Association between the insufficient improvement of the quantitative flow ratio and worsening outcomes in ST-segment elevated myocardial infarction: a multicentre prospective cohort study.

Background: Improved coronary physiological function after percutaneous coronary intervention (PCI) has been shown to improve prognosis in stable ischaemic heart disease, but has not yet been explored in ST-segment elevated myocardial infarction (STEMI). The study sought to determine whether an improvement in the quantitative flow ratio (QFR) could improve the prognosis of STEMI patients undergoing primary PCI. Methods: Patients diagnosed with STEMI who were receiving primary PCI were recruited for the study. Those with thrombolysis in myocardial infarction (TIMI) flow <2 after wiring were excluded. The ΔQFR was calculated using the following formula: ΔQFR = post-PCI QFR - pre-stent QFR. The primary endpoint was the composite event, including recurrent myocardial infarction (MI) and acute heart failure (AHF). Results: In total, 515 STEMI patients with a median follow-up of 364 days were enrolled in the study. Based on the cut-off value from the receiver operator characteristic (ROC) curve, the patients were divided into the following two groups: the lower ΔQFR group (≤0.25, N=332); and the normal ΔQFR group (>0.25, N=183). Patients with a lower ΔQFR had a relatively higher rate of MI/AHF (10.5% vs. 4.4%, P=0.019) and AHF (7.2% vs. 2.7%, P=0.044). A lower ΔQFR was significantly associated with a higher incidence of MI/AHF [hazard ratio (HR) =2.962, 95% confidence interval (CI): 1.358-6.459, P=0.006, respectively] after adjusting for potential confounders. Pre-stent angiographic microvascular resistance [odds ratio (OR) =1.027, 95% CI: 1.022-1.033, P<0.001] and the stent-to-vessel diameter ratio <1.13 (OR =1.766, 95% CI: 1.027-3.071, P=0.04) were independent predictors of a lower ΔQFR. Conclusions: An insufficient improvement in the QFR contributes to worsening outcomes and might be a useful tool for risk stratification in STEMI.

The mediating role of obesity in the development of depression in individuals with diabetes: A population-based study from NHANES 2005-2014.

OBJECTIVE: Depression is one of the common manifestations of diabetes population, and previous studies have shown that there is a correlation between depression and diabetes. This study was conducted retrospectively through the large National Health and Nutrition Examination Survey (NHANES) to explore the risk of depression in different individuals with diabetes. METHODS: We collected data on a total of 33,001 individuals in 5 cycles of NHANES and compared the incidence of depression in the individuals with diabetes, pre-diabetes or without diabetes groups after weighting. A weighted logistic review was used to assess the association between diabetes and depression at different BMI, sex, and age levels. Mediating analysis was used to assess the risk of depression in people with obesity-mediated diabetes. In addition, the non-linear relationship between BMI and depression at different factor levels was evaluated using restricted cubic strips (RCS). RESULTS: Diabetes was significantly associated with depression in obesity, especially for female (OR: 1.45, 95 % CI: 1.20-1.75, P < 0.001) and young (

ASSESS-IE: a Novel Risk Score for Patients with Infective Endocarditis.

Mortality in patients with infective endocarditis (IE) remains high. The existing risk scores are relatively complex with limited clinical application. This study was conducted to establish a new risk model to predict in-hospital and 6-month mortality in IE patients. A total of 1549 adult patients with definite IE admitted to Guangdong Provincial People's Hospital (n=1354) or Xiamen Cardiovascular Hospital (n=195) were included. The derivation cohort consisted of 1141 patients. The score was developed using the multivariate stepwise logistic regression analysis for in-hospital death. Bootstrap analysis was used for validation. Discrimination and calibration were evaluated by the receiver operating characteristic curve and the Hosmer-Lemeshow goodness-of-fit test. Six risk factors were used as score parameters (1 point for each): aortic valve affected, previous valve replacement surgery, severe heart failure, elevated serum direct bilirubin, moderate-severe anemia and acute stage. The predictive value and calibration of the ASSESS-IE score for in-hospital death were excellent in the derivation (area under the curve [AUC]=0.781, p<0.001; Hosmer-Lemeshow p=0.948) and validation (AUC=0.779, p<0.001; Hosmer-Lemeshow p=0.520) cohorts. The score remained excellent in bootstrap validation (AUC=0.783). The discriminatory ability of the ASSESS-IE score for in-hospital (AUC: 0.781 vs. 0.799, p=0.398) and 6-month mortality (AUC: 0.778 vs. 0.814, p=0.040) were similar with that of Park's score which comprised 14 variables. The ASSESS-IE risk score is a new and robust risk-stratified tool for patients with IE, which might further facilitate clinical decision-making.

Prognostic Value of Blood Urea Nitrogen for Short-Term Mortality in Patients with Infective Endocarditis.

INTRODUCTION: Blood urea nitrogen (BUN) is a metabolic product validated to be an independent risk factor in the prognosis of several diseases. However, the prognostic value of BUN in patients with infective endocarditis (IE) remains unevaluated. METHODS: A total of 1371 patients with a diagnosis of IE were included and divided into four groups according to BUN (mmol/L) at admission: < 3.5 (n = 343), 3.5-4.8 (n = 343), 4.8-6.8 (n = 341), and ≥ 6.8 (n = 344). Restricted cubic spline was used to assess the association of BUN with in-hospital mortality. Multivariate analysis was performed to identify the independent risk factors for adverse outcomes. RESULTS: The in-hospital mortality reached 7.4%, while the 6-month mortality was 9.8%. The restricted cubic spline plot exhibited an approximately linear relationship between BUN and in-hospital mortality. Receiver operating characteristics curve analysis showed that the optimal cut-off of BUN for predicting in-hospital death was 6.8 mmol/L. Kaplan-Meier analysis showed that patients with BUN > 6.8 mmol/L had a higher 6-month mortality than other groups (log rank = 97.9, P < 0.001). Multivariate analysis indicated that BUN > 6.8 mmol/L was an independent predictor indicator for both in-hospital [adjusted odds ratio (aOR) = 2.365, 95% confidence interval (CI) 1.292-4.328, P = 0.005] and 6-month mortality [adjusted hazard ratio (aHR) = 2.171, 95% CI 1.355-3.479, P = 0.001]. CONCLUSIONS: BUN is suitable for independently predicting short-term mortality in patients with IE.

Clinical evaluation of Sepsis-1 and Sepsis-3 in infective endocarditis.

BACKGROUND: Sepsis is associated with poor survival outcomes in patients with infective endocarditis (IE). However, the prognostic value of the Sepsis-1 and Sepsis-3 criteria of sepsis for IE patients is unclear. METHODS: A total of 1354 patients with IE was enrolled and classified into the sepsis and non-sepsis groups according to the Sepsis-1 and Sepsis-3. Multivariate regression analysis was performed to test the predictive performances of the Sepsis-1 and Sepsis-3 in assessing the risk of mortality in patients with IE. RESULTS: Sepsis was diagnosed in 347 (25.6%) patients according to the Sepsis-1 and 496 (36.6%) patients with the Sepsis-3. The in-hospital mortality rate was 11.5% in the Sepsis-1 group and 14.3% in the Sepsis-3 group. Kaplan-Meier survival curve analysis showed that both Sepsis-1 (Log-rank = 17.2, p < 0.001) and Sepsis-3 (Log-rank = 94.3, p < 0.001) were significantly associated with 6-month mortality. Multivariate regression analysis demonstrated that the Sepsis-3 was independently associated with the in-hospital mortality (odds ratio = 2.89, 95% CI 1.68-4.97, p < 0.001) and the 6-month mortality (hazard ratio = 3.24, 95% CI 2.08-5.04, p < 0.001). CONCLUSIONS: Sepsis-3 shows better predictive performance than Sepsis-1 criteria in assessing the risk of mortality in patients with IE.

Analysis of risk factors for severe acute kidney injury in patients with acute myocardial infarction: A retrospective study.

Background: Patients with acute myocardial infarction (AMI) complicated by acute kidney injury (AKI) tend to have a poor prognosis. However, the exact mechanism of the co-occurrence of the two diseases is unknown. Therefore, this study aims to determine the risk factors for severe AKI in patients with AMI. Methods: A total of 2022 patients were included in the Medical Information Mart for Intensive Care. Variables were identified via univariate logistic regression, and the variables were corrected via multivariate logistic regression. Restricted cubic splines were used to examine the risks associated with the variables. The Kaplan-Meier method was used to compare the risk of severe AKI among the patients. Results: Patients with severe AKI had a higher in-hospital mortality rate (28.6% vs. 9.0%, P < 0.001) and a longer duration of intensive care (6.5 days vs. 2.9 days, P < 0.001). In patients with AMI, the mean systolic blood pressure (SBP); international normalized ratio (INR); the levels of blood urea nitrogen (BUN), glucose, and calcium; and a history of liver disease were found to be the independent risk factors for developing severe AKI after their admission. Increased levels of BUN and blood glucose and a high INR increased the risk of severe AKI; however, increased levels of calcium decreased the risk; SBP presented a U-shaped curve relationship. Conclusions: Patients with severe AKI have a poor prognosis following an episode of AMI. Furthermore, in patients with AMI, SBP; INR; a history of liver disease; and the levels of BUN, glucose, and calcium are the independent risk factors for developing severe AKI after their admission.

LIN28A attenuates high glucose-induced retinal pigmented epithelium injury through activating SIRT1-dependent autophagy.

AIM: To evaluate the effects of LIN28A (human) on high glucose-induced retinal pigmented epithelium (RPE) cell injury and its possible mechanism. METHODS: Diabetic retinopathy model was generated following 48h of exposure to 30 mmol/L high glucose (HG) in ARPE-19 cells. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot tested the expression of the corresponding genes and proteins. Cell viability as well as apoptosis was determined through cell counting kit-8 (CCK-8) and flow cytometry assays. Immunofluorescence assay was adopted to evaluate autophagy activity. Caspase 3 activity, oxidative stress markers, and cytokines were appraised adopting their commercial kits, respectively. Finally, ARPE-19 cells were preincubated with EX527, a Sirtuin 1 (SIRT1) inhibitor, prior to HG stimulation to validate the regulatory mechanism. RESULTS: LIN28A was downregulated in HG-challenged ARPE-19 cells. LIN28A overexpression greatly inhibited HG-induced ARPE-19 cell viability loss, apoptosis, oxidative damage as well as inflammatory response. Meanwhile, the repressed autophagy and SIRT1 in ARPE-19 cells challenged with HG were elevated after LIN28A overexpression. In addition, treatment of EX527 greatly inhibited the activated autophagy following LIN28A overexpression and partly abolished the protective role of LIN28A against HG-elicited apoptosis, oxidative damage as well as inflammation in ARPE-19 cells. CONCLUSION: LIN28A exerts a protective role against HG-elicited RPE oxidative damage, inflammation, as well as apoptosis via regulating SIRT1/autophagy.

The effect of perioperative diuretic administration on acute kidney injury in patients with acute myocardial infarction after percutaneous coronary intervention: a real-world retrospective study.

PURPOSE: The relationship between diuretic use and contrast-induced acute kidney injury (CI-AKI) after contrast exposure remains unclear. In this study, we conducted a retrospective analysis using propensity score matching (PSM) to investigate the effect of perioperative diuretic administration on contrast-induced acute kidney injury (CI-AKI) in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI). METHODS: A total of 1894 patients with AMI who underwent PCI were retrospectively analyzed using PSM and multivariate models. Depending on whether diuretics were used, the patients were divided into two groups: the perioperative diuretic group (497 patients, 26.2%) and the non-diuretic group (1397 patients, 73.8%). And the relationship between perioperative diuretic administration and CI-AKI was evaluated by multiple regression models. Furthermore, Kaplan Meier survival curve ratio was used to evaluate and compare overall postoperative survival between the two groups. RESULTS: Most patients who received diuretics were older (67 vs. 60 years, respectively, p < 0.001) and women (22.5% vs. 15.2%, p < 0.001) and had combined hypertension (62.8% vs. 47%, p < 0.001), atrial fibrillation (5.4% vs. 1.8%, p < 0.001), stroke (9.3% vs. 4.9%, p < 0.001), and diabetes mellitus (33.4% vs. 23.6%, p < 0.001) compared to those who did not. After the baseline characteristics were balanced using the PSM model, no significant difference was observed in the incidence of postoperative CI-AKI (22.7% vs. 19.5%, p = 0.356) and major cardiovascular adverse events (21.5% vs. 18.7%, p = 0.398). Multiple regression analysis showed no association between perioperative diuretic administration and postoperative CI-AKI occurrence (odds ratio: 1.14, 95% confidence interval: 0.86-1.51, p = 0.371). Further subgroup analysis and sensitivity analysis confirmed the above findings. CONCLUSION: We found no significant association between perioperative diuretic administration and postoperative CI-AKI in patients with AMI who underwent PCI.

Long-term outcomes and potential mechanisms of offspring exposed to intrauterine hyperglycemia.

Diabetes mellitus during pregnancy, which can be classified into pregestational diabetes and gestational diabetes, has become much more prevalent worldwide. Maternal diabetes fosters an intrauterine abnormal environment for fetus, which not only influences pregnancy outcomes, but also leads to fetal anomaly and development of diseases in later life, such as metabolic and cardiovascular diseases, neuropsychiatric outcomes, reproduction malformation, and immune dysfunction. The underlying mechanisms are comprehensive and ambiguous, which mainly focus on microbiota, inflammation, reactive oxygen species, cell viability, and epigenetics. This review concluded with the influence of intrauterine hyperglycemia on fetal structure development and organ function on later life and outlined potential mechanisms that underpin the development of diseases in adulthood. Maternal diabetes leaves an effect that continues generations after generations through gametes, thus more attention should be paid to the prevention and treatment of diabetes to rescue the pathological attacks of maternal diabetes from the offspring.

Inflammatory mechanisms and intervention strategies for sepsis-induced myocardial dysfunction.

Sepsis-induced myocardial dysfunction (SIMD) is the leading cause of death in patients with sepsis in the intensive care units. The main manifestations of SIMD are systolic and diastolic dysfunctions of the myocardium. Despite our initial understanding of the SIMD over the past three decades, the incidence and mortality of SIMD remain high. This may be attributed to the large degree of heterogeneity among the initiating factors, disease processes, and host states involved in SIMD. Previously, organ dysfunction caused by sepsis was thought to be an impairment brought about by an excessive inflammatory response. However, many recent studies have shown that SIMD is a consequence of a combination of factors shaped by the inflammatory responses between the pathogen and the host. In this article, we review the mechanisms of the inflammatory responses and potential novel therapeutic strategies in SIMD.

Hypoglycemic Coma Caused by Methimazole-Induced Insulin Autoimmune Syndrome, a Case Study.

Islet autoimmune syndrome (IAS) is an autoimmune disease caused by high concentrations of insulin autoantibodies (IAA) in the blood. It is characterized by hyperinsulinemia and spontaneous hypoglycemia. The incidence of IAS is low, and the hypoglycemia symptom is usually mild. Hence, the severe manifestations (up to seizures and coma) are rarely reported. Here, we reported two cases of Graves' disease who developed insulin autoimmune syndrome after methimazole treatment. The patients exhibited sudden hypoglycemic coma after receiving methimazole treatment for approximately 2 or 6 months. The patients' serum glucose levels were below 2.8 mmol/L, and laboratory tests showed high levels of serum insulin and high titers of insulin autoantibodies. Patient 1 discontinued methimazole treatment and the hypoglycemic symptoms disappeared after 7 days. However, patient 2 experienced severe hypoglycemia after discontinuation of methimazole, and the patient condition improved after glucocorticoid therapy. He developed thyroid storm during the treatment, and his condition improved after receiving standard treatment procedures for thyroid storm. To the best of our knowledge, this is the first case report of IAS in Graves' disease with thyroid storm.

Klotho alleviates contrast-induced acute kidney injury by suppressing oxidative stress, inflammation, and NF-KappaB/NLRP3-mediated pyroptosis.

BACKGROUND: Contrast-induced acute kidney injury (CI-AKI) is a common complication following percutaneous coronary intervention in coronary artery disease (CAD) patients with >30% incidence. Klotho is a multifunctional protein that inhibits oxidative stress and inflammation, but its role in CI-AKI is poorly understood. The present study aimed to explore the effects of klotho in CI-AKI. METHODS: Six-week-old mice and HK-2 were divided into the control, contrast medium (CM), CM + klotho, and klotho groups. H&E staining evaluated kidney injury. Scr and BUN showed renal function. DHE probe and ELISA kit detected the levels of reactive oxygen species (ROS) in kidney tissue, superoxide dismutase (SOD), and malondialdehyde (MDA) in serum. Western blot detected the expressions of NF-κB and phosphorylated NF-κB (p-NF-κB) and pyroptosis-related protein levels of NLRP3, caspase-1, GSDMD, and cleaved-GSDMD in the kidney of CI-AKI mice. CCK-8 and lactate dehydrogenase (LDH) activity assays determined cell viability and damage. Fluorescent probe dichloro-dihydro-fluorescein diacetate (DCFH-DA) and enzyme-linked immunosorbent assay (ELISA) tested oxidative stress-related indicators. These included intracellular reactive oxygen species (ROS), superoxidase dismutase (SOD), and malondialdehyde (MDA). IL-6, TNF-α, IL-1ß, and IL-18 in the cell supernatant were tested by ELISA assay and used to reflect inflammation responses. Propidium iodide (PI) staining showed the cell death of HK-2. The expressions of NF-κB, p-NF-κB and pyroptosis-related protein levels of NLRP3, caspase-1, GSDMD, and cleaved-GSDMD were detected by Western blot. RESULTS: Exogenous klotho administration reduced kidney histopathological alterations and improved renal function in vivo. The levels of reactive oxygen species (ROS) in renal tissue, superoxide dismutase (SOD), and malondialdehyde (MDA) in serum decreased after the klotho intervention. The expression levels of p-NF-κB and pyroptosis-related proteins, including NLRP3, caspase-1, GSDMD, and cleaved-GSDMD, were decreased in CI-AKI mice after the klotho intervention. In vitro, klotho significantly inhibited CM-induced oxidative stress and the production of IL-6 and TNF-α. Moreover, it was found that klotho inhibited the activation of p-NF-κB and down-regulated pyroptosis-related protein (NLRP3, caspase-1, GSDMD, and cleaved-GSDMD). CONCLUSION: Klotho has a protective effect on CI-AKI via suppressing oxidative stress, inflammation, and NF-κB/NLRP3-mediated pyroptosis that contributes to the potential therapy of CI-AKI.

Impaired retinal microcirculation in patients with non-obstructive coronary artery disease.

PURPOSE: To quantitatively investigate alterations of retinal microcirculation in patients with non-obstructive coronary artery disease (NOCAD) using optical coherence tomography angiography (OCTA), and to identify the ability of retinal microcirculation parameters in differentiating coronary artery disease (CAD) subtypes. METHODS: All participants with angina pectoris underwent coronary computed tomography angiography. Patients with lumen diameter reduction of 20-50 % in all major coronary arteries were defined as NOCAD, while patients with at least one major coronary artery lumen diameter reduction ≥ 50 % were recruited as obstructive coronary artery disease (OCAD). Participants without a history of ophthalmic or systemic vascular disease were recruited as healthy controls. Retinal neural-vasculature was measured quantitatively by OCTA, including peripapillary retinal nerve fiber layer (RNFL) thickness and vessel density (VD) of the optic disc, superficial vessel plexus (SVP), deep vessel plexus (DVP), and foveal density (FD 300). p < 0.017 is considered significant in multiple comparisons. RESULTS: A total of 185 participants (65 NOCAD, 62 OCAD, and 58 controls) were enrolled. Except for the DVP fovea (p = 0.069), significantly reduced VD in all other regions of SVP and DVP was detected in both the NOCAD and OCAD groups compared to control group (all p < 0.017), while a more significant decrease was found in OCAD compared to NOCAD. Multivariate regression analysis showed that lower VD in superior hemi part of whole SVP (OR: 0.582, 95 % CI: 0.451-0.752) was an independent risk factor for NOCAD compared to controls, while lower VD in the whole SVP (OR: 0.550, 95 % CI: 0.421-0.719) was an independent risk factor for OCAD compared to NOCAD. Using the integration of retinal microvascular parameters, the area under the receiver operating characteristic curve (AUC) for NOCAD versus control and OCAD versus NOCAD were 0.840 and 0.830, respectively. CONCLUSION: Significant retinal microcirculation impairment, while milder than that in OCAD was observed in NOCAD patients, indicating retinal microvasculature assessment might provide a new systemic microcirculation observation window for NOCAD. Furthermore, retinal microvasculature may serve as a new indicator to assess the severity of CAD with good performance of retinal microvascular parameters in identifying different CAD subtypes.

Optimal threshold of urinary albumin-to-creatinine ratio (UACR) for predicting long-term cardiovascular and noncardiovascular mortality.

PURPOSE: Traditional cutoff values of urinary albumin-to-creatinine ratio (UACR) for predicting mortality have recently been challenged. In this study, we investigated the optimal threshold of UACR for predicting long-term cardiovascular and non-cardiovascular mortality in the general population. METHODS: Data for 25,302 adults were extracted from the National Health and Nutrition Examination Survey (2005-2014). Receiver operating characteristic (ROC) curve analysis was performed to assess the predictive value of UACR for cardiovascular and non-cardiovascular mortality. A Cox regression model was established to examine the association between UACR and cardiovascular and non-cardiovascular mortality. X-tile was used to estimate the optimal cutoff of UACR. RESULTS: The UACR had acceptable predictive value for both cardiovascular (AUC (95% CI) for 1-year, 3-year and 5-year mortality, respectively: 0.769 (0.711-0.828), 0.764 (0.722-0.805) and 0.763 (0.730-0.795)) and non-cardiovascular (AUC (95% CI) for 1-year, 3-year and 5-year mortality, respectively: 0.772 (0.681-0.764), 0.708 (0.686-0.731) and 0.708 (0.690-0.725)) mortality. The optimal cutoff values were 16 and 30 mg/g for predicting long-term cardiovascular and non-cardiovascular mortality, respectively. Both cutoffs of UACR had acceptable specificity (0.785-0.891) in predicting long-term mortality, while the new proposed cutoff (16 mg/g) had higher sensitivity. The adjusted hazard ratios of cardiovascular and non-cardiovascular mortality for the high-risk group were 2.50 (95% CI 1.96-3.18, P < 0.001) and 1.92 (95% CI 1.70-2.17, P < 0.001), respectively. CONCLUSIONS: Compared to the traditional cutoff value (30 mg/g), a UACR cutoff of 16 mg/g may be more sensitive for identifying patients at high risk for cardiovascular mortality in the general population.

Renal Safety and Renin-Angiotensin-Aldosterone System Inhibitors in Patients With Contrast Media Exposure: A Multicenter Randomized Controlled Study.

ABSTRACT: There is no clear consensus on the safety of renin-angiotensin-aldosterone system inhibitors in patients with contrast media exposure. We aimed to assess the safety of renin-angiotensin-aldosterone system inhibitors in patients exposed to contrast media at 1-year follow-up. Patients treated with angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB) were recruited and randomly divided into 2 groups (1:1 ratio): with ACEI/ARB group (ACEI/ARB continued throughout the study period) and without ACEI/ARB group (ACEI/ARB stopped 24 hours before and continued 48 hours after the procedure). The primary endpoint was contrast-induced acute kidney injury (CI-AKI) and secondary endpoints were major adverse cardiovascular events (MACEs), and the need for renal replacement therapy during hospitalization and at 1-year follow-up. The occurrence rates of CI-AKI were not comparable in the ACEI/ARB group and the without ACEI/ARB group (2.92% and 2.62%, respectively; P = 0.866). No significant between-group differences were found with respect to the frequency of MACEs or renal replacement therapy during hospitalization and at 1-year follow-up. On subgroup analysis, among patients with estimated glomerular filtration rate (eGFR) < 45 mL/min, the incidence of CI-AKI was significantly higher in the ACEI/ARB group [17.95% (14/78) vs. 6.02% (5/83), P = 0.029]. Among patients with eGFR ≥ 45 mL/min, the incidence of CI-AKI was comparable in the 2 groups [0.87% (5/572) vs. 2.12% (12/567), P = 0.094]. The incidence of MACEs and renal replacement therapy was not comparable in the 2 groups, during hospitalization and at 1-year follow-up. ACEI or ARB treatment can safely be continued after exposure to contrast media, but not in patients with eGFR < 45 mL/min.

The effect of medication on serum anti-müllerian hormone (AMH) levels in women of reproductive age: a meta-analysis.

OBJECTIVE: The study aims to address whether serum anti-müllerian hormone (AMH) levels fluctuate in the short term after medication application, including oral contraceptives (OCs), metformin (MET), Gonadotropin-releasing hormone agonist (GnRH-a), dehydroepiandrosterone (DHEA), vitamin D (VD), clomiphene citrate (CC), and letrozole (LET). METHODS: Published literature from PubMed, Embase, and Cochrane central was retrieved up until 19 September 2021. A total of 51 self-control studies with an average Newcastle-Ottawa quality assessment scale (NOS) score of 6.90 were analyzed. The extracted data were entered into Stata software, and the weighted mean difference/standardized mean difference (WMD/SMD) and 95% confidence interval (CI) were used for data analysis. RESULTS: After OCs treatment the AMH level showed a significant decline in women with normal ovarian function, which was significant within 3 months (WMD = -1.43, 95% CI: -2.05 to -0.80, P < 0.00001). After MET treatment, the serum AMH decreased in polycystic ovary syndrome (PCOS) patients (WMD = -1.79, 95% CI: -2.32 to -1.26, P < 0.00001), in both obese and non-obese patients. GnRH-a treatment in endometriosis patients led to dynamic changes in the serum AMH levels, that is, ascent at 1 month (P = 0.05), and descent at 3 months (P = 0.02). After DHEA treatment the serum AMH increased in diminished ovarian reserve (DOR) / poor ovarian response (POR) patients (WMD = 0.18, 95% CI: 0.09 to 0.27, P < 0.0001). After VD treatment the serum AMH increased, and it was obvious in non-PCOS patients (WMD = 0.78, 95% CI: 0.34 to 1.21, P = 0.0004). After CC treatment the serum AMH decreased significantly in PCOS patients, specifically in non-obese patients (WMD = -1.24, 95% CI: -1.87 to -0.61, P = 0.0001). CONCLUSIONS: Serum AMH levels may be affected in the short term after drug application. Specifically, OC, MET and CC lead to decreased AMH level, DHEA and VD lead to increased AMH level, and GnRH-a leads to dynamic variation, which is correlated with PCOS, obesity, age, and duration of medication. The impacts of these medications should be taken into consideration when AMH is used as a marker of ovarian reserve.

Albumin-Bilirubin Score to Predict Outcomes in Patients with Idiopathic Dilated Cardiomyopathy. / Escore Albumina-Bilirrubina para Predizer Desfechos em Pacientes com Cardiomiopatia Dilatada Idiopática.

BACKGROUND: Liver dysfunction is a postulated variable for poor prognosis in dilated cardiomyopathy (DCM). OBJECTIVE: This study aimed to investigate the prognostic value of the albumin-bilirubin (ALBI) score, a relatively new model for evaluating liver function, in patients with idiopathic DCM. METHODS: A total of 1025 patients with idiopathic DCM were retrospectively included and divided into three groups based on ALBI scores: grade 1 (≤ -2.60, n = 113), grade 2 (-2.60 to -1.39, n = 835), and grade 3 (> -1.39, n = 77). The association of ALBI score with in-hospital major adverse clinical events (MACEs) and long-term mortality was analyzed. P-value less than 0.05 was considered statistically significant. RESULTS: The in-hospital MACEs rate was significantly higher in the grade 3 patients (2.7% versus 7.1% versus 24.7%, p < 0.001). Multivariate analysis showed that ALBI score was an independent predictor for in-hospital MACEs (adjusted odds ratio = 2.80, 95%CI: 1.63 - 4.80, p < 0.001). After a median 27-month follow-up, 146 (14.2%) patients died. The Kaplan-Meier curve indicated that the cumulative rate of long-term survival was significantly lower in patients with higher ALBI grade (log-rank = 45.50, p < 0.001). ALBI score was independently associated with long-term mortality (adjusted hazard ratio = 2.84, 95%CI: 1.95 - 4.13, p < 0.001). CONCLUSION: ALBI score as a simple risk model could be considered a risk-stratifying tool for patients with idiopathic DCM.

FUNDAMENTO: A disfunção hepática é uma variável postulada de prognóstico desfavorável na cardiomiopatia dilatada (CMD). OBJETIVO: Este estudo teve como objetivo investigar o valor prognóstico do escore albumina-bilirrubina (ALBI), um modelo relativamente novo para a avaliação da função hepática, em pacientes com CMD idiopática. MÉTODOS: Um total de 1.025 pacientes com CMD idiopática foram incluídos retrospectivamente e divididos em três grupos com base nos escores de ALBI: grau 1 (≤ −2,60, n = 113), grau 2 (−2,60 a −1,39, n = 835) e grau 3 (> −1,39, n = 77). Foi analisada a associação do escore ALBI com eventos clínicos adversos maiores (ECAM) intra-hospitalares e mortalidade a longo prazo. Valor de p inferior a 0,05 foi considerado estatisticamente significativo. RESULTADOS: A taxa de ECAM intra-hospitalares foi significativamente maior nos pacientes com grau 3 (2,7% versus 7,1% versus 24,7%, p < 0,001). A análise multivariada mostrou que o escore ALBI foi um preditor independente para ECAM intra-hospitalares (odds ratio ajustada = 2,80, IC 95%: 1,63 ­ 4,80, p < 0,001). Após seguimento mediano de 27 meses, 146 (14,2%) pacientes morreram. A curva de Kaplan-Meier indicou que a taxa cumulativa de sobrevida a longo prazo foi significativamente menor em pacientes com grau mais alto de ALBI (log-rank = 45,50, p < 0,001). O escore ALBI foi independentemente associado à mortalidade a longo prazo (hazard ratio ajustada = 2,84, IC 95%: 1,95 ­ 4,13, p < 0,001). CONCLUSÃO: O escore ALBI, como modelo de risco simples, pode ser considerado uma ferramenta de estratificação de risco para pacientes com CMD idiopática.

Estimated glomerular filtration rate derived from different formulas and prognosis in acute coronary syndrome: Findings from the improving care for cardiovascular disease in China-acute coronary syndrome project.

BACKGROUND: The optimal formula for the estimation of glomerular filtration rate (GFR) in patients with acute coronary syndrome (ACS) in terms of predicting in-hospital mortality and adverse events remains unclear. METHODS: A nationwide registry study, Improving CCC (Care for Cardiovascular Disease in China) ACS project, was launched in 2014 as a collaborative study of the American Heart Association and Chinese Society of Cardiology. The Cockcroft-Gault, modification of diet in renal disease (MDRD) formula for Chinese (C-MDRD), Mayo, and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formulas were used to calculate estimated GFR in 61,545 ACS patients (38,734 with ST-segment elevation myocardial infarction [STEMI] and 22,811 with non-ST-segment-elevation ACS [NSTE-ACS]). RESULTS: Prevalence of moderate to severe renal dysfunction was inconsistent among four formulas, ranging from 11.6% to 22.4% in NSTE-ACS and from 8.3% to 16.8% in STEMI, respectively. The in-hospital mortality rate in patients with ACS was inversely associated with estimated GFR. In STEMI, the Mayo-derived eGFR exhibited the highest predictive power for in-hospital death compared with the Cockcroft-Gault-derived eGFR (area under the curve [AUC]: 0.782 vs. 0.768, p=0.004), C-MDRD-derived eGFR (AUC: 0.782 vs. 0.740, p<0.001) and CKD-EPI-derived eGFR (AUC: 0.782 vs. 0.767, p<0.001). In NSTE-ACS, the Mayo-derived eGFR exhibited a similar predictive value with the Cockcroft-Gault (AUC: 0.781 vs. 0.787, p>0.05) and CKD-EPI-derived eGFR (AUC: 0.781 vs. 0.784, p>0.05). CONCLUSIONS: The Mayo formula was superior to Cockcroft-Gault, C-MDRD, and CKD-EPI formulas for predicting in-hospital mortality in ACS patients, especially for STEMI. The Mayo-derived eGFR may serve as a risk-stratification tool for in-hospital adverse events in ACS patients. CLINICAL TRIAL REGISTRATION: URL: http://www. CLINICALTRIALS: gov. Unique identifier: NCT02306616.

Corrigendum: Prevalence and Prognostic Significance of Malnutrition in Hypertensive Patients in a Community Setting.

[This corrects the article DOI: 10.3389/fnut.2022.822376.].

Endovascular embolization of spontaneous massive hemorrhage of a facial plexiform neurofibroma: case report and literature review.

BACKGROUND: As a subtype of neurofibromatosis, the plexiform neurofibroma is a benign, autosomally inherited disorder and predisposed to tumour formation. However, life-threatening haemorrhage into facial plexiform neurofibroma is extremely rare. CASE INFORMATION: In the current study, we showed a facial plexiform neurofibroma case with massive haemorrhage in the cranio-maxillofacial region. An emergent selective angiography of the external carotid artery was performed to identify the offending artery, which was then selectively occluded by the combination of detachable coils and Onyx-34. Thus, the minimally invasive drainage surgery was successfully performed to evacuate the haematoma. CONCLUSION: We believe the endovascular embolization achieved its purpose by providing an initial salvage strategy for stopping active haemorrhage in plexiform neurofibroma, allowing surgeons to perform open surgery with lower complications rate.