Angiography-based Fractional Flow Reserve for the Prediction of Clinical Outcomes After Drug-coated Balloon or Plain Old Balloon Angioplasty.

BACKGROUND: AccuFFRangio is a novel method for fast computation of fractional flow reserve (FFR) based on coronary angiography and computational fluid dynamics. The association between the AccuFFRangio and clinical outcomes after drug-coated balloon (DCB) or plain old balloon angioplasty (POBA) remains to be investigated. METHODS: This study included consecutive patients who underwent balloon angioplasty from December 2016 to October 2020. AccuFFRangio was calculated retrospectively based on the post-procedural angiography obtained immediately after angioplasty. The primary endpoint was major adverse cardiac events (MACE), defined as a composite of all-cause death, vessel-related myocardial infarction, and repeat target vessel revascularization. RESULTS: A total of 169 patients were retrospectively analyzed in this study. Post-procedural AccuFFRangio (hazard ratio [HR] per 0.1 increase 0.33, 95% confidence interval [CI] 0.22-0.48, p < 0.001) was an independent predictor for MACE at 2-year follow-up. Post-procedural AccuFFRangio ≤ 0.87 was determined as the optimal cutoff value to predict MACE with an area under the curve (AUC) of 0.872 (95% CI 0.813-0.919, p < 0.001). CONCLUSIONS: AccuFFRangio measured immediately after balloon angioplasty is a promising predictor of unfavorable clinical outcomes.

Triglyceride-glucose index in the prediction of clinical outcomes after successful recanalization for coronary chronic total occlusions.

BACKGROUND: Triglyceride-glucose index (TyG) has been widely used to predict cardiovascular outcomes. However, it remains unclear whether TyG holds prognostic significance for patients with coronary chronic total occlusions (CTO). Thus, our study aimed to evaluate the predictive accuracy and prognostic value of TyG in individuals who underwent successful percutaneous coronary intervention (PCI) for CTO. METHODS: A total of 331 consecutive patients with ≥ 1 successful CTO-PCI were included. The baseline and angiographic data were acquired. The duration of follow-up ranged from 32 to 79 months, with a median of 44 months and an interquartile range of 39 to 67 months. The primary outcome measured was the occurrence of major adverse cardiac and cerebrovascular events (MACCE), including mortality, target vessel revascularization, recurrent myocardial infarction, and stroke. RESULTS: After controlling for confounders, multivariate Cox regression analysis revealed that TyG remained statistically significant, regardless of being a continuous or categorical variable. In the partially adjusted regression model, the Hazard ratio (95%CI) for MACCE was 2.54 (1.12-5.79) in tertile 3 and 1.61 (1.22-2.12) per SD increase in the TyG.Kaplan-Meier survival analysis demonstrated significant differences in MACCE-free survival rates across tertiles of the TyG, as indicated by the log-rank test (p = 0.001). ROC analysis was conducted to evaluate the predictive ability of TyG for MACCE, resulting in an AUC of 0.677. CONCLUSION: The TyG index demonstrates independent predictive capabilities for MACCE in patients who have undergone successful CTO-PCI. These findings suggest that TyG holds the potential as a valuable tool in risk stratification and the identification of patients who may benefit from early intervention in the management of CTO.

Uric acid to high-density lipoprotein cholesterol ratio predicts adverse cardiovascular events in patients with coronary chronic total occlusion.

BACKGROUND AND AIMS: Uric acid to high-density lipoprotein cholesterol ratio (UHR) is a novel index of metabolism and inflammation proposed by recent studies. The prognostic value of UHR is undetermined in patients with coronary chronic total occlusion (CTO). The aim of this study was to investigate the association of UHR with adverse cardiovascular events in patients with CTO. METHODS AND RESULTS: In this retrospective cohort study, we enrolled 566 patients with CTO lesion in our hospital from January 2016 to December 2019. Patients were divided into three groups based on UHR level. The primary endpoint was major adverse cardiovascular event (MACE), defined as a combination of death, non-fatal MI, target vessel revascularization (TVR), and non-fatal stroke. The median follow-up time of this study was 43 months. During the follow-up, 107 (18.9%) MACEs were recorded. Kaplan-Meier survival plots show the cumulative incidence of MACE-free decreased across tertile of UHR (log-rank test, p < 0.001). In the fully adjusted model, the Hazard ratio (95% CI) of MACE was 2.16 (1.17-3.99) in tertile 3 and 2.01 (1.62-2.49) for per SD increase in UHR. CONCLUSION: Elevated UHR predicts an increasing risk of MACE in patients with CTO. UHR is a simple and reliable indicator for risk stratification and early intervention in CTO patients.

The synergy of serum SFRP5 levels and the TyG index in predicting coronary artery disease and prognosing major adverse cardiovascular events.

BACKGROUND AND AIMS: Secreted frizzled-related protein 5 (SFRP5) is a member of the SFRP family that is known for its potent anti-inflammatory properties. Nevertheless, little is known regarding the relevance of SFRP5 in coronary artery disease (CAD). The current study examined the correlation between serum levels of SFRP5 and the triglyceride-glucose (TyG) index in patients who underwent coronary angiography (CAG) as a component of cardiovascular assessment and for the purpose of prognosis evaluation. METHODS: A total of 310 hospitalized patients were enrolled in this study between May 2021 and March 2022 and were divided into three groups based on their CAG results and SYNTAX (synergy between PCI with TAXUS drug-eluting stent and cardiac surgery) scores: the control group, mild lesion group, and moderate-severe lesion group. Univariate and multivariate analyses were employed to investigate the relationships between changes in patients and clinical variables. To investigate the impact of the TyG index and serum SFRP5 levels on the occurrence of major adverse cardiovascular events (MACEs), Kaplan‒Meier curves were plotted. Serum SFRP5 levels were measured utilizing an enzyme-linked immunosorbent assay (ELISA) kit. RESULTS: The serum SFRP5 levels significantly decreased with the increasing severity and complexity of CAD, while the TyG index significantly increased (P < 0.001). Moreover, a significant negative correlation was observed between the serum SFRP5 levels and the TyG index (r = -0.312, P < 0.001). SFRP5 exerts a protective role in different groups of patients. The area under the receiver operating characteristic (ROC) curve indicated that an SFRP5 concentration > 115.58 pg/mL was the best predictive value for CAD (OR:0.87, P < 0.001). MACEs were significantly associated with serum SFRP5 levels and the TyG index, as indicated by both univariate and multivariate Cox regression analyses (P < 0.001). Furthermore, Kaplan‒Meier analysis indicated that as the TyG index decreased and SFRP5 levels increased, the occurrence of MACEs decreased (P < 0.001). Patients with a concentration of SFRP5 > 115.58 pg/mL and a TyG index < 8.49 exhibited a better prognosis for avoiding MACEs (P < 0.001). CONCLUSION: These results suggest that the collaboration between serum SFRP5 levels and the TyG index holds promise in predicting CAD and its prognosis.

Lipoprotein (a) and myocardial infarction: impact on long-term mortality.

BACKGROUND AND AIMS: Lipoprotein (a) [Lp(a)] is a genetically regulated lipoprotein particle that is an independent risk factor for coronary atherosclerotic heart disease. However, the correlation between Lp(a) and left ventricular ejection fraction (LVEF) in patients with myocardial infarction (MI) has been poorly studied. The present study investigated the correlation between Lp(a) and LVEF, as well as the impact of Lp(a) on long-term mortality in patients with MI. METHODS: Patients who underwent coronary angiography resulting in MI diagnosis between May 2018 and March 2020 at the First Affiliated Hospital of Anhui Medical University were included in this study. The patients were divided into groups based on the Lp(a) concentration and LVEF (reduced ejection fraction group: < 50%; normal ejection fraction group: ≥ 50%). Then, correlations between the Lp(a) level and LVEF, as well as the impact of Lp(a) on mortality, were assessed. RESULTS: This study included 436 patients with MI. The Lp(a) level and LVEF were significantly and negatively correlated (r = -0.407, ß = -0.349, P < 0.001). The area under the receiver operating characteristic curve (ROC) indicated that an Lp(a) concentration > 455 mg/L was the best predictive value for reduced ejection fraction (AUC: 0.7694, P < 0.0001). The clinical endpoints did not differ based on the Lp(a) concentration. However, all-cause mortality and cardiac mortality differed based on LVEF. CONCLUSIONS: These results suggest that an elevated Lp(a) concentration predicts reduced ejection fraction and that LVEF predicts all-cause mortality and cardiac mortality in patients with MI.

Effect of Levosimendan on B-type Natriuretic Peptide Levels in Patients with Heart Failure: A Systematic Review and Meta-Analysis.

Objective: This meta-analysis aims to evaluate the effects of levosimendan on B-type natriuretic peptide (BNP) levels in patients with decompensated heart failure and assess the efficacy and safety of levosimendan in treating left heart failure. Methods: Randomized controlled trials (RCTs) were identified through searches in the Chinese Biomedical Literature Database (CBM), Chinese Academic Journal Full Text Database (CNKI), Wanfang Database (CECDB), VIP Chinese Scientific, PubMed, Cochrane Library, and Web of Science. Quality assessment and data extraction were performed for the included studies, and meta-analysis was conducted using Review Manager 5.2 software. Results: The meta-analysis revealed a statistically significant difference in the regulatory effect of levosimendan on BNP levels in patients with stage III heart failure compared to the control group [OR = 2.12, 95% CI (1.22, 3.67), P = .008, I2 = 37%, Z = 2.67]. Additionally, leosimendan showed a significant effect on BNP levels in patients with stage IV heart failure [OR = 1.88, 95% CI (1.27, 2.79), P = .002, I2 = 0%, Z = 3.14], compensatory heart failure [OR=2.97, 95% CI (1.81, 4.86), P < .0001, I2 = 55%, Z = 4.32], and decompensated heart failure [OR = 1.98, 95% CI (1.59, 2.47), P < .00001, I2 = 76%, Z = 6.07]. Conclusions: Levosimendan administration demonstrated improved cardiac function and a significant reduction in plasma BNP levels in patients with decompensated heart failure.

LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88.

OBJECTIVE: Long non-coding RNAs (lncRNAs) play critically in the pathogenesis of myocardial ischemia-reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis. METHODS: miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury was measured. Mice with I/R injury were injected with the gene expression-modified vectors, after which cardiac function, hemodynamics, myocardial enzyme, oxidative stress, and cardiomyocyte apoptosis were analyzed. RESULTS: I/R mice showed LINC00461 and Myd88 up-regulation and miR-185-3p down-regulation. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice. CONCLUSION: LINC00461 knockdown attenuates myocardial I/R injury via elevating miR-185-3p expression to suppress Myd88 expression.

The novel relationship between Sirt3 and autophagy in myocardial ischemia-reperfusion.

Class III histone deacetylases (HDACs) belong to the proteasome family, comprising seven family members identified in mammalian cells, identified Sirt1-Sirt7. As an important member of HDACs, Sirt3 is hotly debated for its multiple functions. It was reported that Sirt3 got involved in the alleviation of multiple diseases, including myocardial infarction, neuron ischemia, hypertrophy, and diabetic myopathy. Through regulating many cellular mechanisms, such as apoptosis, autophagy, and clearance of reactive oxygen species (ROS), Sirt3 played an important role in the alleviation of myocardial ischemia-reperfusion injury. Nowadays Sirt3-induced autophagy was indicated to be involved in the process of the development of myocardial ischemia-reperfusion injury. Sirt3 could both activate and inhibit autophagy process by activating different downstream signal pathways, such as Sirt3-AMP-activated protein kinase pathway, Sirt3-Foxo3a pathway, and Sirt3-superoxide dismutase-mitochondrial ROS pathway. Whereas the Sirt3-induced autophagy in different phases of myocardial ischemia-reperfusion has not been systematically illustrated. In this review, we summarized the regulated mechanisms found in these years and listed the updated research about the relationship between Sirt3 and autophagy which are both positive and negative during myocardial ischemia-reperfusion phase. We anticipated that we may controlled the activation of autophagy by regulating the concentration of Sirt3 in myocyte. By maintaining a proper expression of autophagy in different phases of myocardial ischemia-reperfusion, we could reduce the morbidity of patients with myocardial infarction apparently in the future.

mTOR and Beclin1: Two key autophagy-related molecules and their roles in myocardial ischemia/reperfusion injury.

Autophagy is the general term of lysosomal degradation of substances in cells, which is considered the key to maintaining the normal structure and function of the heart. It also has a correlation with several heart diseases, in particular, myocardial ischemia/reperfusion (I/R) injury. At the stage of myocardial ischemia, autophagy degrades nonfunctional cytoplasmic proteins providing the critical nutrients for the critical life activities, thereby suppressing cell apoptosis and necrosis. However, autophagy is likely to affect the heart negatively in the reperfusion stage. Mammalian target of rapamycin (mTOR) and Beclin1 are two vital autophagy-related molecules in myocardial I/R injury playing significant roles in different stages. In the ischemia stage, mTOR plays its roles through AMPK/mTOR and phosphoinositide 3-kinase/Akt/mTOR pathway, whereas Beclin1 plays its roles through its upregulation in the reperfusion stage. A possible interaction between mTOR and Beclin1 has been reported recently, and further studies need to be done to find the underlying interaction between the two molecules in myocardial I/R injury.

The Predictive Value of Potential Hematological Biomarkers in Acute Coronary Syndrome.

BACKGROUND: To explore the predictive value of potential hematological biomarkers in acute coronary syndrome (ACS). METHODS: A total of 309 patients suffering ACS from June 2014 to June 2016 in The First Affiliated Hospital of Anhui Medical University were enrolled. The clinical data was studied retrospectively. All patients were divided into 3 groups based on the presence of elevated ST-segment including UA (150), STEMI (159), and NSTEMI (100). The association between potential hematological biomarkers of neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), white blood cell count (WBC), monocyte percentage (MO), and platelet width (PLW) and outcome of ACS including cTnI, occlusion of coronary artery, emergent PCI, and 30-day mortality was performed. RESULTS: Mean ± standard deviation was used to describe quantitative data of normal distribution. Inter-group comparison was performed by t or chi-square test and non-parametric test. M (P25, P75) was used to describe quantitative data of skewed distribution. Non-parametric tests revealed, except for PLW, there was significance between NLR, PLR, MO, and WBC and emergent PCI as well as 30-day mortality (p < 0.05). Multivariate logistic regression revealed that NLR was the best predictive factor of 30-day mortality. Meanwhile, it was found that the association between NLR, PLR, WBC, and cTnI was significant (p < 0.05). CONCLUSIONS: NLR is a useful and available factor in predicting outcome of ACS and more significant when combined with PLR, MO, and WBC.

Nicotinamide Phosphate Transferase (NAMPT) Increases in Plasma in Patients with Acute Coronary Syndromes, and Promotes Macrophages to M2 Polarization.

Atherosclerosis is an inflammatory disease; monocytes and macrophages play an important role in the progression of this disease. However, the mechanisms are not fully understood yet. Nicotinamide phosphate transferase (NAMPT) is the rate limiting enzyme in the synthesis of NAD, but extracellular NAMPT shows the characteristics of cytokines/adipokines, suggesting that it may be a link between metabolism and inflammation. In this study, we compared the expression levels of the NAMPT/NAD+/Sirt1 signaling pathway as well as NAMPT, CRP and IL-6 in the peripheral blood mononuclear cell (PBMC), and plasma in patients with acute coronary syndromes and healthy subjects, and analyzed their association with macrophage polarization. The relationship between eNAMPT and iNAMPT and the polarization of macrophages was analyzed by NAD+, NAMPT blocker, and neutralizing antibody treatment. The results showed that the expression of the NAMPT/NAD+/Sirt1 signaling pathway was up-regulated in the peripheral blood of patients with ACS. Inhibition of iNAMPT expression can reduce M1 polarization; however, there was no significant effect on eNAMPT secretion and M2 polarization. Neutralizing eNAMPT by neutralizing antibodies can reduce M2 polarization and decrease the expression levels of IL-10, IL-13, IL-4 and IL-1ra. The addition of NAD+ in the cell culture supernatant had no significant effect on the polarization of M1 but increased the M2 polarization and the expression levels of IL-10 and IL-1ra. Our findings suggested that NAMPT is involved in the pathogenesis of atherosclerosis; the increased expression of eNAMPT in ACS patients may play a protective role by the up regulation of the NAMPT/NAD+/Sirt1 signaling pathway.

Sites of latest mechanical activation as assessed by SPECT myocardial perfusion imaging in ischemic and dilated cardiomyopathy patients with LBBB.

OBJECTIVE: Sites of latest mechanical activation (SOLA) have been recognized as optimal left-ventricular (LV) lead positions for cardiac resynchronization therapy (CRT). This study was aimed to investigate SOLA in ischemic cardiomyopathy (ICM) and dilated cardiomyopathy (DCM) patients with left bundle branch block (LBBB). METHODS: Sixty-four consecutive LBBB patients (47 DCM, 17 ICM), who met the standard indications for CRT and underwent resting SPECT myocardial perfusion imaging (MPI), were selected. Phase analysis was used to assess LV dyssynchrony and SOLA. The Emory Cardiac Toolbox was used to measure perfusion defects. LV dyssynchrony and SOLA were compared between the DCM patients with wide (≥150 ms) and moderate (120-150 ms) QRS durations (QRSd). The relationship between SOLA and perfusion defects was analyzed in the ICM patients. RESULTS: The DCM patients with wide QRSd had significantly more LV dyssynchrony than those with moderate QRSd. Lateral SOLA were significantly more frequent in the DCM patients with wide QRSd than those with moderate QRSd (96% vs. 62%, p = 0.010). In the ICM patients, SOLA were either in the scar segments (82%) or in the segments immediately adjacent to the scar segments (18%), regardless of QRSd. CONCLUSION: Lateral SOLA were more frequent in the DCM patients with wide QRSd than those with moderate QRSd. Such relationship was not observed in the ICM patients, where SOLA were associated with scar location rather than QRSd. These findings support the use of SPECT MPI to aid the selection of potential CRT responders and guide LV lead placement.

Challenges and advances in the management of inflammation in atherosclerosis.

INTRODUCTION: Atherosclerosis, traditionally considered a lipid-related disease, is now understood as a chronic inflammatory condition with significant global health implications. OBJECTIVES: This review aims to delve into the complex interactions among immune cells, cytokines, and the inflammatory cascade in atherosclerosis, shedding light on how these elements influence both the initiation and progression of the disease. METHODS: This review draws on recent clinical research to elucidate the roles of key immune cells, macrophages, T cells, endothelial cells, and clonal hematopoiesis in atherosclerosis development. It focuses on how these cells and process contribute to disease initiation and progression, particularly through inflammation-driven processes that lead to plaque formation and stabilization. Macrophages ingest oxidized low-density lipoprotein (oxLDL), which partially converts to high-density lipoprotein (HDL) or accumulates as lipid droplets, forming foam cells crucial for plaque stability. Additionally, macrophages exhibit diverse phenotypes within plaques, with pro-inflammatory types predominating and others specializing in debris clearance at rupture sites. The involvement of CD4+ T and CD8+ T cells in these processes promotes inflammatory macrophage states, suppresses vascular smooth muscle cell proliferation, and enhances plaque instability. RESULTS: The nuanced roles of macrophages, T cells, and the related immune cells within the atherosclerotic microenvironment are explored, revealing insights into the cellular and molecular pathways that fuel inflammation. This review also addresses recent advancements in imaging and biomarker technology that enhance our understanding of disease progression. Moreover, it points out the limitations of current treatment and highlights the potential of emerging anti-inflammatory strategies, including clinical trials for agents such as p38MAPK, tumor necrosis factor α (TNF-α), and IL-1ß, their preliminary outcomes, and the promising effects of canakinumab, colchicine, and IL-6R antagonists. CONCLUSION: This review explores cutting-edge anti-inflammatory interventions, their potential efficacy in preventing and alleviating atherosclerosis, and the role of nanotechnology in delivering drugs more effectively and safely.

Exploring the mediating role of calcium homeostasis in the association between diabetes mellitus, glycemic traits, and vascular and valvular calcifications: a comprehensive Mendelian randomization analysis.

BACKGROUND: The interplay between diabetes mellitus (DM), glycemic traits, and vascular and valvular calcifications is intricate and multifactorial. Exploring potential mediators may illuminate underlying pathways and identify novel therapeutic targets. METHODS: We utilized univariable and multivariable Mendelian randomization (MR) analyses to investigate associations and mediation effects. Additionally, the multivariable MR analyses incorporated cardiometabolic risk factors, allowing us to account for potential confounders. RESULTS: Type 2 diabetes mellitus (T2DM) and glycated hemoglobin (HbA1c) were positively associated with both coronary artery calcification (CAC) and calcific aortic valvular stenosis (CAVS). However, fasting glucose (FG) was only linked to CAVS and showed no association with CAC. Additionally, CAVS demonstrated a causal effect on FG. Calcium levels partially mediated the impact of T2DM on both types of calcifications. Specifically, serum calcium was positively associated with both CAC and CAVS. The mediation effects of calcium levels on the impact of T2DM on CAC and CAVS were 6.063% and 3.939%, respectively. The associations between T2DM and HbA1c with calcifications were influenced by body mass index (BMI) and smoking status. However, these associations were generally reduced after adjusting for hypertension. CONCLUSION: Our findings suggest a genetically supported causal relationship between DM, glycemic traits, and vascular and valvular calcifications, with serum calcium playing a critical mediating role.

Potential relationship between autophagy and ferroptosis in myocardial ischemia/reperfusion injury.

Autophagy is an evolutionarily conserved process involved in the degradation of long-lived proteins and excessive or dysfunctional organelles. As a pivotal cellular response, autophagy has been extensively studied and is known to be involved in various diseases. Ferroptosis is a recently discovered form of regulated cell death characterized by iron overload, leading to the accumulation of lethal levels of lipid hydroperoxides. Recently, an increasing number of studies have revealed a link between autophagy and ferroptosis. Myocardial ischemia/reperfusion injury (MIRI) is an urgent dilemma after myocardial infarction recanalization, which is regulated by several cell death pathways, including autophagy and ferroptosis. However, the potential relationship between autophagy and ferroptosis in MIRI remains unexplored. In this study, we briefly review the mechanisms of autophagy and ferroptosis, including their roles in MIRI. Moreover, we provide an overview of the potential crosstalk in MIRI. Clarifying the relationship between different cell death pathways may provide new ideas for the treatment of MIRI in the future.

Corrigendum to "Safety and efficacy of ablation index-guided high-power ablation for the treatment of atrial fibrillation" [Heliyon 9 (4), (April 2023) Article e15311].

[This corrects the article DOI: 10.1016/j.heliyon.2023.e15311.].

Safety and efficacy of ablation index-guided high-power ablation for the treatment of atrial fibrillation.

Objective: To study the safety and efficacy of high-power ablation for atrial fibrillation (AF) guided by lesion size index (LSI) and impedance cutoff. Method: A total of 223 patients who underwent radiofrequency catheter ablation of atrial fibrillation (including paroxyparal atrial fibrillation and persistent atrial fibrillation) in the Department of Cardiology of Anhui Provincial Hospital from February 2019 to July 2020 were enrolled, and were divided into 123 patients in the high-power ablation group (HPAI) and 100 patients in the conventional power ablation group (CPAI). The HPAI group adopted high-power (40-50 W) ablation by impedance cutoff, and the CPAI group adopted conventional-power (30-35 W) ablation. Patients in both groups were ablated guided by the same LSI. For both groups, we analyzed the pulmonary vein single-circle isolation rate, ablation time, X-ray exposure, impedance drop value, incidence of complications, and recurrence rate within one year after operation. Results: There was no significant difference in the success rate of pulmonary vein single-circle isolation, X-ray perspective time, and X-ray exposure quantity between the HPAI group and the CPAI group (88.60% vs 82.00%, P = 0.161; 8.7 ± 3.74 min vs 7.82 ± 3.86 min, P = 0.067; 54.74 ± 28 min vs 52.78 ± 39.58 min, P = 0.139); the annular pulmonary vein ablation time and total ablation time were less in the HPAI group (35.74 ± 7.25 min vs 65.49 ± 7.34 min, P < 0.01; 55.42 ± 11.61 min vs 76.9 ± 6.79 min, P < 0.01); the impedance drop values at 10-15Ω and 15-20Ω were higher in the HPAI group (25.3% vs 19.1%, P < 0.05; 24.1% vs 19.1%, P < 0.05); there was no significant difference in the recurrence rate within one year after operation between the two groups; and no serious complications occurred in the two groups. Conclusion: High-power ablation guided by LSI and impedance cutoff could significantly shorten the AF ablation time and reduce complications.

The interaction between uric acid and high-density lipoprotein cholesterol on the prognosis of patients with acute myocardial infarction.

Background: The significance of uric acid (UA) and high-density lipoprotein cholesterol (HDL-C) in the prognosis of acute myocardial infarction (AMI) remains controversial. This study investigated the effect of the interaction between UA and HDL-C on the prognosis of patients with AMI. Methods: In total, 480 patients with AMI were included in this study. Baseline and follow-up data were collected, and the primary endpoint was major adverse cardiovascular events (MACE). The secondary endpoint was all-cause death. Both additive and multiplicative interactions were calculated to evaluate their interaction with prognosis. Then, the impact of UA and HDL-C ratio (UHR) on prognosis was assessed. Results: Over a median follow-up period of 41 (30,46) months, 136 (28.3%) MACEs, and 44 (9.2%) deaths were recorded. There was a positive additive interaction between UA and HDL-C for MACEs. The attributable proportion (AP) showed that 46% of the estimated effect (MACE in patients) was attributable to this interaction. The synergy index (SI) was 2.04 (1.07,3.88) for MACE, indicating that the risk for patients presenting with both risk factors was greater than the sum of the risk factors alone. Multivariate Cox regression analysis revealed that UHR independently predicted MACEs and mortality. Kaplan-Meier survival curves according to tertiles of UHR showed statistically significant differences in MACE (log-rank test, P < 0.001). Receiver operating characteristic (ROC) analysis showed that the area under the curve (AUC) of UHR for predicting MACE was 0.716. Conclusion: The coexistence of high UA and low HDL-C has a synergistic effect and provides further information for risk stratification of patients with AMI. UHR is a simple and easily available prognostic indicator independent of traditional risk factors.

Acetylation, ferroptosis, and their potential relationships: Implications in myocardial ischemia-reperfusion injury.

Myocardial ischemia-reperfusion injury (MIRI) is a serious complication affecting the prognosis of patients with myocardial infarction and can cause cardiac arrest, reperfusion arrhythmias, no-reflow, and irreversible myocardial cell death. Ferroptosis, an iron-dependent, peroxide-driven, non-apoptotic form of regulated cell death, plays a vital role in reperfusion injury. Acetylation, an important post-translational modification, participates in many cellular signaling pathways and diseases, and plays a pivotal role in ferroptosis. Elucidating the role of acetylation in ferroptosis may therefore provide new insights for the treatment of MIRI. Here, we summarized the recently discovered knowledge about acetylation and ferroptosis in MIRI. Finally, we focused on the acetylation modification during ferroptosis and its potential relationship with MIRI.

Anticoagulation therapy and clinical outcomes following transcatheter mitral valve repair for patients with mitral regurgitation: A meta-analysis.

Transcatheter mitral valve repair (TMVR) using MitraClip (MC) is now an established technique in the interventional treatment of mitral regurgitation. Common complications after MC procedure are bleeding and ischemic events. However, 2017 ESC/EACTS and 2020 ACC/AHA did not give a clear antithrombotic protocol, the policy has been based on clinical experience. Here, we performed a meta-analysis comparing outcomes with and without the addition of anticoagulants after TMVR. We searched the Cochrane Library, EMBASE, PubMed, and Web of Science from inception to October 6, 2022 to identify studies with or without the use of anticoagulants after TMVR. From each study, we extracted the number of people with bleeding, stroke, combined endpoints, and all-cause death. Five observational cohort studies were included, enrolling a total of 1892 patients undergoing TMVR who were assigned to either the anticoagulation group (n = 1209) or the no-anticoagulation group (n = 683). Pooled analysis showed a significantly lower stroke rate in the anticoagulated group (at least 4 weeks duration) compared with the non-anticoagulated group (RR [95% CI] = 0.14 [0.0-0.77], p = 0.02), and similar rates of bleeding, combined endpoints, and all-cause death in both groups (RR [95% CI] = 0.76 [0.48-1.22], p = 0.26), (RR [95% CI] = 0.52 [0.10-2.63], p = 0.43), and (RR [95% CI] = 0.89 [0.58-1.35], p = 0.58). We observed a reduced risk of stroke without elevated risk of bleeding, combined endpoints, or all-cause death in patients using anticoagulants (at least 4 weeks duration) after TMVR compared to no anticoagulants.