Hypertensive patients with snoring and elevated plasma homocysteine levels are common. When these factors are combined, the risk of coronary heart disease (CHD) is high. Herein, we developed and validated an easy-to-use nomogram to predict high-risk CHD in snoring hypertensive patients with elevated plasma homocysteine.

Snoring patients (n = 1,962) with hyperhomocysteinemia and hypertension were divided into training (n = 1,373, 70%) and validation (n = 589, 30%) sets. We extracted CHD predictors using multivariate Cox regression analysis, then constructed a nomogram model. Internal validation using 1,000 bootstrap resampling was performed to assess the consistency and discrimination of the predictive model using the area under the receiver operating characteristic curve (AUC) and calibration plots.

We constructed a nomogram model with the extracted predictors, including age, waist-height ratio, smoking, and low-density lipoprotein cholesterol levels. The AUCs of the training and validation cohorts at 80 months were 0.735 (95% CI: 0.678-0.792) and 0.646 (95% CI: 0.547-0.746), respectively. The consistency between the observed CHD survival and the probability of CHD survival in the training and validation sets was acceptable based on the calibration plots. A total of more than 151 points in the nomogram can be used in the identification of high-risk patients for CHD among snoring hypertensive patients with elevated plasma homocysteine.

We developed a CHD risk prediction model for snoring hypertension patients with hyperhomocysteinemia. Our findings provide a useful clinical tool for the rapid identification of high-risk CHD at an early stage.

Recently, the supra-normal left ventricular ejection fraction (snLVEF) has been proposed, based on extensive datasets indicating increased all-cause mortality in individuals with an LVEF exceeding 65%. However, the implications of an LVEF > 65% in the context of acute coronary syndrome (ACS) remain underexplored.

The aim of the present study was to investigate the correlation between supra-normal left ventricular ejection fraction (snLVEF) and major adverse cardiovascular events (MACE) in patients with ACS.

Methods: A total of 874 ACS patients (560 men, mean age 59.5 ± 10.0; 314 women, mean age 61.5 ± 8.9) who underwent their first coronary angiography during the period from March 2013 to October 2015 were divided into 2 groups: normal LVEF (nLVEF) (55% ≤ EF ≤ 65%) and snLVEF (EF > 65%), according to their echocardiography results. The patients were evaluated for MACE after surgery by collecting clinical data and long-term follow-up data. This correlation was further analyzed by Kaplan-Meier analysis and Cox regression analysis.

The follow-up data revealed a significantly higher incidence of MACE among snLVEF patients compared to the nLVEF group (15.6% versus 7.4%; P = 0.020). This heightened risk persisted even after adjustment for multiple variables, indicating a strong association between snLVEF and increased MACE risk (HR: 2.346; 95% CI: 1.196-4.602; P = 0.013).

SnLVEF was independently associated with poor prognosis after ACS. Enhanced management strategies for snLVEF patients could potentially reduce the incidence of MACE in ACS patients.

Although acute myocardial infarction (AMI) currently has a high survival rate, the treatment and prognosis are still diffuse negative life events for patients, which will affect their quality of life (QOL) and psychological health. Based on an integrated physiological-psychological-social-medical model, it is necessary to design an intervention program for safeguarding the physical and mental health of AMI patients.

This study aimed to explore the influence of psychological intervention on negative emotions and QOL of AMI patients using a randomized controlled trial (RCT) design.

Based on convenience sampling and double-blinded group assignment, 101 patients from August 2019 to January 2020 were randomly divided into 2 groups. An intervention group received comprehensive psychological intervention, while a control group received general supportive nursing. Both groups answered questionnaires before and after the intervention, including assessments of anxiety, depression, and QOL.

Before the intervention, there were no significant differences between the groups. After intervention, anxiety and depression in the intervention group (n = 48) were significantly lower (P < 0.001) and QOL was markedly improved (P < 0.05) compared to that of the control group (n = 53).

Comprehensive psychological intervention contributed to ameliorate negative emotions, enhance confidence in treatment, and improve the QOL of AMI patients.

Bull's eye view for the display of myocardial single-photon emission computed tomography (SPECT) 3-D perfusion maps does not reflect left ventricular (LV) volume, an important parameter. We created and evaluated a myocardial SPECT display method that reflects the LV volume.

Using Digital Imaging and Communications in Medicine data, short-axis slices from the apex to the base were reconstructed and interpolated into 0.5-mm thickness. We obtained the radial lengths at 1° intervals throughout 360°, and calculated the length of the LV long axis and half circumference (1/2 circ). Myocardial perfusion was displayed as 2 ellipsoidal developments that exhibited the left anterior descending coronary artery (LAD) and non-LAD regions. We created a system that can display these processes on a personal computer. Myocardial SPECT data from 526 individuals without heart disease were analyzed. The long axis and 1/2 circ were compared with the body size, LV end-diastolic diameter (LVDd) obtained by echocardiography, and the end-diastolic volume (EDV) obtained by electrocardiogram-gated SPECT analysis. The 1/2 circle correlated with the LVDd and EDV. The images obtained allowed a diagnosis comparable to that made using the conventional coordinate display system.

The new myocardial display reflects ischemia and LV volume within a single image, which cannot be achieved with conventional SPECT image display. Additional studies of this display system are required to allow its application to patients with heart disease.

The relationship between dietary magnesium intake and the risk of stroke is controversial. This study aimed to examine the association of dietary magnesium intake with the risk of stroke among American adults.

The relationship between dietary magnesium intake and the risk of stroke was analyzed using the National Health and Nutrition Examination Survey (NHANES) 2007-2018 data with 29,653 adults. The amount of magnesium from the diet was assessed by two 24-hour dietary recalls. Stroke outcomes were defined using the results of the self-reported questionnaires. The association between dietary magnesium intake and the risk of stroke was evaluated using logistic regression models and restricted cubic spline.

In our study, an inverse association between dietary magnesium intake and the risk of stroke was found. For the highest versus lowest quartile of dietary magnesium intake, the multivariate-adjusted odds ratio (95% confidence interval) of stroke was 0.56 (0.36-0.86). The magnesium intake of women was negatively associated with stroke risk, but this negative association was not found in men. Then, the inverse association was statistically significant among the 40-59 year-old group. The results from the dose-response analysis show a linear relationship between dietary magnesium intake and the risk of stroke.

Dietary magnesium intake was inversely associated with the risk of stroke, especially in women. Therefore, our study emphasizes the importance of appropriately increasing dietary magnesium intake.

This study aimed to investigate the relationship between blood urea nitrogen to albumin ratio (BAR) and the prognosis of heart failure (HF).

A total of 2125 patients with HF were included in this single-center prospective cohort study between February 2012 and December 2017. Using a receiver operating characteristic curve, we determined the cutoff value of BAR as 0.24. All patients were divided into two groups according to the cutoff value of BAR.

Among 2125 HF patients, the mean age was 56.7 ± 14.3. During a median follow-up time of 22 months, 516 end-point events occurred. Compared with patients in the low BAR group, those in the high BAR group were older; more likely to be male; had a higher percentage of hypertension, diabetes, smoking, and β-blocker use; and higher levels of alanine aminotransferase, glycosylated hemoglobin, creatinine, log-transformed NTproBNP, and Blood urea nitrogen but lower levels of albumin, triglycerides, high-density lipoprotein, ApoA1, and hemoglobin. Prognosis analysis indicated that high BAR was associated with increased mortality risk of HF (Hazard Ratio = 1.497, 95% CI = 1.234-1.816; P < 0.001) in the multivariate Cox proportional hazard regression model. Subgroup analysis revealed that stratification by age, gender, history of hypertension, diabetes, smoking, β-blocker use, and levels of hemoglobin, glycosylated hemoglobin, and creatinine have no obvious effect on the association between BAR ratio and the prognosis of HF. Furthermore, patients with high BAR represented a decreased left ventricular ejection fraction and increased left ventricular end-diastolic diameter.

High BAR was an independent predictor for the mortality risk of HF.

Atrial fibrillation (AF) is closely related to abnormal cerebral blood flow. Inflammation and oxidative stress have always been important factors in the pathophysiology of AF. It remains unknown whether inflammation and oxidative stress are correlated to hippocampal perfusion in patients with AF.

Sixty-three patients with AF with normal hippocampal blood perfusion (NHBP) were compared to 71 patients with AF with abnormal hippocampal blood perfusion (AHBP) using a case-control study design. The serum levels of inflammation and oxidative stress were measured. The hippocampal perfusion was detected.

(1) The serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and oxidized low-density lipoprotein (ox-LDL) were statistically higher in the AHBP group than in the NHBP group. In the AHBP subgroup analysis, the serum levels of hs-CRP and IL-6 were statistically higher in patients with persistent AF than those with paroxysmal AF. (2) The relative cerebral blood volume (rCBV), mean transit time (MTT), and the time-to-peak (TTP) were statistically higher in the AHBP group than in the NHBP group. Moreover, cerebral blood flow (rCBF) was statistically lower in the AHBP group than in the NHBP group. (3) relative cerebral blood volume (rCBV), rCBF, MTT, and TTP were passively associated with serum hs-CRP and IL-6; rCBV, rCBF, and MTT were positively associated with ox-LDL. The serum levels of hs-CRP, IL-6, and ox-LDL were associated with AHBP in patients with AF after multivariate logistic regression analysis.

Oxidative stress and inflammatory biomarkers were increased in patients with AF with AHBP, in which the serum levels of hs-CRP and IL-6 in the persistent AF group were statistically higher than those in the paroxysmal AF group. The serum levels of hs-CRP, IL-6, and ox-LDL were associated with AHBP in patients with AF.

The number of TV-PM implantations in elderly people is increasing. Although frailty syndrome is common in elderly patients, the relationship between the pre-procedural frailty status and clinical outcomes has not been fully elucidated in elderly TV-PM recipients.

This study included 103 consecutive patients over 80 years old who were newly implanted with a TV-PM (age 85.7 ± 4.2, 41.7% male). We assessed the relationship between the clinical outcome and predictive factors, especially for the pre-procedural frailty status after the TV-PM implantation. The pre-procedural frailty status was retrospectively assessed from the medical records and classified on the basis of impairments in 3 domains (walking, cognition, and activities of daily living). The primary endpoint was defined as a heart failure admission.

During the follow-up period (4.1 ± 2.3 years), 20 patients (19.4%) met the primary endpoint. Frailty syndrome was identified in 40 patients (38.8%). In univariate analysis, the LVEF (HR 0.97, 95% CI 0.96-1.00 P = 0.0492), an RV pacing burden over 40% (HR 1.58, 95% CI 1.00-2.54 P = 0.0473), and presence of a frailty status (HR 1.82, 95% CI 1.13-2.87 P = 0.0134) were found to be statistically significant predictors for the study endpoint. In multivariate analysis, having frailty syndrome was the only predictive factor for a heart failure admission (HR 1.83, 95% CI 1.12-2.93 P = 0.0157).

The presence of frailty syndrome and incidence of clinical events were high and a pre-procedural frailty status assessment was key in determining the clinical outcomes in TV-PM recipients over 80 years old.

This study investigates the effect of sacubitril/valsartan (Sac/Val) in patients diagnosed with nonvalvular atrial fibrillation (AF) without systolic heart failure (SHF).

Nonvalvular AF patients without SHF admitted to the People's Hospital of Bortala Mongol Autonomous Prefecture from December 2020 to December 2021 were enrolled and randomly divided into Sac/Val treatment group (group T) and valsartan treatment group (group C, control). For subgroup analysis, patients were divided into subgroups with and without diastolic heart failure (DHF). After 1-month adaptive phase and subsequent 3-month treatment period, patients were followed up in the cardiology clinic. Plasma levels of biochemical markers and echocardiographic parameters before and after treatment were evaluated, and DHF scores were computed to assess diastolic function.

Of 61 enrolled patients, 46 patients completed follow-up. Sac/Val treatment did not increase the percentage of sinus rhythm. Although N-terminal pro-B-type natriuretic peptide (NT-proBNP) expression tended to be reduced in both groups after 3 months of treatment, the differences compared with respective baseline levels and between groups were not significant. According to subgroup analysis, although NT-proBNP expression in the subgroup with DHF was lower at follow-up compared to baseline, the difference was not statistically significant. Similarly, no marked differences in echocardiographic parameters or tissue Doppler parameters related to DHF were detected between the groups (P > 0.05). Additionally, a subgroup analysis found no significant variations in the echocardiographic measures (P > 0.05).

Sac/Val is not superior to valsartan for the short-term treatment of patients suffering with AF without SHF in improving NT-proBNP level and cardiac function.

The prognosis of patients with nonvalvular atrial fibrillation (NVAF) with a low CHA₂DS₂-VASc score (0-1) following a stroke is not well studied. In this investigation, stroke risk factors and prognostic markers in low-risk NVAF patients who are nonetheless at risk for stroke were examined.

From January 2012 to January 2022, we retrospectively assessed atrial fibrillation (AF) patients at Xiamen University's Zhongshan Hospital for ischemic stroke. Along with a control group of patients with CHA₂DS₂-VASc scores of 0-1 who weren't suffering from a stroke, patients with CHA₂DS₂-VASc scores of 0-1 at the time of stroke were included in the study. Using multivariate logistic regression, independent risk factors were identified. To assess the cumulative occurrences of in-hospital mortality in patients with NVAF-related stroke, the Kaplan-Meier method was used.

The study included 156 out of 3.237 inpatients with AF-related stroke who had CHA₂DS₂-VASc ratings of 0-1. Left atrial diameter (LAD) (odds ratio [OR]: 1.858, 95% confidence interval (CI) 1.136-3.036, P = 0.013), D-dimer (OR: 2.569, 95% CI 1.274-5.179, P = 0.008), and NT-proBNP (OR: 4.558, 95% CI 2.060-10.087, P = 0.000) were found to be independent risk factors for stroke in NVAF patients with a low CHA₂DS₂-VASc score. During hospitalization, nine patients with NVAF-related stroke died. In patients with NVAF-related stroke, NT-proBNP (hazard ratio: 3.504, 95% CI 1.079-11.379, P = 0.037) was an indicator of mortality risk.

Patients with NVAF and CHA₂DS₂-VASc scores of 0-1 had independent risk factors for stroke in the form of LAD, D-dimer, and NT-proBNP. Notably, in low-risk NVAF patients with stroke, NT-proBNP was discovered to be a potent predictor of in-hospital death.

Genetic factors may be involved in postoperative atrial fibrillation (PoAF) development and cardiac injury. However, the associations of the apolipoprotein E (ApoE) gene polymorphisms with PoAF and cardiac injury after coronary artery bypass graft surgery (CABG) remain unclear.

We recruited 150 patients with CABG, comprising 92 and 58 cases for the ApoE4 and ApoE3 groups, respectively, and analyzed PoAF incidence and the levels of cardiac biomarkers, including N-terminal prohormone of brain natriuretic peptide, cardiac troponin T (cTnT), and cardiac troponin I (cTnI). The linear regression model or logistic regression analysis was applied to investigate the associations of ApoE gene polymorphisms with PoAF and biomarkers for cardiac injury.

A total of 58 (38.7%) patients with CABG developed PoAF, with 40 and 18 cases in the ApoE4 and ApoE3 groups (43.5% versus 31.0%, P < 0.05), respectively. Logistic regression analysis revealed that the ApoE4 allele was an independent risk factor for PoAF (OR = 3.340, P = 0.001), while the ApoE3 allele was a protective factor for the PoAF (OR = 0.841, P = 0.043). Patients carrying the ApoE4 allele had higher levels of cTnT and cTnI than those carrying the ApoE3 allele. ApoE3 was a protective factor for cardiac injury (β = −0.220, P = 0.001), whereas ApoE4 was a risk factor for cTnI (β = 0.335, P = 0.015).

Our study reveals that the ApoE allele contributes to the occurrence of PoAF and severity of cardiac injury in an allele-dependent manner, with the ApoE4 allele increasing the risk and the ApoE3 allele reducing the risk.

Dilated cardiomyopathy (DCM) is a common cause of heart failure. In this study, we screened the immune infiltration-related genes associated with DCM to explore the potential molecular mechanisms and provide a basis for the early diagnosis and development of new immunotherapeutic targets. A dataset related to DCM was downloaded from the Gene Expression Omnibus (GEO) database. R software was applied to the genetic differential analysis of patients with DCM and healthy individuals, and the obtained differential expressed genes (DEGs) were screened for differentially expressed immune-related genes (DEIRGs) after comparison with the immune microsatellite database. Gene functional analysis established a protein interaction network (PPI). The immune infiltration in patients with DCM versus normal controls was assessed using the CIBERSORT algorithm, the hub genes were screened using the MOCDE app, and the hubs were validated in multiple datasets. A total of 246 DEGs were screened (adj. P < 0.05 and |logFC| > 0.3), and a total of 170 DEIRGs were compared. Gene Ontology analysis showed significant (adj. P < 0.05) Biological Process entries of 591, Cellular Component of 10, and Molecular Function of 39; Kyoto Encyclopedia of Genes and Genomes showed 20 significant entries, mainly focused on cytokines involved in immune-related response, etc. A protein interaction network comprising 28 hub DEGs was constructed in combination with the PPI network interactions. DEIRG was mainly distributed in the T-cell receptor pathway by immune infiltration detection analysis, and significant changes in central memory T-cells were found by analyzing T-cell-related subpathways, where INSR, HLA-B, IFITM1, and HBEGF were significantly differentially expressed. We selected 632 hospitalized patients for validation and found that INSR and HLA-B expression were associated with DCM development by Nomogram. The expression of HLA-B in peripheral blood T-cells was higher in DCM patients than in the normal group, as verified by qRT-PCR. However, the detailed mechanism needs to be further explored.

Sodium zirconium cyclosilicate (SZC), a newly-introduced potassium binder, can be used to manage hyperkalemia especially in patients with chronic kidney disease and in those on medical therapy which may raise serum potassium levels. The medication may incur additional costs but may in turn have a significant benefit in the effect of maintaining guideline-directed medical therapy for heart failure. We aimed to investigate the financial impact of SZC therapy in patients with systolic heart failure.

Patients with systolic heart failure who received SZC for hyperkalemia between July 2020 and March 2023 were included. In-hospital medical costs were compared between the patients who discontinued SZC and those who continued SZC. For the continue group, the cost of SZC was added. All patients were followed for 2 years or until May 2023.

A total of 36 patients (median age 81 years, 56% male, median left ventricular ejection fraction 43%) were included. Total medical costs were significantly lower in the continue group (n = 12) compared to the discontinue group (n = 24) (3.1 [3.1, 6.2] versus 12.1 [3.8, 48.6] × 10⁴ JPY per month, P = 0.039). In the continue group, serum potassium levels were decreased, renin-angiotensin-aldosterone system inhibitor doses were up-titrated, and the left ventricular ejection fraction was increased, whereas these parameters remained unchanged or worsened in the discontinue group.

SZC may have the potential to assist in the up-titration of potassium-sparing heart failure-specific medications, prevent readmissions, and minimize medical costs, by preventing recurrent hyperkalemia in patients with systolic heart failure.

Sacubitril/valsartan improves outcomes in patients with heart failure (HF) with reduced ejection fraction. However, the relationship between longitudinal changes in natriuretic peptides and echocardiographic parameters in patients with HF treated with sacubitril/valsartan across the left ventricular ejection fraction (LVEF) range is not fully understood.

In patients with HF treated with sacubitril/valsartan, comprehensive data on natriuretic peptides, including atrial natriuretic peptide (ANP), N-terminal pro-brain-type natriuretic peptide (NT-proBNP), BNP, and echocardiography, were measured after 6 months of treatment. We assessed the change in natriuretic peptides and echocardiographic parameters in LVEF classification subgroups.

Among 49 patients, the median ANP concentration increased from 55 pg/mL at baseline to 78 pg/mL (P < 0.001). The NT-proBNP concentration decreased from 250 pg/mL to 146 pg/mL (P < 0.001). No significant change was observed in the BNP concentration (P = 0.640). The trajectories of each natriuretic peptide in patients with LVEF > 40% (n = 22) were similar to those in individuals with LVEF ≤ 40% (n = 27). Regardless of LVEF classification, echocardiography at 6 months showed a significant improvement in LVEF, left ventricular end-diastolic volume, and the ratio of early diastolic mitral inflow velocity to early diastolic mitral annulus velocity (E/e'). The reduction in natriuretic peptide concentration was related to LV reverse remodeling and decreased left and right atrial pressures assessed by E/e' and inferior vena cava diameter.

Sacubitril/valsartan induced an increase in ANP, a reduction in NT-proBNP, and no change in plasma BNP, regardless of LVEF. It caused LV reverse remodeling, and the natriuretic peptide concentration changes were associated with structural and functional echocardiographic parameters.

Perfluoroalkyl and polyfluoroalkyl substance (PFAS) is a large group of fluorinated synthetic chemicals, e.g., perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorohexanesulfonic acid (PFHxS), perfluorodecanoic acid (PFDA), and perfluorononanoic acid (PFNA). Many epidemiological studies have found that PFAS exposure is associated with hypertension risk, but others possess a different opinion. Overall, the relationship between PFASs and hypertension risk remains controversial. We sought to conduct a systematic review and meta-analysis to clarify the association between PFAS exposure and human risk of hypertension.

We conducted a meta-analysis based on population-involving studies published from 1975 to 2023, which we collected from Web of Science, PubMed, and Embase databases. The odds ratio (OR) and standardized mean difference (SMD), with their 95% confidence interval (CI), were used to assess the risk of hypertension with PFAS exposure. The statistical heterogeneity among studies was assessed with the Q-test and I² statistics. Research publications related to our meta-analysis topic were systematically reviewed.

Fourteen studies involving 71,663 participants, in which 26,281 suffered hypertension, met the inclusion criteria. Our analyses suggest that exposure to general PFAS (OR = 1.09, 95% CI = 1.04-1.14) or PFOS (OR = 1.17, 95% CI = 1.05-1.30) is associated with hypertension risk. Specifically, elevated levels of general PFAS (SMD = 0.25, 95% CI = 0.08-0.42), PFHxS (SMD = 0.17, 95% CI = 0.07-0.27), and PFDA (SMD = 0.08, 95% CI = 0.02-0.13) are associated with a high risk of hypertension.

Our meta-analysis indicates that PFAS exposure is a risk factor for hypertension, and increased hypertension risk is associated with higher PFAS levels. Further study may eventually provide a better and more comprehensive elucidation of the potential mechanism of this association.

Simplifying the estimation of internal jugular venous pressure (JVP) as visible or not visible above the right clavicle in the sitting position has attracted attention for risk assessment in patients with heart failure (HF). It remains unclear whether this simple assessment, combined with its inspiration response known as Kussmaul's sign, is useful in patients with HF who vary in features such as HF with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF).

This study consisted of 246 patients who were admitted for the management of HF. JVP was assessed before discharge and considered high if visible at rest. The inspiration response was also examined. The primary outcome was a composite of all-cause death and hospitalization for worsening HF.

One year after discharge, primary outcome events occurred in 91 patients (37%). The incidence of primary outcome was higher in patients with a high JVP at rest (odds ratio, 5.06; 95% confidence interval, 2.31-11.1; P = 0.0001) or with inspiration (odds ratio, 5.93; 95% confidence interval, 2.14-16.4; P < 0.01) than in patients without high JVP conditions. These findings were similarly observed among patients with HFrEF and HFpEF (odds ratios, 3.53 and 6.76; 95% confidence intervals, 1.68-8.68 and 2.19-15.5; P = 0.01 and < 0.01, respectively) and in subgroup analysis stratified by baseline characteristics of the patients.

A high JVP at rest and with inspiration as assessed by this simple, practical method may be useful for risk assessment in patients with HF, independent of baseline characteristics.

Patients with persistent heart failure (HF) with reduced ejection fraction (HFrEF) have a poorer prognosis than those with HF with improved ejection fraction (HFimpEF). However, data on the predictive value of echocardiographic parameters for persistent HFrEF are lacking. We retrospectively studied 443 patients who were diagnosed with HFrEF (EF ≤ 40%) during hospitalization and underwent echocardiography at the 1-year follow-up. We divided them into the 2 groups: HFimpEF (EF > 40%) and persistent HFrEF group at 1-year follow-up, and assessed the predictive value of echocardiographic parameters at discharge for persistent HFrEF. In total, 301/443 patients (68%) were diagnosed with persistent HFrEF and 142/443 (32%) with HFimpEF at the 1-year follow-up. Kaplan-Meier analysis revealed that the persistent HFrEF group had a poorer prognosis than the HFimpEF group (log-rank, P < 0.001). Receiver operating characteristic curve analysis revealed that left ventricular end-systolic diameter (LVESD) had the highest area under the curve (AUC) (0.70; 95% confidence interval [CI]: 0.64-0.75; cutoff value: 55 mm) among various echocardiographic parameters. LVESD was an independent predictor of persistent HFrEF at the 1-year follow-up (odds ratio: 1.07, 95%CI: 1.02-1.12) upon multivariable logistic regression analysis. The incidence of persistent HFrEF was higher in patients with an LVESD ≥ 55 mm than in those with an LVESD < 55 mm (81% versus 55%, Fisher's exact test, P < 0.001). In conclusion, an LVESD (≥ 55 mm) was associated with persistent HFrEF. Focusing on LVESD in daily practice may help clinicians with risk stratification for decision-making regarding management in patients with advanced HF refractory to guideline-directed medical therapy.

The worldwide incidence rates of heart failure (HF) are approaching pandemic status due to aging societies. Board-certified cardiologists (BCCs) of the Japanese Circulation Society (JCS) are cardiologists who have completed the respective fellowship program and passed the examination. However, in rural areas, patients have limited access to medical care for social or geographical reasons. The clinical features of the specialist's follow-up for HF patients in rural areas are unclear.

This study consists of 205 consecutive discharged elderly patients who were admitted to our hospital due to acute HF (AHF). All patients were recommended for follow-up with BCCs-JCS by the multidisciplinary HF team at the discharge-care planning meeting. The aim of this study was to investigate the clinical features and impact of BCC follow-up for discharged elderly patients with AHF in rural areas.

A total of 156 patients chose follow-up with BCCs-JCS (BCC group), and 49 patients chose follow-up with non-BCCs-JCS (non-BCC group). Patients in the BCC group were younger (83 [76-86] versus 89 [75-93] years old, P < 0.001) and had more frequent use of β-blockers (67% versus 39%, P < 0.001). The degree of frailty assessed by the clinical frailty scale was more severe in the non-BCC group than in the BCC group (4 [3-5] versus 6 [4-7], P < 0.001). The non-BCC group lived in nursing homes more frequently than the BCC group (16% versus 5%, P = 0.011).

The HF patients followed by BCCS-JCS in rural areas were younger and had less frailty.

Acute myocardial infarction (AMI) is a common coronary artery disease. This study attempted to reveal the impact of circ-SUZ12 (hsa_circ_0042961) on cardiomyocyte injury after exposure to hypoxia.

Circ-SUZ12 was screened out from the GEO dataset GSE169594. RNA expression and protein level were detected by quantitative real-time PCR (qRT-PCR) and Western blot, respectively. The characteristics of circ-SUZ12 were identified by measuring its resistance to Rnase R or actinomycin D (Act D) treatment. CCK-8 and EdU assays were performed to explore the viability of AC16 cells. Cell apoptosis was assessed through TUNEL assay and flow cytometry analysis. Mechanism experiments were performed to investigate the downstream molecular mechanism of circ-SUZ12.

Circ-SUZ12 was highly expressed in blood samples of AMI patients in the GEO dataset and lowly expressed in hypoxia-treated cardiomyocytes. Overexpression of circ-SUZ12 reversed hypoxia-induced cardiomyocyte injury. Circ-SUZ12 regulated SUZ12 polycomb repressive complex 2 subunit (SUZ12) expression by recruiting FUS protein. SUZ12 activated the Wnt/β-catenin signaling pathway by increasing the H3K27me3 level in microRNA (miR)-526b-5p promoter to release catenin beta 1 (CTNNB1). CTNNB1 depletion reversed the effect of circ-SUZ12 on the viability and apoptosis of hypoxia-induced cardiomyocytes.

Circ-SUZ12 protects cardiomyocytes from hypoxia-induced dysfunction through upregulating SUZ12 expression to activate the Wnt/β-catenin signaling pathway.

This study aimed to observe the mechanism and effect of circ_0004771 on cardiomyocyte injury in acute myocardial infarction (AMI). The differences in circ_0004771 expression in the blood of AMI patients and healthy volunteers were observed by Real-Time Quantitative Reverse Transcription-Polymerase Chain Reaction. AMI cell models were constructed by hypoxia/reoxygenation (H/R)-induced injury in human cardiomyocytes (AC16 cells). The changes of circ_0004771 expression in AMI cells were observed. After transfection with the knockdown or overexpression of circ_0004771 vector in AMI cells, Cell Counting Kit-8 (CCK-8) assay and propidium iodide/FITC-Annexin V staining were performed to detect cell proliferation and apoptosis levels, extracellular lactate dehydrogenase (LDH) activity, malondialdehyde (MDA) concentration, and superoxide dismutase (SOD) activity. Expression levels of Mitogen-activated protein kinase (MAPK) signaling pathway-related proteins (p-MEK1/2, MEK1/2, p-ERK1/2, ERK1/2), and endoplasmic reticulum (ER) stress proteins (GRP78 and CHOP-1) were observed in each group of cells by western blot method. The expression level of circ_0004771 was significantly reduced in both clinical samples and cells of AMI. When circ_0004771 was knocked down in AMI cells, it resulted in a decrease in cell proliferation level and significant increase in apoptosis level. The inhibition of circ_0004771 expression caused leakage of LDH in AMI cells, accumulation of intracellular MDA, and inhibition of SOD activity. In addition, the knockdown of circ_0004771 significantly increased the levels of p-MEK1/2, p-ERK1/2, GRP78, and CHOP-1 in H/R-induced AC16 cells. However, the overexpression of circ_0004771 resulted in the opposite result as when circ_0004771 was knocked down. A low level of circ_0004771 in AMI activates the MAPK signaling pathway in cardiomyocytes as well as encourages intracellular oxidative stress and ER stress, thereby inhibiting cell proliferation and promoting apoptosis.

Given the potential role of microRNA (miRNA) in the pathological process of ischemic heart disease, clinical patients with acute myocardial infarction (AMI) were recruited and serum miR-127-3p levels in the patients were tested. In vitro, the effects of miR-127-3p on cardiomyocyte apoptosis and inflammation induced by hypoxia and reoxygenation (H/R) were also elucidated in AC16 cells.

Collection of serum samples from 113 AMI patients and 104 healthy controls was done. Human cardiomyocyte cell line AC16 was exposed to the H/R condition for the cell function experiments. qRT-PCR was applied for mRNA detection, and cell viability and apoptosis were evaluated. To assess inflammatory response, an enzyme-linked immunosorbent assay was carried out. For the target gene analysis, luciferase reporter assay was accomplished.

MiR-127-3p was significantly reduced in the serum of AMI patients, which was negatively correlated with CDKN3 mRNA levels. Serum miR-127-3p was negatively correlated with Scr, cTnI, CK-MB, IL-6, and TNF-α. CDKN3 serves as a target gene of miR-127-3p, its mRNA levels were reduced by miR-127-3p overexpression. H/R treatment caused the suppression of cell viability and the promotion of cell apoptosis, which was changeover by miR-127-3p overexpression. Furthermore, MiR-127-3p overexpression inhibited cell inflammatory response. The rescue experiments revealed that CDKN3 overexpression canceled the protective influence of miR-127-3p against cardiomyocyte injury and inflammatory response.

MiR-127-3p can alleviate AMI-induced cardiomyocyte apoptosis and cardiac dysfunction, which is related to its anti-inflammatory effect and its downstream CDKN3 gene.

Ventricular septal defect (VSD), the most common type of congenital heart disease (CHD), is primarily caused by cardiac dysplasia. Heart and neural crest derivatives expressed 2 (HAND2) participates in developing the right heart. The loss of HAND2 expression in humans is closely connected with ventricular septal defects. We used a case-control study to analyze the genetic variations in the HAND2 promoter region in VSD patients and controls. Some statistical analysis methods were used to analyze the association of single nucleotide polymorphisms (SNPs) with VSD. The dual-luciferase reporter assay and electrophoretic mobility shift assay (EMSA) were used to conduct functional analysis and molecular mechanism study of genetic variations. Through sequencing, we identified nine genetic variants in patients with VSD. The SNP rs2276940 G>T and rs2276941 G>A were associated with an increased risk of VSD. The dual-luciferase reporter assay showed that SNP rs2276940 G>T and rs138531627 C>G decreased the transcriptional activity of the HAND2 promoter. Transcription factors (TFs) predicting suggested that all three SNPs may change the binding of TFs. The result of EMSA showed that rs138531627 C>G may create a new binding site for TFs while rs2276940 G>T enhanced the binding affinity for TFs. These results indicated that genetic variants of the HAND2 promoter may increase the risk of VSD, and the molecular mechanism may be the change of the binding affinity of TFs.

Astragalus (Astragalus mongholicus) alleviates myocardial remodeling caused by hypertension. However, the detailed molecular mechanism is unclear.

This study aims to investigate the effect of Astragalus on ventricular remodeling in ovariectomized spontaneous hypertensive rats (OVX-SHR).

Female SHR/NCrl rats were subjected to bilateral ovariectomy to establish the OVX-SHR model and treated with Astragalus extract by gavage. The hemodynamics and cardiac function parameters were measured. HE and Masson staining were used to detect the pathological structure of myocardial remodeling and observe the hyperplasia of myocardial collagen fibers. The immunohistochemistry tested the level of α-SMA. The expression levels of inflammatory cytokines, IκB, p65, Cleaved-Caspase3, RhoA, and ROCK1/2 were detected using Western blot. The method of qRT-PCR measured the expression of matrix metalloproteinase (MMP-2 and MMP-9).

Hemodynamic and cardiac function parameters were significantly improved after a high dose of Astragalus extract and Valsartan treatment. The myocardial integrity of the model group was significantly reduced, arranged loosely, and disordered, while the expression of α-SMA was increased. However, Astragalus extract and Valsartan treatments significantly reduced the pathological damage and α-SMA. The levels of TNF-α, IL-1β, IL-6, TGF-β, MMP-2, and MMP-9 in the model group were increased but decreased after Astragalus extract treatment. Adding an ESR1 inhibitor attenuated the improvement effect of Astragalus extract on myocardial remodeling and restored the expression of RhoA and ROCK1/2.

Astragalus extract attenuates the cardiac damage in OVX-SHR by downregulating the RhoA/ROCK pathway through ESR1.

A 59-year-old man who had been diagnosed with human immunodeficiency virus-associated cardiomyopathy was referred for catheter ablation of ventricular tachycardia (VT). An electrocardiogram (ECG) waveform revealed that the clinical VT originated from the epicardium. A deceleration zone (DZ) was identified on an isochronal late activation map. Moreover, 2 forms of monomorphic VT were induced by different cycle length burst pacings from near the DZ. The morphologies of the 2 VTs with an identical cycle length were very likely to use a shared common pathway with bi-directional conduction around the slow conduction area in the left ventricle posterolateral small epicardial surface area. After ablation of the DZ, the VT was uninducible.

Persistent left superior vena cava is the most common thoracic venous anomaly. It is usually asymptomatic, but it can make implanting intracardiac devices difficult.

We present a novel technique to facilitate desfibrillator lead implantation in patients with persistent left superior vena cava and the absence of the right superior vena cava. We used a fixed-curve Selectra 3D 65-42 cm sheath (Biotronik), orienting it toward the tricuspid valve (TV) by rotating it counter-clockwise. During follow-up, the electrodes remained stable.

Our technique was safe, simple, and feasible for patients with this complex venous anatomy.

We are pleased to announce that the following 3 articles have been selected for the UEDA Heart Awards for the Year 2023.

FIRST PLACE

Atherosclerotic Progression Is Related to Immune-Related Adverse Events

Atsumasa Kurozumi, Kayo Sakamoto, Takashi Nakagawa, Futoshi Matsunaga, Akihiko Shimomura, Chikako Shimizu, Hisao Hara, Yukio Hiroi

Int Heart J 2022; 63 (2): 293-298.

SECOND PLACE

Functional Evaluation of Human Bioengineered Cardiac Tissue Using iPS Cells Derived from a Patient with Lamin Variant Dilated Cardiomyopathy

Koichiro Miura, Katsuhisa Matsuura, Yu Yamasaki Itoyama, Daisuke Sasaki, Takuma Takada, Yoshiyuki Furutani, Emiko Hayama, Masamichi Ito, Seitaro Nomura, Hiroyuki Morita, Masashi Toyoda, Akihiro Umezawa, Kenji Onoue, Yoshihiko Saito, Hiroyuki Aburatani, Toshio Nakanishi, Nobuhisa Hagiwara, Issei Komuro, Tatsuya Shimizu

Int Heart J 2022; 63 (2): 338-346.

THIRD PLACE

A Novel Knitted Polytetrafluoroethylene Patch for Cardiovascular Surgery: Feasibility Study in a Swine Model

Katsunari Terakawa, Haruo Yamauchi, Yangsin Lee, Minoru Ono

Int Heart J 2022; 63 (1): 122-130.