Wei Liu

Purpose: Evidence that left bundle branch area pacing (LBBAP) is more effective than conventional right ventricular (RV) pacing in enhancing left atrial (LA) outcomes is lacking. The aim of this study was to investigate LA outcomes using 2-dimensional speckle tracking echocardiography (2D-STE) and real-time 3-dimensional echocardiography (RT-3DE) at 6-months of follow-up in patients that received LBBAP, RV septal pacing (RVSP), or RV apical pacing (RVAP). Methods: A total of 90 patients with normal left ventricular ejection fraction (LVEF) underwent dual-chamber pacemaker implantation for bradycardia at Beijing Anzhen Hospital between January 2021 and July 2021. Patients were divided into three groups based on the pacing site: LBBAP, RVSP, or RVAP. Results: There were no significant differences in baseline characteristics and echocardiographic findings among patients that received LBBAP, RVSP, or RVAP. At 6-months of follow-up, left atrial volume index (LAVI), LA reservoir strain (LASr), LA contractile strain (LASct), global longitudinal strain (GLS), global circumferential strain (GCS), and synchronization parameters (Tmsv-16SD, Tmsv-12SD, Tmsv-6SD, longitudinal Tϵ-dif, circumferential Tϵ-dif) were significantly improved in patients that received LBBAP, while they had significantly worsened with RVSP and RVAP. Compared to baseline, at 6-months of follow-up, patients that received LBBAP had significantly improved LASr (28.17± 10.12% vs 35.4± 17.17%, P=0.024), LASct (− 12.03± 2.15% vs − 17.53± 7.37%, P=0.045), E/e’ ratio(12.61± 3.8 vs 10.85± 3.75,P=0.014) and LVEF (65.74± 7.90% vs 68.81± 5.92%, P=0.023). The 6-minute walking distance significantly increased at 6-months of follow-up compared to baseline in all patients, but the increase was most prominent for LBBAP (403.00± 98.46 m vs. 469.34± 59.32m, P=0.015). LBBAP was associated with a lower risk of new-onset atrial fibrillation. Conclusion: In pacemaker-dependent patients, LBBAP achieved better LA strain, LV strain, and LV synchronization than RVSP or RVAP at 6-months of follow-up. Plain Language Summary: This registered prospective study (ChiCTR2100048503) used two-dimensional speckle tracking echocardiography (STE) and real-time 3D echocardiography (RT-3DE) to comprehensively evaluate LA and LV function and mechanical synchrony in LBBAP. This study demonstrates that LBBAP can achieve better LA strain, LV strain and LV synchronization than RVSP or RVAP at 6-months of follow-up.

Background: Venous thromboembolism (VTE) is influenced by both genetic and acquired risk factors, with protein S (PS) deficiency recognized as a well-established inherited thrombophilia. Introduction: We report the case of a 32-year-old male patient presenting with mesenteric venous thrombosis and pulmonary embolism caused by a missense mutation in PROS1 during the COVID-19 pandemic.Methods: The patient presented with pleuritic chest pain and low-grade fever 15 days after a confirmed COVID-19 infection. Despite initial treatment with glucocorticoids and a macrolide antibiotic, his symptoms worsened and his D-dimer level increased. CT pulmonary angiography confirmed an acute pulmonary embolism.Results: Clinical history revealed a prior episode of mesenteric vein thrombosis and multiple acquired risk factors, including obesity, sedentariness, COVID-19 infection, glucocorticoid treatment, inflammatory response (elevated CRP and serum ferritin levels), and metabolic abnormalities (non-alcoholic fatty liver disease, hyperuricemia, and hyperlipidemia). Laboratory testing showed decreased PS activity, and genetic sequencing identified a heterozygous missense mutation in PROS1, c.683G>A (p.Cys228Tyr). The patient was treated with low-molecular-weight heparin (LMWH) followed by rivaroxaban. Discussion: No recurrence of VTE of bleeding events was observed during a one-year follow-up, suggesting effective management of thrombosis in the context of both inherited and acquired prothrombotic conditions.

Background: Circulating fibrinogen-to-albumin ratio (FAR) has been proposed as a novel inflammatory biomarker in patients with heart failure and malignant tumor. However, the prospective association in patients with atherosclerotic cardiovascular disease (ASCVD) remains to be investigated.Methods: The trial enrolled 821 patients with ASCVD from United States National Health and Nutrition Examination Survey from 1999-2002, with mortality follow-up through December 31st, 2019. Participants were divided into high-level FAR (FAR_H) and low-level FAR (FAR_L) groups. Kaplan-Meier and Cox proportional risk models were used to investigate the relationship between FAR and all-cause mortality in middle-aged and older persons with diabetes mellitus (DM).Results: During the median follow-up time of 15.6 years, 608 (weighted, 74.1%) ASCVD patients developed mortality. The incidence of mortality differed significantly between the FAR groups in patients with or without DM. Compared with FAR_L group, the FAR_H group has increased 90% mortality in the ASCVD patients with DM (HR = 1.90, 95%CI 1.22 - 3.00; P = 0.005). Moreover, the FAR and DM have a significant interaction (P = 0.016) in the ASCVD patients.Conclusions: In this prospective cohort study, a higher level of FAR was independently associated with 15-year mortality among ASCVD patients with DM. The combination of FAR and DM in ASCVD patients may aid in risk stratification and prognosis.

As a novel indicator reflecting metabolic status and visceral adiposity distribution, the cardiometabolic index (CMI) has gained attention in cardiovascular risk stratification. This investigation employed optical coherence tomography (OCT) to examine potential associations between CMI and vulnerable plaque, as well as the role of inflammation. This study conducted a cross-sectional analysis of 270 acute coronary syndrome (ACS) patients who had OCT imaging evaluation. Patients were categorized based on CMI tertiles, with CMI calculated using the formula [waist (cm)/height (cm)]×[triglycerides (mmol/L)/HDL-C (mmol/L)]. OCT was used to assess plaque events in culprit lesions and plaque components in non-culprit lesions, and inflammatory markers were measured. A mediation analysis framework was implemented to investigate inflammatory pathways in CMI-vulnerable plaque relationships. CMI tertiles were linked to vulnerable plaque traits: thin-cap fibroatheromas (TCFA), macrophages (Tertiles1 vs. Tertiles2 vs. Tertiles3, TCFA: 10.0% vs. 20.0% vs. 26.7%, P = 0.016; macrophages: 17.8% vs. 28.9% vs. 36.7%, P = 0.019). Multivariate regression demonstrated CMI elevation independently predicted a higher prevalence of TCFA (OR:1.40, 95%CI: 1.25–2.89, P = 0.003), more macrophage infiltration (OR:1.61, 95% CI:1.09–2.37, P = 0.017), reduced FCT (β:-30.65, 95% CI:-50.72-10.57, P = 0.003), and enlarged maximum lipid arc (β:20.78, 95% CI:6.55–35.01, P = 0.004). Moreover, CMI was positively related to hsCRP, WBC, and neutrophils. Mediation analysis revealed that hsCRP mediated about 17.0% of the association between CMI and minimum FCT [Indirect effect=-5.21, 95% CI=(-12.70, -1.27), P = 0.016]. CMI is a key forecaster of vulnerable plaque in patients with ACS. Systemic inflammation is associated with the relationship between CMI and vulnerable plaque features, suggesting a potential mechanistic link.

Objective: The prevalence of acute myocardial infarction, a severe ischemic cardiac disease, is on the rise annually. The establishment of coronary collateral circulation in the border zone of the infarct can effectively relieve myocardial ischemia and impede cell death, while angiogenesis can promote the formation of collateral circulation in the ischemic tissues. Over the past two decades, studies related to angiogenesis in acute myocardial infarction have increased rapidly. However, there is a lack of bibliometric studies in this particular field.Methods: For this study, we employed bibliometric analysis to outline focal points and patterns in scientific and clinical research. The collection of literature was gathered using the Web of Science Core Collection database. Bibliometric and visual analysis were conducted. Knowledge maps were generated using CiteSpace and VOSviewer software.Results and conclusions: With the deepening of the research, therapeutic angiogenesis will become a treatment direction for acute myocardial infarction in the future.

Background: Left bundle branch area pacing (LBBAP) has evolved into a practical and secure pacing procedure. However, previous studies of LBBAP focused on left heart function and synchronization and lacked assessment of right heart structure and function and interventricular synchrony. The objective of this study was to examine the impacts of LBBAP, right ventricular (RV) septal pacing (RVSP), and RV apical pacing (RVAP) on right heart structure, function and interventricular synchrony. Methods: Between January and July 2021, A total of 90 patients exhibited a normal left ventricular (LV) ejection fraction and received dual chamber pacemaker implantation for bradycardia at Beijing Anzhen Hospital. The patients were assigned to three groups based on the pacing site: LBBAP, RVSP, or RVAP. RV function was evaluated using right ventricular fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), tissue Doppler–derived tricuspid lateral annular systolic velocity (S'), right ventricular myocardial performance index (RVMPI), global longitudinal strain of the right ventricle (GLSRV), and right ventricular free wall longitudinal strain (RVFWLS). Tricuspid regurgitation (TR) was assessed using vena contracta magnitude (VCM) and the ratio of TR jet area to right atrial area (RAA). Interventricular mechanical synchrony was evaluated using interventricular mechanical delay (IVMD) and left ventricular to right ventricular time-to-peak standard deviation (LV-RV TPSD). Results: Baseline echocardiographic parameters and characteristics were comparable among the three groups. No significant differences were observed in the LBBAP group from baseline to follow-up for QRS duration (p = 0.783), TAPSE (p = 0.122), RVFAC (p = 0.679), RVMPI (p = 0.93), GLSRV (p = 0.511), RVFWLS (p = 0.939), VCM (p = 0.467), and TR jet area/RAA (p = 0.667). In contrast, a significant decline was observed in the RVAP group (all p < 0.05). RVSP resulted in a similar percentage reduction in TAPSE, GLSRV, and RVFWLS (all p > 0.05). However, there were significant differences in RVFAC (p = 0.009), RVMPI (p = 0.037), TRVCM (p = 0.046), and TR jet area/RAA (p = 0.033) in the RVSP group. Moreover, compared to baseline, a 1-year follow-up showed that LBBAP significantly reduced IVMD (from 17.3 ± 26.5 ms to 8.6 ± 7.1 ms, p < 0.05) and LV-RV TPSD [from 16.41 (8.81–42.5) to 12.28 (5.64–23.7), p < 0.05], while RVSP and RVAP worsened IVMD and LV-RV TPSD (all p < 0.05). Conclusions: Compared with RVSP or RVAP, LBBAP can maintain RV function and improve electrical and interventricular synchrony, with limited TR deterioration after a 1-year follow-up. Clinical Trial Registration: No. ChiCTR2100048503, https://www.chictr.org.cn/showproj.html?proj=129290.

Background: Inflammasomes have emerged as an important and promising area of investigation in atherosclerosis. This field, however, lacks bibliometric studies. To help understand how basic and clinical research on inflammasomes in atherosclerosis will develop in the future, we used bibliometric analysis to visualize hotspots and trends.Methods: Studies related to inflammasomes in atherosclerosis were collected from the Web of Science Core Collection database. Each study was analyzed bibliometrically and visually. CiteSpace and VOSviewer software were used to generate knowledge maps.Results: A total of 894 articles were identified. Sixty-two countries and 338 institutions led by China and the United States contributed to these publications. The leading research institutions were Harvard Medical School and Columbia University. Circulation was the most frequently cited journal in this field. Among the 475 authors determined, Eicke Latz authored the most studies, and Peter Duewell has been cocited the most. NLRP3 inflammasome, NF-kappa B, macrophage and oxidative stress are the most commonly used keywords.Conclusion: There has been a blooming of research on inflammasomes in atherosclerosis during the last two decades. Future studies will likely explore the molecular mechanism of inflammasomes in cell death. More compellingly, researchers may further delve into the potential clinical value of affecting pathological changes in atherosclerosis by modulating the initial transcription immune response and intracellular multiprotein assembly process of the NLRP3 inflammasome. Our research will be helpful to scholars focusing on inflammation—a much-needed breakthrough in the pathophysiological alterations of atherosclerosis—with a novel perspective.

Background: Cardiac injury is recognized as one of the most common critical complications during exacerbation of coronavirus disease 2019 (COVID-19). This study aimed to investigate the effect of cardiac injury on the clinical course of COVID-19 and to examine its potential mechanism and treatments. Methods and Results: A total of 222 hospitalized patients with COVID-19 from Wuhan were selected for the study during February 10 to March 28, 2020. Demographic, laboratory, and clinical data on admission and during hospitalization were compared between patients with COVID-19 with or without cardiac injury. On admission, cardiac injury (n = 29) was associated with advanced age, more underlying coronary artery disease, and a lower PaO₂. Troponin levels were correlated with inflammatory markers (C-reactive protein: r = 0.348, P < 0.001; interleukin 6: r = 0.558, P < 0.001) and D-dimer levels (r = 0.598, P < 0.001). During hospitalization, another six patients suffered from cardiac injury and cardiac injury (n = 35), resulting in higher rates of ventilation (invasive: 51.4 vs. 1.6%, P < 0.001; non-invasive: 31.4 vs. 1.1%, P < 0.001) and mortality (54.3 vs. 1.1%, P < 0.001). Cardiac injury on admission was a predictive factor for mortality (adjusted hazard ratio = 4.73, 95% confidence interval = 1.35–16.63, P = 0.015). Receiver operating characteristic curve analysis showed that, on admission, a troponin level of 36.35 pg/mL was predictive for mortality with a sensitivity of 73.7% and a specificity of 92.1%. Conclusions: Cardiac injury complicates the disease course and increases the mortality rate of COVID-19. Troponin levels should be checked at admission and during hospitalization for triage, better monitoring, and managing those with COVID-19, especially in the most severe patients. Condensed Abstract: Cardiac injury is not uncommon in COVID-19. In a cohort of 222 patients with COVID-19, cardiac injury was found in 29 patients on admission and in another 6 patients during hospitalization. The admission level of troponin was well-correlated with inflammatory factors and D-dimer levels and strongly predicted mortality. Cardiac injury is a manifestation secondary to hypoxia and systemic infection, but which nevertheless further complicates the disease course and increases the mortality rate. Troponin levels should be checked at admission and during hospitalization for triage, better monitoring, and managing those with COVID-19, especially in the most severe patients.