Analysis of Risk Factors and Construction of a Predictive Model for Readmission in Patients with Coronary Slow Flow Phenomenon.

Background: Coronary slow flow phenomenon (CSFP) is a phenomenon in which distal vascular perfusion is delayed on angiography, but coronary arteries are not significantly narrowed and there is no other organic cardiac disease. Patients with CSFP may be repeatedly readmitted to the hospital because of chest pain or other symptoms of precordial discomfort, and there is a risk of adverse events. In order to investigate the risk factors affecting the readmission of CSFP patients, a prediction model was constructed with the aim of identifying patients at risk of readmission at an early stage and providing a reference for further clinical intervention. Methods: In this study, we collected clinical data from 397 CSFP patients between June 2021 and January 2023 in Xinjiang Medical University Hospital. Telephone follow-up clarified whether the patients were readmitted to the hospital. A predictive model for readmission of CSFP patients was constructed using multifactorial logistic regression. Nomogram was used to visualize the model and bootstrap was used to internally validate the model. ROC, DCA and Calibration curve were plotted to evaluate the calibration and discriminative ability of the column line graphs, respectively. Calibration and resolution of the column line graphs, respectively. Results: A total of 34 of 397 CSFP patients experienced readmission. Smoking history, creatine kinase isoenzyme-MB, total cholesterol, and left ventricular ejection fraction were the predictors of readmission in patients with CSFP. The area under the curve of the Nomogram model was 0.87, which indicated that the model had good predictive ability and differentiation, and the DCA and Calibration curves also indicated that the model had good consistency and was clinically useful. Conclusion: A readmission prediction model for patients with CSFP may facilitate early identification of patients at potential risk for readmission and timely interventional therapy to improve patient prognosis.

Transcatheter Aortic Valve Replacement in Elderly Patients: Opportunities and Challenges.

Over the past two decades, the rapid evolution of transcatheter aortic valve replacement (TAVR) has revolutionized the management of severe aortic stenosis (AS) in the elderly. The prevalence of comorbidities in elderly AS patients presents a considerable challenge to the effectiveness and prognosis of patients after TAVR. In this article, we aim to summarize some of the clinical aspects of the current use of TAVR in elderly patients and attempt to highlight the challenges and issues that need further consideration.

The Tp-e/QT ratio as a predictor of nocturnal premature ventricular contraction events in patients with obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is significantly associated with a higher risk of ventricular arrhythmia (VA). QT, the Tp-e/QT ratio, and QT dispersion (QTd) are used to evaluate myocardial repolarization and are highly correlated with VA. The aim was to evaluate the predictive value of the Tp-e/QT ratio and other electrocardiogram (ECG) parameters for nocturnal premature ventricular contractions (PVCs) in patients with OSA. METHODS: We retrospectively analyzed data from patients with OSA and conducted a 1:1 matched cohort study. Patients diagnosed with OSA who met our criteria for the PVC group, and sex- and age-matched patients with OSA who met our criteria for the control group were enrolled in the study. The Tp-e, Tp-e/QT ratio, corrected QT interval (QTc), corrected Tp-e interval (Tp-ec), and QTd were measured, calculated and analyzed. RESULTS: Patients in the PVC group (n = 31) showed a greater Tp-e, Tp-ec, QTc, Tp-e/QT ratio, and QTd than patients in the control group (n = 31). In the univariate binary logistic regression analysis, higher Tp-ec (OR: 1.025; P = 0.042), QTc (OR: 1.014; P = 0.036), Tp-e/QT ratio (OR: 1.675; P < 0.001), and QTd (OR: 1.052; P = 0.012) values were all significantly associated with nocturnal PVCs. In multivariate analysis and receiver operating characteristic analysis, a higher Tp-e/QT ratio (OR: 2.168; 95% CI: 0.762-0.952; P < 0.001) was an independent predictor of nocturnal PVCs. CONCLUSIONS: The QTc, Tp-e/QT ratio, and QTd in patients with OSA with nocturnal PVCs were significantly increased compared with those in patients without nocturnal PVCs. A prolonged Tp-e/QT ratio was an independent predictor of nocturnal PVCs in patients with OSA.

NLRC5 enhances autophagy via inactivation of AKT/mTOR pathway and ameliorates cardiac hypertrophy.

The aim of this study was to investigate the effect of nucleotide-binding oligomerization domain (NOD)-like receptor family CARD domain containing 5 (NLRC5) in cardiac hypertrophy, and to explore the mechanism implicated in this effect Cardiac hypertrophy was induced in neonatal rat cardiac myocytes using 1 µM of angiotensin II (Ang II) for 12, 24 and 48 h. Overexpression of NLRC5 was induced in H9C2 cells, and the NLRC5 + Ang II-treated cells were exposed to SC9 and 3-methyladenine (3MA). An immunofluorescence assay was used for α-actinin staining, and quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) was performed for NLRC5, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) determination. Western blot analysis was applied to measure the levels of NLRC5, microtubule-associated protein 1A/1B-light chain 3 type I (LC3I), LC3II, sequestosome 1 (p62), protein kinase B (AKT), phosphorylated Akt (pAKT), mammalian target of rapamycin (mTOR) and phosphorylated mTOR (pmTOR). The level of NLRC5 was significantly decreased after Ang II treatment in cardiomyocytes, but the levels of ANP and BNP were increased. Overexpression of NLRC5 reduced the cell size, downregulated the levels of ANP and BNP, increased LC3II / LC3I, but decreased p62 in Ang II-induced cardiomyocyte hypertrophy. In addition, the results from Western blot showed that overexpression of NLRC5 distinctly decreased the ratios of pAKT/AKT and pmTOR/mTOR in cardiomyocyte hypertrophy. SC79 and 3MA significantly downregulated the ratio of LC3I/LC3II but increased the level of p62 in NLRC5 + Ang II-treated cells. These results provide a possible novel therapeutic strategy for cardiac hypertrophy that might be useful in a clinical setting.

Effects of Pacemaker Implantation on Sudden Cardiac Death Rate and Quality of Life in Atrial Fibrillation Patients With Ventricular Pauses.

Ventricular arrest is a rare arrhythmic disease in the clinic; 35% to 55% of cases are associated with atrial fibrillation (AF). It is well known that ventricular arrest for ≥3 seconds can lead to brain symptoms such as dizziness and even syncope, but it is not clear whether ventricular pauses (≥3 seconds) with AF will lead to sudden cardiac death. If the implantation of a pacemaker can improve the quality of life of patients with permanent AF with ventricular arrest and whether it has a long-term protective effect on sudden cardiac death. To this end, we conducted a prospective follow-up observation study, which was conducted through telephone interviews and clinical hospital observation to obtain information on the quality of life, survival rate, and other details. The results show that for patients with permanent AF with ventricular arrest, pacemaker implantation cannot reduce sudden cardiac death, cardiovascular events, and stroke nor can it improve the cumulative survival rate. Fortunately, the implantation of pacemakers can improve the quality of life of patients.

The Contribution of Psychological Distress to Resting Palpitations in Patients Who Recovered from Severe COVID-19.

BACKGROUND: Increasing numbers of patients have recovered from severe coronavirus disease 2019 (COVID-19) in Wuhan, China. This study aimed to evaluate the association of psychological distress with resting palpitations in recovered patients. METHODS: In this prospective cohort study, consecutive patients who recovered from severe COVID-19 and complained of resting palpitations were included. Dynamic electrocardiogram (ECG) was continuously monitored for 2 hours while patients were at rest. A survey using a palpitation frequency scale and the Hospital Anxiety and Depression Scale (HADS) was administered to all participants. RESULTS: Of the 289 consecutive patients who recovered from severe COVID-19, 24 patients (8.3%) suffered resting palpitation symptoms, and 22 patients were finally included. Two-hour Holter monitoring showed that 18 (81.8%) patients had tachyarrhythmias, of which the most common was sinus tachycardia (17/22, 77.3%). However, patients with sinus tachycardia showed a similar frequency of palpitation episodes compared to those without sinus tachycardia. Anxiety (68.2%) and depression (59.1%) were prevalent among these recovered patients. Patients with anxiety or depression symptoms had a higher frequency of palpitation episodes than those without anxiety or depression symptoms. In addition, both the HADS-anxiety score (r =0.609, P<0.01) and HADS-depression score (r =0.516, P=0.01) were positively related to the frequency of palpitation episodes. CONCLUSION: Symptoms of resting palpitations, manifested mainly by sinus tachycardia, are not uncommon in patients who recovered from severe COVID-19. Psychological distress (anxiety and depression) may be responsible, at least in part, for resting palpitation symptoms.

Ganglionated Plexi Ablation Suppresses Chronic Obstructive Sleep Apnea-Related Atrial Fibrillation by Inhibiting Cardiac Autonomic Hyperactivation.

Background: Previous studies have reported that right pulmonary artery ganglionated plexi (GP) ablation could suppress the onset of atrial fibrillation (AF) associated with obstructive sleep apnea (OSA) within 1 h. Objective: This study aimed to investigate the effect of superior left GP (SLGP) ablation on AF in a chronic OSA canine model. Methods and Results: Fifteen beagles were randomly divided into three groups: control group (CTRL), OSA group (OSA), and OSA + GP ablation group (OSA + GP). All animals were intubated under general anesthesia, and ventilation-apnea events were subsequently repeated 4 h/day and 6 days/week for 12 weeks to establish a chronic OSA model. SLGP were ablated at the end of 8 weeks. SLGP ablation could attenuate the atrial effective refractory period (ERP) reduction and decrease ERP dispersion, the window of vulnerability, and AF inducibility. In addition, chronic OSA leads to left atrial (LA) enlargement, decreased left ventricular (LV) ejection fraction, glycogen deposition, increased necrosis, and myocardial fibrosis. SLGP ablation reduced the LA size and ameliorated LV dysfunction, while myocardial fibrosis could not be reversed. Additionally, SLGP ablation mainly reduced sympathovagal hyperactivity and post-apnea blood pressure and heart rate increases and decreased the expression of neural growth factor (NGF), tyrosine hydroxylase (TH), and choline acetyltransferase (CHAT) in the LA and SLGP. After SLGP ablation, the nucleotide-binding oligomerization domain (NOD)-like receptor signaling pathway, cholesterol metabolism pathway, and ferroptosis pathway were notably downregulated compared with OSA. Conclusions: SLGP ablation suppressed AF in a chronic OSA model by sympathovagal hyperactivity inhibition. However, there were no significant changes in myocardial fibrosis.

A prospective comparison of four methods for preventing pacemaker pocket infections.

This study aims to evaluate four pacemaker pocket cleaning methods for preventing implantation-related infections. This single-center trial prospectively randomized 910 patients undergoing first-time pacemaker implantation or replacement into four pocket cleaning methods: hemocoagulase (group A, n = 228), gentamicin (group B, n = 228), hemocoagulase plus gentamicin (group C, n = 227), and normal saline (group D, n = 227). Before implanting the pacemaker battery, the pockets were cleaned with gauze presoaked in the respective cleaning solutions. Then, these patients were followed up to monitor the occurrence of infections for 1 month after implantation. Twelve implantation-related infections occurred in 910 patients (1.32%): four patients from group A (1.75%), three patients from group B (1.32%), two patients from group C (0.88%), and three patients from group D (1.32%) (P > .05). Furthermore, two patients developed bloodstream infections (0.22%), and both of these patients were associated with pocket infection (one patient was from group A, while the other patient was from group C, respectively). No cases of infective endocarditis occurred. The differences in the number of infections in these study groups were not statistically significant. The application of hemocoagulase, gentamicin, hemocoagulase plus gentamicin, or normal saline on the presoaked gauze before implantation was equally effective in preventing pocket-associated infections.

Atrial fibrillation in obstructive sleep apnea: Neural mechanisms and emerging therapies.

Obstructive sleep apnea (OSA) has been reproducibly identified as a risk factor for initiation and progression of atrial fibrillation (AF) and reduces the efficacy of antiarrhythmic drugs, electrical cardioversion, and catheter ablation in AF. It is still controversial whether continuous positive airway pressure ventilation (CPAP) could improve the successful rate of AF treatment in OSA patients. Besides, CPAP has shown relative low compliance in patients with OSA. Therefore, novel optional therapies might be needed to improve the control of AF associated with OSA. A growing body of evidence suggests that autonomic activation contributes to the pathogenesis of AF in OSA. Acute apneic episodes result in sympathovagal co-activation, shortening atrial refractoriness and promoting the initiation of AF. Chronic OSA-induced sympathetic activation plays a crucial role in atrial autonomic, structural, and electrical remodeling, thus providing substrates for AF maintenance and recurrence. Therefore, the autonomic nervous system may be a promising therapeutic target for OSA and AF. Autonomic modulation as a treatment for OSA-associated AF has been well established in several preclinical studies. Further clinical studies are needed to provide a more precise definition of the role of autonomic modulation in the treatment of AF in OSA.

In-Hospital Management and Outcomes of Acute Myocardial Infarction Before and During the Coronavirus Disease 2019 Pandemic.

The outbreak of coronavirus disease 2019 (COVID-19) has rapidly spread worldwide. This study sought to share our experiences with in-hospital management and outcomes of acute myocardial infarction (AMI) during the COVID-19 pandemic. We retrospectively analyzed consecutive AMI patients, including those with ST-elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI), from February 1, 2020, to April 15, 2020 (during the COVID-19 pandemic), and from January 1, 2019, to December 31, 2019 (before the COVID-19 pandemic), respectively. Fifty-three AMI patients (31 STEMI, 22 NSTEMI) during the COVID-19 pandemic were matched to 53 AMI patients before the pandemic. Baseline characteristics were comparable between the matched patients. STEMI patients during the COVID-19 pandemic had a longer delay time, less primary or remedial PCI and more emergency thrombolysis than those before the pandemic. Less coronary angiography and stenting were performed in AMI patients during the COVID-19 pandemic than before the pandemic. There were no statistically significant differences in the clinical outcomes between the matched patients. However, STEMI patients during the COVID-19 pandemic had a 4-fold (12.9% vs. 3.2%) increase in all-cause mortality rate compared with those before the pandemic. AMI combined with COVID-19 infection was associated with higher rates of mortality than AMI alone. This study demonstrates that the COVID-19 pandemic results in significant reperfusion delays in STEMI patients and has a marked impact on the treatment options selection in AMI patients. The mortality rate of STEMI patients exhibits an increasing trend during the pandemic of COVID-19.

Low-Level Vagus Nerve Stimulation Reverses Obstructive Sleep Apnea-Related Atrial Fibrillation by Ameliorating Sympathetic Hyperactivity and Atrial Myocyte Injury.

Background: Previous studies have proved that low-level vagus nerve stimulation (LLVS) could suppress acute obstructive sleep apnea (OSA), which is associated with atrial fibrillation (AF). Objective: This study investigates the underlying electrophysiological, neural, and cardiomyocyte injury mechanisms on acute OSA-induced AF, examining whether LLVS can attenuate or reverse this remodeling. Methods and Results: Eighteen mongrel dogs received endotracheal intubation under general anesthesia and were randomly divided into three groups: the OSA group (simulated OSA with clamping of the trachea cannula at the end of expiration for 2min followed ventilation 8min, lasting 6h, n=6), the OSA+LLVS group (simulated OSA plus LLVS, n=6), and a control group (sham clamping the trachea cannula without stimulation, n=6). In the OSA+LLVS group, the atrial effective refractory period was significantly lengthened while the sinus node recovery time and AF duration decreased after the 4th hour, and the expression level of Cx40 and Cx43 was significantly increased compared to the OSA group. Norepinephrine, TH, and ChAT were significantly decreased in the OSA+LLVS group compared with the OSA group. Mitochondrial swelling, cardiomyocyte apoptosis, and glycogen deposition, along with a higher concentration of TNF-α, IL-6 were observed in the OSA group, and the LLVS inhibited the structural remodeling and expression of inflammatory cytokines. Conclusion: LLVS decreased the inducibility of AF partly by ameliorating sympathetic hyperactivity and atrial myocyte injury after acute OSA-induced AF.

MicroRNA-155 inhibition attenuates endoplasmic reticulum stress-induced cardiomyocyte apoptosis following myocardial infarction via reducing macrophage inflammation.

Endoplasmic reticulum stress (ERS)-induced cardiomyocyte apoptosis plays an important role in the pathological process following myocardial infarction (MI). Macrophages that express microRNA-155 (miR-155) mediate cardiac inflammation, fibrosis, and hypertrophy. Therefore, we investigated if miR-155 regulates ERS-induced cardiomyocyte apoptosis after MI using a mouse model, lipopolysaccharide (LPS)-induced rat bone marrow derived macrophages (BMDMs)and hypoxia-induced neonatal rat cardiomyocytes (NRCMs). In vivo, miR-155 levelswere significantly higher in the MI group compared to the sham group. MI increasedmacrophage infiltration, nuclear factor-κB (NF-κB) activation, ERS induced-apoptosis, and SOCS1 expression, all of which were attenuated by the miR-155 antagomir, with the exception of SOCS1 expression. Additionally, post-MI cardiac dysfunction was significantly improved by miR-155 inhibition. In vitro, LPS upregulated miR-155 expression in BMDMs, and the miR-155 antagomir decreased LPS-induced macrophage inflammation and NF-κB pathway activation, but increased expression of SOCS1. Hypoxia increased NF-κB pathway activation, ERS marker expression, and apoptosis in NRCMs. Interestingly, conditioned medium from LPS-induced macrophages in combination with the miR-155 antagomir decreased, while the miR-155 agomir increased, the hypoxia-induced effects in NRCM's. The miR-155 agomir effects were reversed by inhibiting the NF-κB pathway in cardiomyocytes. Moreover, SOCS1 knockdown in LPS-induced macrophages promoted NF-κB pathway activation and ERS-induced cardiomyocyte apoptosis in the hypoxia-induced NRCMs, but the SOCS1-siRNA-induced effects were markedly decreased by miR-155 antagomir treatment. These data suggest that miR-155 inhibition attenuates ERS-induced cardiomyocyte apoptosis after MI via reducing macrophage inflammation through the SOCS1/NF-κB pathway.

Idiopathic premature ventricular complexes originating from the distal great cardiac vein: Clinical, cardiac and electrophysiological characteristics and catheter ablation outcome.

AIMS: Although catheter ablation for idiopathic ventricular arrhythmia (VA) has been generally well-established, VA originating from the great cardiac vein (GCV) may be clinically challenging due to its epicardial origin, proximity to coronary arteries and limited accessibility. The purpose of this study was to explore its electrophysiological characteristics and identify effective mapping/ablation strategies for idiopathic premature ventricular complexes (PVCs) originating from the GCV. MATERIALS AND METHODS: Between January 2013 to January 2018, 12 patients (who were diagnosed with PVCs originating from the GCV) among the 305 patients with idiopathic left ventricular outflow tract tachycardia were included. The origin of the ectopy was localized by mapping, the characteristics of the electrocardiogram (ECG) were analyzed, and all the patients with PVCs originating from GCV were treated by radiofrequency catheter ablation (RFCA). The safety and efficacy of RFCA were evaluated. KEY FINDINGS: The origin of the ectopy was successfully localized in GCV for all 12 patients by mapping, and access to GCV via the coronary sinus was feasible. Successful RFCA was achieved in 11 of 12 patients (91.67% acute procedural success) without perioperative complications. During a median follow-up of 12.6 ±â€¯6.5 months, only one patient had recurrent VA (recurrence rate: 9.1%). SIGNIFICANCE: ECG characteristics may be helpful for identifying patients with PVCs originating from the GCV. RFCA within the coronary venous system appears to be safe and effective for these patients, and should be considered when routine RFCA from the endocardium or aortic sinus of the Valsalva is not effective.

Effect of bone marrow mesenchymal stem cell transplantation on acute hepatic failure in rats.

The aim of the present study was to investigate the effectiveness of bone marrow mesenchymal stem cell (BMSC) transplantation in the treatment of acute hepatic failure (AHF) in rats. BMSCs were isolated from rat bone marrow, cultured and analyzed by flow cytometry. Following BMSC transplantation into rats with AHF, the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB), direct bilirubin (DBIL) and indirect bilirubin (IBIL) in the serum were measured using an automatic biochemical analyzer. Hematoxylin and eosin (H&E) staining and a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay were performed to analyze the pathological changes and apoptosis rate. Levels of cluster of differentiation (CD)163 and interleukin (IL)-10 in the serum and liver tissue were detected by an enzyme-linked immunosorbent assay (ELISA) assay and western blot analysis. Compared with the levels in the control group, the serum levels of ALT, AST, DBIL, IBIL, CD163 and IL-10 in the BMSC transplantation groups were significantly lower at 120 and 168 h, while the serum levels of ALB were significantly higher at 168 h after BMSC transplantation. The pathological features of liver failure were alleviated by BMSC transplantation. The expression levels of CD163 and IL-10 in the liver tissue were also significantly decreased following transplantation. The results indicate that BMSCs have a therapeutic effect on AHF in rats, and CD163 and IL-10 may be used as sensitive serum prognosis indicators in the early assessment of patients following liver transplantation.

Transplantation of induced bone marrow mesenchymal stem cells improves the cardiac function of rabbits with dilated cardiomyopathy via upregulation of vascular endothelial growth factor and its receptors.

Bone marrow mesenchymal stem cells (BMMSCs) have shown promise in repairing injured myocardium. However, few studies have explored the potential of BMMSC transplantation for dilated cardiomyopathy (DCM). In this study we aimed to examine whether BMMSC transplantation improves the cardiac function of dilated cardiomyopathy and investigate the underlying mechanism. We established a DCM model in rabbit, then transplanted BMMSCs induced by 5-azacytidine into the rabbit, and determined the left ventricular pressure and the expression of vascular endothelial growth factor (VEGF) and its receptors. Immunohistochemistry, ultrastructural and reverse transcription polymerase chain reaction (RT-PCR) analysis proved that 5-azacytidine induced the differentiation of BMMSCs into cardiomyocyte-like cells. Upon transplantation of the induced BMMSCs into a DCM model, significantly higher maximum rates of rise and decline (±dp/dt) of left ventricular pressure and left ventricular systolic pressure, as well as much lower left ventricular diastolic pressure, were observed compared with the control group (P < 0.05). After four weeks, deposition of collagen fibers in the myocardium of transplantation group was reduced, accompanied by increased expression of VEGF and its receptors as detected by RT-PCR. Taken together, our results suggest that BMMSC transplantation could alleviate DCM through angiogenesis via the upregulation of VEGF and its receptors.