1.76, P  = 0.008); whereas within the 138–147 mmol/L range, the risk gradually decreased (HR 0.88, 95% CI 0.80–0.98, P  = 0.014). Baseline serum sodium concentrations are significantly associated with long-term cardiovascular risk in newly diagnosed CHD patients, showing an inverted U-shaped relationship, whereas low serum sodium may be specifically linked to higher risks of death and nonfatal myocardial infarction. Further research is needed to explore the impact of long-term changes in serum sodium concentrations on disease prognosis.

Background This study aimed to determine the potential interference of calcium dobesilate in two urinary total protein detection methods. Methods Urine samples from patients receiving calcium dobesilate were collected, and drug concentrations were quantified using liquid chromatography‐tandem mass spectrometry. Paired‐difference testing was used to assess if calcium dobesilate interfered with the total protein concentration measurement. The interference effect of calcium dobesilate on the detection method was evaluated using dose–effect experiments. Results In total, 22 24‐h urine samples and 50 spot urine samples were collected. The calcium dobesilate concentrations ranged from 76 to 738 mg/L (median: 243 [161, 328] mg/L) and 60–2236 mg/L (median: 370 [195, 667] mg/L) in the 24‐h and spot urine samples, respectively. Paired‐difference testing showed that the total protein results deviated by 0.8%–12.1% and 13.0%–286.4% with the pyrogallol red‐molybdate and benzethonium chloride methods, respectively, when the calcium dobesilate concentration was 4500 mg/L. The dose–response experiment with the benzethonium chloride method demonstrated a “J‐shaped” effect; negative interference on the total protein concentration occurred at low and medium calcium dobesilate concentrations, but positive interference occurred at high calcium dobesilate concentrations. Conclusions Calcium dobesilate did not significantly interfere with the pyrogallol red‐molybdate method but did significantly interfere with the benzethonium chloride method. The direction and degree of interference were related to the urinary protein and drug concentrations. Discontinuing calcium dobesilate for 1–2 days before obtaining a urine sample for total protein detection is recommended. Graphical illustrating the interference of calcium dobesilate in two urinary total protein detection methods. Urine calcium dobesilate concentrations were measured by LC‐MS/MS. The pyrogallol red‐molybdate method showed no significant interference, whereas the benzethonium chloride method exhibited significant interference.

Cyhalofop-butyl is an aryloxyphenoxypropionate post-emergence herbicide widely used around the world in agriculture. The acute toxicity of cyhalofop-butyl to embryos, larvae (12 and 72 h post-hatching), and adult zebrafish, as well as the short-term developmental toxicity of cyhalofop-butyl to embryo and sac-fry stages, was tested. The results showed that the 96-h LC 50 values of cyhalofop-butyl to embryos, 12 h post-hatching larvae, 72 h post-hatching larvae, and adult fish were 2.03, 0.58, 1.42, and 3.49 mg/L, respectively, suggesting zebrafish early life stages were more sensitive to cyhalofop-butyl than adult stage. Cyhalofop-butyl would inhibit the spontaneous movement, heartbeat, hatching rate of embryos, and the body length of surviving larvae of zebrafish at 1.00 mg/L or higher concentrations. Morphological abnormalities, including pericardial edema, yolk sac edema, deformation of tail, and deformation of spine, were induced by cyhalofop-butyl. The results indicated that cyhalofop-butyl had significant negative impacts on zebrafish at different life stages, and spontaneous movement and hatching rate were sensitive endpoints for assessing short-term developmental toxicity of cyhalofop-butyl.

Gemcitabine is an antineoplastic drug commonly used in the treatment of several types of cancers including pancreatic cancer and non–small cell lung cancer. Although gemcitabine-induced cardiotoxicity is widely recognized, the exact mechanism of cardiac dysfunction causing arrhythmias remains unclear. The objective of this study was to electrophysiologically evaluate the proarrhythmic cardiotoxicity of gemcitabine focusing on the human rapid delayed rectifier potassium channel, hERG channel. In heterologous hERG expressing HEK293 cells (hERG-HEK cells), hERG channel current ( I hERG ) was reduced by gemcitabine when applied for 24 h but not immediately after the application. Gemcitabine modified the activation gating properties of the hERG channel toward the hyperpolarization direction, while inactivation, deactivation or reactivation gating properties were unaffected by gemcitabine. When gemcitabine was applied to hERG-HEK cells in combined with tunicamycin, an inhibitor of N-acetylglucosamine phosphotransferase, gemcitabine was unable to reduce I hERG or shift the activation properties toward the hyperpolarization direction. While a mannosidase I inhibitor kifunensine alone reduced I hERG and the reduction was even larger in combined with gemcitabine, kifunensine was without effect on I hERG when hERG-HEK cells were pretreated with gemcitabine for 24 h. In addition, gemcitabine down-regulated fluorescence intensity for hERG potassium channel protein in rat neonatal cardiomyocyte, although hERG mRNA was unchanged. Our results suggest the possible mechanism of arrhythmias caused by gemcitabine revealing a down-regulation of I hERG through the post-translational glycosylation disruption possibly at the early phase of hERG channel glycosylation in the endoplasmic reticulum that alters the electrical excitability of cells.