Jailed high-pressure balloon technique is superior to jailed wire technique in protecting side branch of coronary bifurcation lesions.

Objectives. This study investigated the influence of higher pressure protection with a small diameter balloon of side branch (SB) on bifurcation lesions. Background. Of the different coronary stent implantation techniques, the modified jailed balloon technique has become a viable option for bifurcation lesions. However, there was no detailed study on the relationship between the balloon inflation pressure of the main vessel (MV) and SB. Methods. In this study, we collected information of patients who underwent percutaneous coronary intervention (PCI) for bifurcated lesions between March 2019 and December 2022. They were divided into two groups according to the operation way: active jailed balloon technique (A-JBT) group and jailed wire technique (JWT) group. Results. A total of 216 patients were enrolled. The A-JBT group had a larger SB stenosis diameter (1.53 ± 0.69 vs. 0.95 ± 0.52, p < .001), the lower degree of stenosis (44.34 ± 18.30 vs. 63.69 ± 17.34, p < .001) compared to the JWT group. However, the JWT group had a higher incidence of SB occlusion (18.0% vs. 1.9%, p < .001) compared to the A-JBT group. Nevertheless, the success rate for both groups was 100%. Conclusions. This novel high inflation pressure and small diameter balloon approach we propose has significant advantages. There is a lower rate of SB occlusion and SB dissection, which is more cost-effective and provides better clinical outcomes for the patient. This method should be considered in the future for treating bifurcation lesions.

Complexities of Coexisting Cardiac Amyloidosis and Coronary Artery Disease: A Contemporary Review of Diagnostic and Treatment Approaches.

Cardiac amyloidosis (CA) represents an emerging challenge in cardiovascular medicine, with notable clinical overlaps and diagnostic complexities when coexisting with coronary artery disease (CAD). This integrative review navigates the intricate terrain of CA and CAD, elucidating epidemiology, clinical presentations, and diagnostic considerations. Examining both immunoglobulin light chain amyloidosis (AL) and transthyretin amyloidosis, we underscore their shared demographic associations, diagnostic intricacies, and potential diagnostic confounders with CAD. Notably, we emphasize the impact of CA on epicardial coronary arteries and the consequential implications for coronary microcirculation. Further exploration reveals the connection between CA and acute myocardial infarction, emphasizing early recognition as pivotal. In terms of differential diagnosis, we underscore the significance of clinical symptoms, electrocardiography, echocardiography, cardiac magnetic resonance, and bone scintigraphy. Additionally, we scrutinize the intricate realm of treatment, encompassing medication selection, antithrombotic strategies, and revascularization modalities. Our review addresses the distinctive challenges posed by CA patients' limited tolerance for conventional therapies. This comprehensive synthesis serves as an invaluable resource for clinicians confronting the intricate intersection of CA and CAD. By offering insights into diagnostic refinement and innovative therapeutic avenues, we aim to enhance patient outcomes and quality of life within this complex clinical landscape.

The percentage of circulating fibrocytes is associated with increased morbidity of pulmonary hypertension in patients on hemodialysis.

INTRODUCTION: Pulmonary hypertension (PH) is highly prevalent in patients receiving dialysis. The precise mechanisms underlying PH in hemodialysis (HD) patients have not been adequately addressed. Emerging experimental evidence indicates that circulating fibrocytes may contribute significantly to this process. METHODS: We measured the proportion of circulating fibrocytes using flow cytometry analysis and prospectively analyzed patients during HD from February 1, 2017, to February 1, 2022. Then we investigated correlations between circulating fibrocytes, inflammation cytokines, PH, and their affective factors that predict the prognosis of HD patients. RESULTS: The cohort included 192 patients. During a follow-up of 5 years, we registered 66 all-cause deaths, and 11 patients received kidney transplantation. The incidence of PH among HD patients was 30.9%. We found that the circulating fibrocyte level significantly correlated with pulmonary arterial systolic pressure (r = 0.412, p < 0.05). In the multiple logistic regression analysis, the percentage of circulating fibrocytes was an independent predictor of PH (odds ratio [OR]: 2.080, 95% confidence interval [CI]: 1.539-2.812, p < 0.001). Controlling for confounding covariates in the multivariate Cox regression models, the presence of PH conferred an increased risk of all-cause mortality in HD patients [hazard ratio (HR): 2.183, 95% CI:1.257-3.788, p = 0.006]. CONCLUSION: The prevalence of PH was high in HD patients and was associated with higher all-cause mortality. Higher circulating fibrocyte level was an independent predictor of the presence of PH; these fibrocytes may serve as early detection markers and novel therapeutic targets.

Proteomic sequencing analysis in a rat model of atrial fibrosis caused by chronic intermittent hypoxia.

Background: Atrial fibrosis caused by long-term atrial fibrillation influences the outcomes of clinical treatment. An improved understanding of the mechanisms underlying atrial fibrillation may reveal new therapeutic targets. This study was conducted to analyze the changes in protein levels in the atrial tissue of a rat model of atrial fibrillation based on proteome sequencing. Methods: Sprague-Dawley rats were used to develop a model of atrial fibrillation induced by chronic intermittent hypoxia (CIH). Histopathological changes were detected using hematoxylin and eosin staining and Masson's staining, and immunohistochemistry and western blotting for the levels of fibrosis biomarkers. Atrial fibrosis tissue samples were also evaluated by proteome sequencing. Differentially expressed proteins (DEPs) between the CIH and control groups were evaluated in functional assay. The expression levels of several key proteins were validated using western blotting. Results: CIH resulted in atrial fibrosis and induced atrial fibrillation. We identified 145 DEPs between the CIH and control groups. These included Myh7, Myl2, Myl3, and Atpla3, which are involved in signaling pathways related to hypertrophic cardiomyopathy, glycerolipid metabolism, and cardiac muscle contraction. Western blotting revealed the upregulation of Myh7, Myl2, and Myl3 and the downregulation of Atpla3 in the CIH group compared with the control group. These results were consistent with the sequencing results. Conclusions: Myh7, Myl2, Myl3, and Atpla3 may play key roles in the progression of atrial fibrillation through their involvement in cardiovascular-disease-related signaling pathways.

Cfa-circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosis.

Background and aims: The role of circular RNAs (circRNAs) in the pathophysiology of cardiovascular disease is gradually being elucidated; however, their roles in atrial fibrillation (AF)-related fibrosis are largely unknown. This study aimed to characterize the different circRNA profiles in the rapid-pacing atria of dogs and explore the mechanisms involved in atrial fibrosis. Methods: A rapid right atrial-pacing model was established using electrical stimulation from a pacemaker. After 14 days, atrial tissue was collected for circRNA sequencing analysis. In vitro fibrosis was established by stimulating canine atrial fibroblasts with angiotensin II (Ang II). The fibroblasts were transfected with siRNA and overexpressing plasmids to explore the effects of cfa-circ002203 on fibroblast proliferation, migration, differentiation, and the expression of fibrosis-related proteins. Results: In total, 146 differentially expressed circRNAs were screened, of which 106 were upregulated and 40 were downregulated. qRT-PCR analysis showed that cfa-circ002203 was upregulated in both in vivo and in vitro fibroblast fibrosis models. The upregulation of cfa-circ002203 enhanced proliferation and migration while weakening the apoptosis of fibroblasts. Western blotting showed that cfa-circ002203 overexpression increased the protein expression levels of fibrosis-related indicators (Col I, Col III, MMP2, MMP9, and α-SMA) and decreased the protein expression levels of pro-apoptotic factors (Bax and Caspase 3) in Ang II-induced fibroblast fibrosis. Conclusion: Cfa-circ002203 might serve as an active promoter of the proliferation, migration, and fibrosis of atrial fibroblasts and is involved in AF-induced fibroblast fibrosis.

Combination of SVI/S' and diagnostic scores for heart failure with preserved ejection fraction.

The diagnosis of heart failure with preserved ejection fraction (HFpEF) remains a challenge. There are three methods proposed as diagnostic tools. H2 FPEF score was determined by six weighted clinical characteristics and echocardiographic variables. Heart Failure Association (HFA)-PEFF algorithm consists of various functional and morphological variables as well as natriuretic peptides. SVI/S' is a novel echocardiographic parameter calculated by stroke volume index and mitral annulus systolic peak velocity. This study aimed to compare the three approaches in patients with suspected HFpEF. Patients referred to right heart catheterization for suspected HFpEF were classified into low-, intermediate- and high-likelihood groups according to H2 FPEF or HFA-PEFF scores. A diagnosis of HFpEF was confirmed by pulmonary capillary wedge pressure (PCWP) of ≥15 mm Hg according to the guidelines. In result, a total of 128 patients were included. Of these, 71 patients with PCWP ≥15 mm Hg and 57 patients with PCWP <15 mm Hg. Moderate correlations were observed between H2 FPEF score, HFA-PEFF score, SVI/S' and PCWP. The area under curve of SVI/S' was 0.82 for diagnosis of HFpEF, compared with 0.67 for H2 FPEF score and 0.75 for HFA-PEFF score by receiver-operating characteristics analysis. Combining SVI/S' with diagnostic scores showed higher Youden index and accuracy than each score alone. Kaplan-Meier analysis reported that the high-likelihood group showed poorer outcomes regardless the method used for diagnosis. Among the contemporary tools for identifying HFpEF in this study, the combination of SVI/S' with risk scores showed best diagnostic ability. Each of the strategies can determine rehospitalisation because of heart failure.

Integrated whole transcriptome analysis for the crucial regulators and functional pathways related to cardiac fibrosis in rats.

BACKGROUND: Cardiac fibrosis has gradually gained significance in the field of cardiovascular disease; however, its specific pathogenesis remains unclear. This study aims to establish the regulatory networks based on whole-transcriptome RNA sequencing analyses and reveal the underlying mechanisms of cardiac fibrosis. METHODS: An experimental model of myocardial fibrosis was induced using the chronic intermittent hypoxia (CIH) method. Expression profiles of long non-coding RNA (lncRNA), microRNA (miRNA), and messenger RNA (mRNA) were acquired from right atrial tissue samples of rats. Differentially expressed RNAs (DERs) were identified, and functional enrichment analysis was performed. Moreover, a protein-protein interaction (PPI) network and competitive endogenous RNA (ceRNA) regulatory network that are related to cardiac fibrosis were constructed, and the relevant regulatory factors and functional pathways were identified. Finally, the crucial regulators were validated using qRT-PCR. RESULTS: DERs, including 268 lncRNAs, 20 miRNAs, and 436 mRNAs, were screened. Further, 18 relevant biological processes, such as "chromosome segregation, " and 6 KEGG signaling pathways, such as "cell cycle, " were significantly enriched. The regulatory relationship of miRNA-mRNA-KEGG pathways showed eight overlapping disease pathways, including "pathways in cancer." In addition, crucial regulatory factors, such as Arnt2, WNT2B, GNG7, LOC100909750, Cyp1a1, E2F1, BIRC5, and LPAR4, were identified and verified to be closely related to cardiac fibrosis. CONCLUSION: This study identified the crucial regulators and related functional pathways in cardiac fibrosis by integrating the whole transcriptome analysis in rats, which might provide novel insights into the pathogenesis of cardiac fibrosis.

Effects of radiofrequency balloon angioplasty on the abdominal aorta in atherosclerotic rabbits.

OBJECTIVES: A novel temperature-controlled intravascular radiofrequency balloon angioplasty (RFBA) technique was designed and developed for atherosclerosis (AS) management. METHODS: After establishing an AS model based on a balloon denudation injury of the abdominal aorta and a high cholesterol diet in rabbits, 46 animals were randomly assigned to the RFBA group (n = 28) or the plain balloon angioplasty (PBA) group (n = 28). The groups were further subdivided based on post-treatment euthanasia times (1 hour, 7 days, 14 days, and 28 days). Histopathological changes were observed by hematoxylin and eosin and Masson's staining. Immunohistochemistry, western blotting, and real-time quantitative polymerase chain reaction were used to detect changes in pro-inflammatory, anti-inflammatory, and apoptotic factors; TGF-ß/Smad-2 pathway protein Immune levels; and mRNA levels in tissues, respectively. RESULTS: The vascular lumen area in the RFBA group was larger than that in the PBA group at the same time points, although the change in the vascular lumen area was not different between groups. The expression of Bax, TGF-ß, Smad-2, and Caspase-3 in the RFBA group was significantly higher than that in the PBA group. The expression levels of Bcl-2 in the RFBA group were significantly lower than those in the PBA group. CONCLUSIONS: At 28 days, RFBA dilated the atherosclerotic blood vessels and thickened the fibrous cap of atherosclerotic plaques to promote plaque stability. RFBA was also found to activate apoptotic factors and the TGF-/Smad-2 inflammatory pathway.

Structurally Ordered PtNi Intermetallic Nanoparticles as Efficient and Stable Cathode Catalysts for Proton Exchange Membrane Fuel Cells.

Exploring oxygen reduction reaction (ORR) catalysts with superior electrochemical performance and long-term stability is crucial to the development of proton exchange membrane fuel cells (PEMFCs). In this work, graphited carbon with high specific surface area was obtained under relatively low temperature using Ni catalyst, then ordered nanoparticles (NPs) PtNi catalysts attaching to graphited carbon were synthesized via polyol reduction and thermal treatment. Benefiting from graphitized carbon support and appropriate order degree, PtNi/GC-700 NPs catalyst exhibits excellent electrocatalytic ORR performance with specific and mass activities as high as 2.8-fold and 3.7-fold of the commercial Pt/C catalyst, respectively. Besides, the as-prepared PtNi/GC-700 catalyst exhibits superior stability with negligible degradation after 10000 potential cycles, due to its ordered chemical structure. The work described herein highlights the potential of structurally ordered electrocatalysts for efficient and durable fuel cell cathodic catalysts.

CircRNA_0263 and circRNA_1507 are dysregulated in a rat model of atrial fibrosis induced by chronic intermittent hypoxia.

Aims: This study aimed to characterize circular RNA (circRNA) profiles associated with atrial fibrosis-related atrial fibrillation (AF) and reveal critical circRNAs for AF. Methods: Sprague Dawley rats were randomly divided into control and atrial fibrosis-related AF groups (n = 15 in each group). The rats in the atrial fibrosis-related AF group were induced by chronic intermittent hypoxia (CIH), and then confirmed by electrocardiograms, echocardiography, hematoxylin-eosin staining, Masson staining, immunohistochemistry assays and western blotting. After that, the atrial tissues were sent for circRNA sequencing, and the differentially expressed circRNAs were identified and validated by quantitative real-time polymerase chain reaction (qRT-PCR). Finally, a series of cell experiments were performed to explore the roles of two crucial circRNAs in rat atrial fibroblasts. Results: A CIH-induced AF model was successfully established in the rats. After sequencing, five upregulated and 11 downregulated circRNAs were identified in the CIH-induced AF group. These dysregulated circRNAs were primarily associated with "carbohydrate metabolism" and "cardiovascular diseases". Two circRNAs (circRNA_0263 and circRNA_1507) were predicted to regulate target gene expression by interacting with corresponding miRNAs, including rno-miR-29b-5p, rno-miR-29b-3p, rno-miR-496-5p, rno-miR-136-5p, and novel123-mature. Additionally, circRNA_0263 knockdown and circRNA_1507 overexpression inhibited the cell viability of fibroblasts, and downregulated the expression of fibrosis-related proteins. Conclusion: A series of circRNAs were identified as dysregulated in an AF rat model, and circRNA_0263 and circRNA_1507 might be crucial for atrial fibrosis-related AF development by competing with several miRNAs.

Antiplatelet therapy for patients with COVID-19: Systematic review and meta-analysis of observational studies and randomized controlled trials.

Background: Hyperinflammation and coagulopathy are hallmarks of COVID-19 and synergistically contribute to illness progression. Antiplatelet agents have been proposed as candidate drugs for COVID-19 treatment on the basis of their antithrombotic and anti-inflammatory properties. A systematic review and meta-analysis that included early observational studies and recent randomized controlled trials (RCTs) was performed to summarize and compare evidence on this issue. Methods: PubMed, Embase, and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched to identify studies published up to Nov 7, 2021, and the results of registered clinical trials were followed up to Mar 30, 2022. We included RCTs and observational studies assessing the effect of antiplatelet therapy in adult patients with COVID-19. Data on baseline patient characteristics, interventions, controls, and outcomes were extracted by two independent reviewers. The primary outcome was mortality. Data were pooled using a random-effects model. Results: Twenty-seven studies were included, of which 23 observational studies were pooled in a meta-analysis, and the remaining four RCTs (ACTIV-4B, RECOVERY, ACTIV-4a, and REMAP-CAP) were narratively synthesized. Based on 23 observational studies of 87,824 COVID-19 patients, antiplatelet treatment favors a lower risk of mortality [odds ratio (OR) 0.72, 95% confidence interval (CI) 0.61-0.85; I 2 = 87.0%, P < 0.01]. The narrative synthesis of RCTs showed conflicting evidence, which did not support adding antiplatelet therapy to the standard care, regardless of the baseline illness severity and concomitant anticoagulation intensity. Conclusion: While the rationale for using antiplatelet treatment in COVID-19 patients is compelling and was supported by the combined result of early observational studies, evidence from RCTs did not confirm this approach. Several factors that could explain this inconsistency were highlighted alongside perspectives on future research directions.

[Mechanism and experimental verification of "Polygoni Cuspidati Rhizoma et Radix-Ligustri Lucidi Fructus" combination in treatment of acute gouty arthritis based on network pharmacology].

Based on network pharmacology, the mechanism of Polygoni Cuspidati Rhizoma et Radix-Ligustri Lucidi Fructus(PL) combination against acute gouty arthritis(AGA) was explored and preliminarily verified by animal experiment. The chemical components and corresponding targets of PL were retrieved from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP). The active components with oral bioavailability(OB)≥30% and drug-likeness(DL)≥0.18 were screened based on literature, and the related protein targets were collected. Then the protein targets were standardized with the help of UniProt database. The AGA-related targets were searched from GeneCards, NCBI, and DrugBank. The common targets of the disease and the medicinals were yielded by FunRich V3, and the protein-protein interaction(PPI) network was constructed to screen the key targets, followed by Gene Ontology(GO) term enrichment analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analysis of the key targets. Afterwards, some of the key targets were verified by sodium urate crystal-induced AGA mouse model. A total of 25 active components and 287 targets of PL, 811 targets of AGA, and 88 common targets were screened out. PPI network analysis showed that tumor necrosis factor(TNF), interleukin-6(IL-6), and interleukin-1ß(IL-1ß) may be the core targets of PL in the treatment of AGA. The key targets were mainly involved in 566 GO terms(P<0.05), including multiple biological processes such as inflammatory response and immune response. Moreover, they were related to 116 KEGG pathways and these pathways were involved in inflammation and immunity, mainly including NOD-like receptor signaling pathway and TNF signaling pathway. Animal experiment confirmed that PL can alleviate ankle swelling, improve abnormal gait, and down-regulate the protein expression of TNF-α, IL-6, and IL-1ß in AGA mice, indicating that PL can treat AGA through TNF-α, IL-6, and IL-1ß and the feasibility of network pharmacology to predict drug targets. This study preliminarily discussed the key targets and biological signaling pathways involved in the treatment of AGA with PL combination, which reflected the multi-pathway and multi-target action characteristics of Chinese medicine. Moreover, this study laid a scientific basis for research on the treatment of AGA with PL combination, as well as the mechanism of action.

A Novel Three-Dimensional and Tissue Doppler Echocardiographic Index for Diagnosing and Prognosticating Heart Failure With Preserved Ejection Fraction.

INTRODUCTION: The diagnosis of heart failure with preserved ejection fraction (HFpEF) remains challenging. In this study, a novel echocardiography index based on three-dimensional and tissue Doppler echocardiography for diagnosing and estimating prognosis in HFpEF. MATERIALS AND METHODS: Patients with symptoms and/or signs of heart failure and normal left ventricular ejection fraction (LVEF ≥50%) who underwent right heart catheterization were screened. Patients were divided based on pulmonary capillary wedge pressure (PCWP) of ≥15 mmHg and PCWP <15 mmHg. A diagnosis of HFpEF was confirmed by PCWP of ≥15 mmHg according to ESC guidelines. A novel index was calculated by the ratio between stroke volume standardized to body surface area (SVI) and tissue Doppler mitral annulus systolic peak velocity S' (SVI/S'). Its diagnostic and prognostic values were determined. RESULTS: A total of 104 patients (mean age 64 ± 12 years) were included. Of these, 63 had PCWP ≥15 mmHg and 41 patients had PCWP <15 mmHg. Compared to the PCWP <15 mmHg group, the ≥15 mmHg group had a significantly lower SVI/S' (P < 0.001). Logistic regression showed that SVI/S' was associated with high PCWP measured invasively. The SVI/S' had an area under the curve of 0.761 for diagnosing classifying between PCWP ≥15 mmHg and <15 mmHg. Kaplan-Meier analysis showed that the lower SVI/S' group showed a poorer prognosis. CONCLUSIONS: SVI/S' is a non-invasive index calculated by three-dimensional and tissue Doppler echocardiography. It is a surrogate measure of PCWP and can be used to diagnose and determine prognosis in HFpEF.

Establishment of a lncRNA-miRNA-mRNA network in a rat model of atrial fibrosis by whole transcriptome sequencing.

PURPOSE: Dysregulation of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) plays important roles in atrial fibrillation (AF). This study aimed to identify crucial lncRNAs, miRNAs, and mRNAs in AF based on whole transcriptome sequencing. METHODS: Thirty Sprague Dawley rats were randomly stratified into control and chronic intermittent hypoxia (CIH) groups (n = 15 in each). Hematoxylin-eosin staining, Masson staining, immunohistochemical assay, and western blotting were used to evaluate this model. Thereafter, atrial tissues were sent for whole transcriptome sequencing. Finally, fibrosis-related competing endogenous RNA (ceRNA) regulatory networks were built, and the relative levels of lncRNAs, miRNAs, and mRNAs were validated by real-time quantitative polymerase chain reaction (RT-qPCR) or western blotting. RESULTS: A CIH-induced atrial fibrosis rat model was successfully constructed. After sequencing, 268 differentially expressed lncRNAs (DELs), 20 differentially expressed miRNAs (DEMs), and 436 differentially expressed genes (DEGs) were identified. Functional analyses showed that these DEGs were associated with several processes and pathways, including "cell division," "IL-17 signaling pathway," "NOD-like receptor signaling pathway," and "cell adhesion molecules." Fibrosis-related ceRNA networks were then built, comprising five lncRNAs, seven miRNAs, and 19 DEGs. RT-qPCR and western blotting results showed that the patterns of lncRNAs (NONRATT016396.2, NONRATT001596.2, NONRATT011456.2), miRNAs (miR-10b-3p, miR-29b-3p), and mRNAs (Gng7 and Wnt2b) were consistent with sequencing analyses. CONCLUSIONS: The DELs, DEMs, and DEGs identified in this study may participate in atrial fibrosis processes, and the occurrence and progression of AF.

CD36+/CD61+ Microparticles Correlate with the Risk of Percutaneous Cardiac Interventions in Coronary Artery Disease Patients and the Effects of Ticagrelor.

PURPOSE: The CD36 scavenger receptor is a mediator of both atherogenesis and thrombosis. We aimed to investigate the prognostic value of CD36+ microparticles (MPs) released from platelets for cardiovascular event presentation in coronary artery disease (CAD) patients and the effects of different antiplatelet drugs on MPs. METHODS: A total of 101 aspirin-treated CAD patients, who were planned to undergo coronary angiography (CAG), were randomized to either a standard clopidogrel regimen or ticagrelor treatment. Total Annexin V-(AV)+ MPs, CD61+/AV+ MPs, and CD36+/CD61+/AV+ MPs were quantified by flow cytometry at baseline, before and immediately after the operation. The ADP-induced platelet inhibition rate was measured by thromboelastogram (TEG) examination 1 h before the operation. RESULTS: The baseline levels of CD36+/CD61+/AV+ MPs were significantly increased in percutaneous coronary intervention (PCI) patients (n = 52) compared to no-PCI patients (n = 49) (p < 0.05). A ROC-curve clustered model for CD36+/CD61+/AV+ MPs at baseline predicted an increased risk of PCI [p = 0.009, AUC = 0.761 (95%CI: 0.601 to 0.922)]. Moreover, TEG examination showed that the preoperative proportion of CD36+/CD61+/AV+ MPs was significantly negatively correlated with R time and K time (r = - 0.236, p = 00.026; r = - 0.288, p = 0.006), and positively correlated with MAADP (r = 0.226, p = 0.045). Subgroup analysis of PCI group showed that the platelet inhibition rate of ticagrelor was significantly higher (66.05% ± 28.76% vs.31.01% ± 27.33%, p < 0.001), and the number of AV+ MPs, CD61+/AV+ MPs, and CD36+/CD61+/AV+ MPs before the operation was significantly lower than clopidogrel (p < 0.05, all). CONCLUSION: The high levels of CD36+ MPs derived from activated platelets are related to an increased risk of PCI in CAD patients. Ticagrelor significantly reduced the number of CD61+/AV+ MPs and CD36+/CD61+/AV+ MPs. This trial registration number is ChiCTR1800014908 and the date of registration is 2018.05.01.

Loading doses of ticagrelor versus clopidogrel in preventing periprocedural myocardial infarction in Asian patients with acute coronary syndrome.

BACKGROUND: Periprocedural myocardial infarction is a common complication following percutaneous coronary intervention. The present study was conducted with an aim to compare the safety and efficacy of loading doses of ticagrelor versus clopidogrel in preventing periprocedural myocardial infarction in Asian patients with acute coronary syndrome undergoing elective percutaneous coronary intervention. METHODS: A total of 114 patients with acute coronary syndrome undergoing elective percutaneous coronary intervention were assigned to clopidogrel group (n = 57, the loading and maintenance doses were 300 and 75 mg qd for clopidogrel, and 300 and 100 mg qd for aspirin), or ticagrelor group (n = 57, the loading and maintenance doses were 180 and 90 mg bid for ticagrelor, and 300 and 100 mg qd for aspirin). Cardiac biomarkers were measured before, 8 hours, and 24 hours after percutaneous coronary intervention. The percutaneous coronary intervention-related periprocedural myocardial infarction was defined according to the fourth universal definition of myocardial infarction (2018). RESULTS: The overall incidence of percutaneous coronary intervention-related periprocedural myocardial infarction was 21.1%. The ticagrelor group showed a significantly lower incidence of periprocedural myocardial infarction (12.3% vs 29.8%, p = 0.022) and numerically lower bleeding events (3.5% vs 8.8%, p = 0.242) as compared with clopidogrel group. No patient had major adverse cardiovascular events during the 1-month follow-up. The levels of high-sensitivity C-reactive protein did not differ significantly between the two groups (p > 0.05), indicating that the benefits of ticagrelor were not from its anti-inflammatory effects. Multivariable analysis showed that the use of ticagrelor (odds ratio: 0.50; 95% confidence interval: 0.29-0.87; p = 0.014) and number of stents (odds ratio: 2.75; 95% confidence interval: 1.25-6.06; p = 0.012) were independent predictors of periprocedural myocardial infarction. CONCLUSION: Pretreatment with a loading dose of ticagrelor seems to be superior in reducing the incidence of percutaneous coronary intervention-related periprocedural myocardial infarction in Asian patients with acute coronary syndrome as compared with clopidogrel.

The Potential Effects of Aliskiren on Atrial Remodeling Induced by Chronic Intermittent Hypoxia in Rats.

PURPOSE: Atrial remodeling takes part in the pathogenesis of atrial fibrillation (AF). Aliskiren, as a direct renin inhibitor, has been shown to exert protective effects against arrhythmia. The aim of this study was to investigate the potential role of aliskiren in atrial remodeling in a chronic intermittent hypoxia (CIH) rat model. METHODS: A total of 45 Sprague-Dawley rats were randomly assigned into three groups (n=15 per group): control group; CIH group; and CIH with aliskiren (CIH-A) group. CIH and CIH-A rats were subjected to CIH for 6 h per day for 4 weeks. Atrial fibrosis was evaluated using Masson's trichrome staining. Electrophysiological tests were conducted in the isolated perfused hearts to assess the atrial effective refractory period and inducibility of AF. Atrial ionic remodeling was measured using the whole-cell patch-clamp technique, and Western blotting and real-time quantitative polymerase chain reactionwere performed to evaluate changes in ion channels. RESULTS: CIH induced obvious collagen deposition, and the abnormal fibrosis was significantly attenuated by aliskiren. The inducibility of AF was increased significantly in the CIH group compared with the control and CIH-A groups (23±24.5% vs 2.0±4.2% vs 5.0±7.0%, respectively; P<0.05). Compared with the control group, the densites of the calcium current (I CaL) and sodium current (I Na) were reduced significantly in the CIH group (I CaL: -3.16±0.61 pA/pF vs -7.13±1.98 pA/pF; I Na: -50.97±8.71 pA/pF vs -132.58±25.34 pA/pF, respectively; all P<0.05). Following intervention with aliskiren, the reductions in I CaL and I Na were significantly improved, and the ionic modeling changes assessed at the mRNA and protein levels were also significantly improved. CONCLUSION: CIH could alter atrial modeling and subsequently promote the occurrence and development of AF, which could be attenuated by treatment with aliskiren.

Doxycycline Improves Fibrosis-Induced Abnormalities in Atrial Conduction and Vulnerability to Atrial Fibrillation in Chronic Intermittent Hypoxia Rats.

BACKGROUND The structural remodeling of atrial architecture, especially increased amounts of fibrosis, is a critical substrate to atrial fibrillation (AF). Doxycycline (Doxy) has recently been shown to exert protective effects against fibrogenic response. This study investigated whether doxycycline (Doxy) can sufficiently ameliorate the fibrosis-induced changes of atrial conduction and AF vulnerability in a chronic intermittent hypoxia (CIH) rat model. MATERIAL AND METHODS Sixty rats were randomized into 3 groups: Control, CIH, and CIH with Doxy treatment (DOXY) group. CIH rats were exposed to CIH (6 h/d) and Doxy-treated rats were treated with Doxy during processing CIH. After 6 weeks, echocardiographic and hemodynamic parameters were measured. Isolated atrial epicardial activation mapping and heart electrophysiology were performed. The extent of atrial interstitial fibrosis were estimated by Masson's trichrome staining. The expression levels of TGF-ß1 and downstream factors were determined by real-Time PCR, immunohistochemistry, and Western blot analysis. RESULTS Compared to Control rats, the CIH rats showed significant atrial interstitial fibrosis, longer inter-atrial conduction time, and elevated conduction inhomogeneity and AF inducibility, and the expression of TGF-ß1, TGF-ßRI, TGF-ßRII, P-Smad2/3, alpha-SMA, CTGF, and Collagen I were significantly increased, whereas the velocity of atrial conduction and the expression of miR-30c were dramatically decreased. All of these changes were significantly improved by Doxy treatment. CONCLUSIONS The findings suggested that Doxy can profoundly mitigate atrial fibrosis, conduction inhomogeneity as well as high AF inducibility secondary to fibrosis in a CIH rat model through suppressing the TGF-ß1 signaling pathway.

Effects of nicorandil infusion on ECG parameters in patients with unstable angina pectoris and percutaneous coronary intervention.

BACKGROUND: Percutaneous coronary intervention (PCI) is effective in treating patients with acute coronary syndrome (ACS) but is associated with some serious complications. Nicorandil is an anti-anginal agent acting to improve microvascular circulation and to increase coronary blood flow. The objective of this article is to evaluate the effects of intracoronary injection followed with continuous intravenous injection of nicorandil on ECG parameters in patients with unstable angina pectoris (UA) undergoing PCI. METHODS: A single-center, self-controlled clinical trial was conducted at the Second Hospital of Tianjin Medical University between January 2019 and April 2019. Sixty-three consecutive patients with UA who received coronary angiography and selective PCI were enrolled. ECG was recorded and analyzed before and 24 hr after nicorandil infusion. RESULTS: Patients were divided into three groups: control group (n = 23, aged 63.43 ± 12.55 years), short-term, and prolonged use with nicorandil group (n = 20 and 20, aged 66.45 ± 8.06 years and 65.80 ± 9.49 years, respectively). Clinical characteristics and ECG parameters were similar before PCI among three groups (p > .05). In nicorandil treatment groups, intervals of QTd and Tp-e in patients post-PCI were significantly shorter than that in control and pre-PCI (p < .05). CONCLUSIONS: Nicorandil infusion reduces QTd and Tp-e interval in patients with UA. Further studies will be needed to determine whether these electrophysiological changes are associated with a reduction of ventricular arrhythmias and improved outcomes.

Beneficial effects of tolvaptan on atrial remodeling induced by chronic intermittent hypoxia in rats.

INTRODUCTION: Atrial remodeling in the form of fibrosis is considered as the substrate for the development of atrial fibrillation (AF). The aim of this study was to investigate the effects of tolvaptan on chronic intermittent hypoxia (CIH) induced atrial remodeling and the mechanisms underlying such changes. METHODS: A total of 45 Sprague-Dawley rats were randomized into three groups: Control group, CIH group, CIH with tolvaptan treatment (CIH-T) group (n = 15). CIH rats were subjected to CIH 6 hour/d for 30 days, and CIH-T rats were administrated tolvaptan while they received CIH. After the echocardiography examination, rats were sacrificed in the 31 days. In each group, 5 rats were randomly selected for isolated heart electrophysiology testing, for other 10 rats, the tissues of atria were sampled for histological and molecular biological experiments, Masson's trichrome staining was used to evaluate the extent of atrial fibrosis, expression levels of microRNA-21 (miR-21), Sprouty-1 (Spry1), phosphatase, and tensin homolog (PTEN), extracellular regulated protein kinase (ERK), phospho-extracellular regulated protein kinase (p-ERK), matrix metalloprotein 9 (MMP-9), phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), phospho-protein kinase B (p-AKT), nuclear factor-k-gene binding (NF-κB), phosphor-nuclear factor-k-gene binding (p-NF-κB) were measured. RESULTS: Compared to the Control rats, CIH rats showed higher atrial interstitial collagen deposition and AF inducibility, mRNA levels of miR-21, MMP-9, PI3K, AKT, and protein levels of ERK, p-ERK, MMP-9, NF-κB, p-NF-κB were significantly increased, whereas mRNA levels of Spry1, ERK, and protein levels of Spry1, PTEN, PI3K, AKT, p-AKT were significantly decreased. Treatment with tolvaptan attenuated CIH-induced atrial fibrosis, reduced AF inducibility, expression levels of miR-21 and its downstream factors were also improved. CONCLUSIONS: CIH-induced significant atrial remodeling in our rat model, which was attenuated by tolvaptan. These changes may be explained due to alterations in miR-21/Spry1/ERK/MMP-9, miR-21/PTEN/PI3K/AKT, and NF-κB pathways by tolvaptan.