Exploring new frontiers: a rare case of catheter ablation for persistent atrial fibrillation in a patient with cor triatriatum sinister guided by intracardiac echocardiography.

BACKGROUND: Cor triatriatum sinister (CTS) is an uncommon congenital cardiac anomaly. Atrial fibrillation (AF) is commonly the initial symptom in patients with CTS, occurring in approximately 32% of the cases. The complexity of performing AF catheter ablation, particularly in cases with persistent AF, increases in patients with CTS due to its unique structural challenges. CASE PRESENTATION: We report the treatment course of a 60-year-old male patient diagnosed with CTS, who underwent catheter ablation of drug-refractory, persistent AF. The complex anatomical structure of the condition made catheter ablation of AF challenging. To navigate these challenges, we performed comprehensive assessments using transthoracic echocardiography and transesophageal echocardiography, along with cardiac computed tomography angiography, prior to treatment initiation. The intricate anatomy of CTS was further clarified during the procedure via intracardiac echocardiography (ICE). Additionally, the complexity of catheter manipulation was further reduced with the aid of the VIZIGO sheath and the vein of Marshall ethanol infusion to achieve effective mitral isthmus blockage, thereby circumventing the impact of the CTS membrane. CONCLUSIONS: This case underscores the complexity and potential of advanced ablation techniques in managing cardiac arrhythmias associated with unusual cardiac anatomies. During the procedure, ICE facilitated detailed modeling of the left atrium, including the membranous structure and its openings, thus providing a clearer understanding of CTS. It is noteworthy that the membrane within the CTS may serve as a potential substrate for arrhythmias, which warrants further validation through larger sample studies.

Teneligliptin mitigates diabetic cardiomyopathy by inhibiting activation of the NLRP3 inflammasome.

BACKGROUND: Diabetic cardiomyopathy (DCM), which is a complication of diabetes, poses a great threat to public health. Recent studies have confirmed the role of NLRP3 (NOD-like receptor protein 3) activation in DCM development through the inflammatory response. Teneligliptin is an oral hypoglycemic dipeptidyl peptidase-IV inhibitor used to treat diabetes. Teneligliptin has recently been reported to have anti-inflammatory and protective effects on myocardial cells. AIM: To examine the therapeutic effects of teneligliptin on DCM in diabetic mice. METHODS: Streptozotocin was administered to induce diabetes in mice, followed by treatment with 30 mg/kg teneligliptin. RESULTS: Marked increases in cardiomyocyte area and cardiac hypertrophy indicator heart weight/tibia length reductions in fractional shortening, ejection fraction, and heart rate; increases in creatine kinase-MB (CK-MB), aspartate transaminase (AST), and lactate dehydrogenase (LDH) levels; and upregulated NADPH oxidase 4 were observed in diabetic mice, all of which were significantly reversed by teneligliptin. Moreover, NLRP3 inflammasome activation and increased release of interleukin-1ß in diabetic mice were inhibited by teneligliptin. Primary mouse cardiomyocytes were treated with high glucose (30 mmol/L) with or without teneligliptin (2.5 or 5 µM) for 24 h. NLRP3 inflammasome activation. Increases in CK-MB, AST, and LDH levels in glucose-stimulated cardiomyocytes were markedly inhibited by teneligliptin, and AMP (p-adenosine 5'-monophosphate)-p-AMPK (activated protein kinase) levels were increased. Furthermore, the beneficial effects of teneligliptin on hyperglycaemia-induced cardiomyocytes were abolished by the AMPK signaling inhibitor compound C. CONCLUSION: Overall, teneligliptin mitigated DCM by mitigating activation of the NLRP3 inflammasome.

JinJiang ablation catheter is no inferior than Johnson ablation catheter in radiofrequency ablation of paroxysmal supraventricular tachycardia.

BACKGROUND: Paroxysmal supraventricular tachycardia (PSVT) is characterized by episodes of rapid tachycardia with sudden onset and sudden termination. PSVT treatment has evolved considerably over the past 30 years. Currently, radiofrequency catheter ablation is the first-line treatment. HYPOTHESIS: We conducted a randomized controlled trial to compare safety and effectiveness of PSVT ablation between the Jinjiang and Johnson (J&J) catheters in 57 patients in our hospital. METHODS AND RESULTS: Patients were randomly assigned to ablation procedures using either the Jinjiang system or the J&J Carto system. Follow-up was performed 3 days, 1, and 6 months after the procedure. Success rate, ablation time, frequency of ablation, and rates of complications and recurrence did not significantly differ between the groups. One Jinjiang group patient (3.6%) experienced arrhythmia recurrence during the 6-month follow-up. CONCLUSIONS: The Jinjiang catheter for radiofrequency ablation of PSVT is as safe and effective as the J&J catheter.

Downregulation of MicroRNA-29-3p Following Percutaneous Coronary Intervention: An Implication of YY1/IRAK1 Pathway in the Post-Vascular Injury Inflammation.

This study explored the expression of microRNA (miR)-29b-3p following percutaneous coronary intervention (PCI) and the implication of its downstream Yin Yang 1 (YY1)/interleukin (IL)-1 receptor-associated kinase 1 (IRAK1) pathway in post-vascular injury inflammation. Blood samples were collected for analysis of plasma miR-29b-3p from patients with acute coronary syndrome before surgery, 1 day after PCI, and 30 days after PCI. Lipopolysaccharide (LPS)-treated human coronary artery endothelial cells (HCAECs) were transfected with miR-29b-3p mimic/inhibitor or YY1 shRNA and underwent viability tests. Enzyme-linked immunosorbent assay was performed to detect the levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), IL-1ß, IL-6, and tumor necrosis factor (TNF)-α in serum and cell culture supernatant. Dual-luciferase reporter and RNA/chromatin immunoprecipitation were used to confirm the targeting relationships among miR-29b-3p, YY1, and IRAK1. A rat model of intraluminal injury of the common femoral artery was established to address the role of miR-29b-3p and relevant mechanisms. miR-29b-3p was lowly expressed, and sVCAM-1, IL-1ß, IL-6, and TNF-α were upregulated 1 day after PCI and 24 h after LPS treatment. miR-29b-3p overexpression or YY1 knockdown alleviated LPS-induced inflammatory responses and improved the viability of HCAECs. miR-29b-3p inhibition aggravated LPS-induced inflammatory injury in HCAECs. miR-29b-3p bound to YY1 mRNA and inhibited the expression of YY1 protein. YY1 bound to the IRAK1 promoter and activated the transcription of IRAK1. Upregulation of miR-29b-3p suppressed the inflammatory response after intraluminal injury of the common femoral artery in rats. In conclusion, dysregulation of the YY1/IRAK1 pathway via miR-29b-3p downregulation may be implicated in post-vascular injury inflammation.

Thioredoxin Reductase 2 Synergizes with Cytochrome c, Somatic to Alleviate Doxorubicin-Induced Oxidative Stress in Cardiomyocytes and Mouse Myocardium.

Doxorubicin (DOX) may cause multiple side effects, which include cardiotoxicity. Hence, to ascertain the impact of thioredoxin reductase 2 (TXNRD2) and cytochrome c, somatic (CYCS) on DOX-induced oxidative stress (OS) in cardiomyocytes and mouse myocardium, this study was implemented. DOX was utilized to treat cardiomyocytes and mice, and TXNRD2 and CYCS expression in cell supernatant and mouse myocardial tissues was detected. TXNRD2 and/or CYCS were overexpressed in DOX-induced cardiomyocytes and mice. In cardiomyocytes, cell viability and the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and glutathione (GSH) were measured. In mice, pathologic changes of the heart, ejection fraction (EF), fractional shortening (FS), and heart weight (HW) /tibial length (TL) ratio, and the contents of lactic dehydrogenase (LDH), creatine kinase-MB (CK-MB), and cardiac troponin I (cTnI) were analyzed. To assess the binding between TXNRD2 and CYCS, coimmunoprecipitation and glutathione S-transferase pull-down assays were performed. TXNRD2 and CYCS were downregulated in DOX-treated cardiomyocytes and mice. Mechanistically, TXNRD2 interacted with CYCS. Overexpression of TXNRD2 or CYCS augmented viability and SOD, CAT, and GSH levels but reduced ROS and MDA contents in DOX-induced cardiomyocytes, which was further facilitated by simultaneous overexpression of TXNRD2 or CYCS. Moreover, TXNRD2 or CYCS upregulation improved the pathologic changes in myocardial tissues, along with increases in EF, FS, and HW/TL ratio of the heart and SOD, CAT, and GSH levels and decreases in LDH, CK-MB, cTnI, ROS, and MDA levels. TXNRD2 coordinated with CYCS to alleviate DOX-induced OS in cardiomyocytes and mouse myocardium.

Salmonella pathogenicity island 1 knockdown confers protection against myocardial fibrosis and inflammation in uremic cardiomyopathy via down-regulation of S100 Calcium Binding Protein A8/A9 transcription.

BACKGROUND/AIM: Uremic cardiomyopathy (UCM) is a characteristic cardiac pathology that is commonly found in patients with chronic kidney disease. This study dissected the mechanism of SPI1 in myocardial fibrosis and inflammation induced by UCM through S100A8/A9. METHODS: An UCM rat model was established, followed by qRT-PCR and western blot analyses of SPI1 and S100A8/A9 expression in myocardial tissues. After alterations of SPI1 and S100A8/A9 expression in UCM rats, the blood specimens were harvested from the cardiac apex of rats. The levels of creatine phosphokinase-MB (CK-MB), blood creatinine, blood urea nitrogen (BUN), and inflammatory cytokines (interleukin [IL]-6, IL-1ß, and tumor necrosis factor-α [TNF-α]) were examined in the collected blood. Collagen fibrosis was assessed by Masson staining. The expression of fibrosis markers [transforming growth factor (TGF)-ß1, α-smooth muscle actin (SMA), Collagen 4a1, and Fibronectin], IL-6, IL-1ß, and TNF-α was measured in myocardial tissues. Chromatin immunoprecipitation and dual-luciferase reporter gene assays were conducted to test the binding relationship between SPI1 and S100A8/A9. RESULTS: S100A8/A9 and SPI1 were highly expressed in the myocardial tissues of UCM rats. Mechanistically, SPI1 bound to the promoter of S100A8/A9 to facilitate S100A8/A9 transcription. S100A8/A9 or SPI1 knockdown reduced myocardial fibrosis and inflammation and the levels of CK-MB, blood creatinine, and BUN, as well as the expression of TGF-ß1, α-SMA, Collagen 4a1, Fibronectin, IL-6, TNF-α, and IL-1ß in UCM rats. CONCLUSION: SPI1 knockdown diminished S100A8/A9 transcription, thus suppressing myocardial fibrosis and inflammation caused by UCM.

Relationship between Serum miR-106 and MYL4 Levels and the Prevalence, Risk Stratification, and Prognosis of Atrial Fibrillation.

Objective: To analyze the predictive value of serum microRNA-106 (miRNA-106), miR-106, and myosin light chain 4 (MYL4) levels on the prevalence of atrial fibrillation and to explore the relationship between serum miR-106 and MYL4 and the risk stratification and prognosis of atrial fibrillation, thereby providing basis for them to become clinical targets for the treatment of atrial fibrillation in the future. Methods: 300 patients with atrial fibrillation treated in our hospital from May 2017 to March 2019 were selected as the atrial fibrillation group, and 300 healthy people who came to our hospital for physical examination in the same period were selected as the control group. The general data of the subjects in the two groups were collected. The serum miR-106 level of the subjects in the two groups was detected by fluorescence quantitative polymerase chain reaction (PCR), and the level of MYL4 was detected by enzyme-linked immunosorbent assay (ELISA). The expression of miR-106 and MYL4 in the myocardium was observed by immunohistochemistry. The relationship between the levels of serum miR-106 and MYL4 and the prevalence of atrial fibrillation and the score of atrial fibrillation thromboembolism risk stratification scoring system (cha2ds2) was compared between the two groups. The relationship between serum level of miR-106 and prognosis of patients with atrial fibrillation was analyzed. Results: The systolic blood pressure, diastolic blood pressure, total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and left anterior descending artery (LAD) in the atrial fibrillation group were significantly higher than those in the control group, while HDL-C and left ventricular ejection fraction (LVEF) were significantly lower than those in the control group (P < 0.01). The level of serum miR-106 in patients with atrial fibrillation was significantly higher than that in the control group, whereas the level of MYL4 was significantly lower than that in the control group (P < 0.01). miR-106 was mainly localized in the cytoplasm, and the positive expression rate of miR-106 was 71.43% (81/115) in patients with atrial fibrillation and 21.74% (25/115) in patients with sinus rhythm. MYL4 was mainly located in the cell membrane and the positive expression rate of MYL4 was 24.35% (28/115) in patients with atrial fibrillation and 64.35% (74/115) in patients with sinus rhythm. With the increase of the severity of atrial fibrillation, the level of serum miR-106 gradually increased and the level of MYL4 gradually decreased, which were statistically significant compared with the control group (P < 0.05). With the increase of miR-106 level and the decrease of MYL4 level, the prevalence of atrial fibrillation gradually increased. With the increase of cha2ds2 score, the level of serum miR-106 increased and the level of MYL4 decreased. The survival rate of patients with miR - 106 ≤ 1.96 was significantly higher than that of patients with miR - 106 > 1.96. The survival rate of patients with MYL4 ≥ 0.24 was significantly higher than that of patients with MYL4 < 0.24. At the same time, TC and LDL-C were included in the analysis. The results showed that the survival rate of patients with TC ≤ 4.5 mmol/L was significantly higher than that of patients with TC > 4.5 mmol/L, and that of patients with LDL-C ≤ 2.6 mmol/L was significantly higher than that of patients with LDL-C > 2.6 mmol/L. Conclusion: Serum miR-106 and MYL4 levels are closely related to the prevalence of atrial fibrillation, which can reflect the risk of thromboembolism in patients with atrial fibrillation and can be used as a biological indicator to predict the prognosis of patients with atrial fibrillation.

Pirfenidone attenuates cardiac hypertrophy against isoproterenol by inhibiting activation of the janus tyrosine kinase-2/signal transducer and activator of transcription 3 (JAK-2/STAT3) signaling pathway.

Cardiovascular risk factors have attracted increasing attention in recent years with the acceleration of population aging, amongst which cardiac hypertrophy is the initiating link to heart failure. Pirfenidone is a promising agent for the treatment of idiopathic pulmonary fibrosis and has recently proven to exert inhibitory effects on the inflammatory response. This study proposes to explore the potential pharmacological action of Pirfenidone in treating cardiac hypertrophy in a rodent model. Four groups of mice were used in the present study: the control, ISO (5 mg/kg/day) for 7 days, Pirfenidone (200 mg/kg/day) for 14 days, and Spironolactone (SPI) (200 mg/kg/day) for 14 days groups. Increased heart weight index, left ventricle (LV) weight index, LV wall thickness, declined LV volume, and elevated serum levels of CK-MB, AST, and LDH were observed in ISO-challenged mice, all of which were dramatically reversed by the administration of Pirfenidone or SPI. Furthermore, an elevated cross-sectional area of cardiomyocytes in the wheat germ agglutinin (WGA) staining of heart cross-sections, upregulated atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), ß Myosin Heavy Chain (ß-MHC), and excessively released tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) in cardiac tissues were observed in the ISO group but greatly alleviated by Pirfenidone or SPI. Lastly, the promoted expression levels of p-JAK-2/JAK-2 and p-STAT3/STAT-3 in the cardiac tissues of ISO-challenged mice were significantly repressed by Pirfenidone or SPI. Collectively, our data reveals a therapeutic property of Pirfenidone on ISO-induced cardiac hypertrophy in mice.

Promoting role of circ-Jarid2/miR-129-5p/Celf1 axis in cardiac hypertrophy.

Cardiac hypertrophy is imposed much pressure on heart and threatening our live. Previous study suggested that dysregulation of Celf1 is largely connecting to neonatal cardiac dysfunction. Hence, we aimed to explore the precise function and probable regulatory mechanism upstream of Celf1in cardiac hypertrophy. Here, Ang-II treatment was implemented to stimulate hypertrophic phenotypes inH9C2 and MCM cells. Immunofluorescence assay was conducted to measure the surface area of cardiomyocytes. And qRT-PCR assay was conducted to investigate gene expression. Moreover, western blot assay was conducted to probe the protein levels. Results uncovered that Celf1 expression was increased dependent on elevated Ang-II concentration, and that inhibited Celf1 could relieve the Ang-II-caused cardiac hypertrophy. Significantly, Celf1was found to be targeted by miR-129-5p but then released via the sponging role of circ-Jarid2. Furthermore, circ-Jarid2 was found to promote cardiac hypertrophy, whereas miR-129-5p played suppressing parts in hypertrophic cardiomyocytes. Moreover, we verified circ-Jarid2 contributed to cardiac hypertrophy via miR-129-5p/Celf1 axis both in vitro and in vivo. In conclusion, circ-Jarid2/miR-129-5p/Celf1 axis aggravates cardiac hypertrophy, which provides new ideas for developing treatment strategies for patients with cardiac hypertrophy.

SIRT4 suppresses the PI3K/Akt/NF­κB signaling pathway and attenuates HUVEC injury induced by oxLDL.

Atherosclerosis is a chronic and progressive disease. Its morbidity and mortality rates have demonstrated an increase in recent years. The present study aimed to explore the role of sirtuin (SIRT) 4 in the development of atherosclerosis. Alterations in SIRT4 expression in response to oxidized low density lipoprotein (oxLDL) were quantified in human umbilical vein endothelial cells (HUVECs) using western blotting. Cell counting kit­8 and flow cytometry assays were used in order to explore the effects of SIRT4 on HUVEC proliferation and apoptosis. The effect of SIRT4 on the expression of inflammatory factors in HUVECs was analyzed using ELISA. The expression and phosphorylation of proteins in the phosphoinositide 3­kinase (PI3K)/protein kinase B (Akt)/nuclear factor (NF)­κB pathway were comparatively analyzed using western blotting. Nuclear translocation of p65 NF­κB was examined using immunofluorescence. The present study indicated that oxLDL treatment decreased the expression of SIRT4 in HUVECs in a dose­ and time­dependent manner. SIRT4 overexpression promoted oxLDL­induced HUVEC proliferation and inhibited cell apoptosis. Furthermore, SIRT4 overexpression suppressed the PI3K/Akt/NF­κB pathway by inhibiting PI3K phosphorylation and phosphorylated (p)­Akt, p­nuclear factor of kappa light polypeptide gene enhancer in B­cells inhibitor α and p­p65 NF­κB expression; blocking p65 NF­κB nuclear translocation and decreasing interleukin (IL)­1ß, IL­6, and tumor necrosis factor α expression in oxLDL­induced HUVECs. In conclusion, SIRT4 overexpression enhanced HUVEC survival, suppressed the PI3K/Akt/NF­κB signaling pathway and inhibited the expression of inflammatory cytokines in oxLDL­induced HUVECs.

Silencing CTGF/CCN2 inactivates the MAPK signaling pathway to alleviate myocardial fibrosis and left ventricular hypertrophy in rats with dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is characterized by left ventricular dilation associated with systolic dysfunction. The purpose of the current study is to clarify the effect of connective tissue growth factor (CTGF/CCN2) on myocardial fibrosis and left ventricular hypertrophy (LVH) of rats with DCM through the mitogen-activated protein kinase (MAPK) signaling pathway. First, DCM rat models were established and sh-CTGF/CCN2 lentiviral expression vectors were constructed. Then, by observing the pathological changes and myocardial ultrastructure as well as detecting cardiac functions, myocardial fibrosis, and LVH of rats, the effect of CTGF/CCN2 gene silencing on rats with DCM was investigated. To further explore how CTGF/CCN2 gene silencing affects rats with DCM, the expression of CTGF/CCN2 and the related genes of the MAPK signaling pathway was detected. Sh-CTGF/CCN2-2 and sh-CTGF/CCN2-3 with lower CTGF/CCN2 expression were selected for further experimentation. CTGF/CCN2 gene silencing improved cardiac function and alleviated myocardial fibrosis and LVH of rats with DCM. It was also verified that CTGF/CCN2 gene silencing could relieve the pathology of rats with DCM by inactivation of the MAPK signaling pathway. We conclude that CTGF/CCN2 gene silencing inhibits the activation of the MAPK signaling pathway, thus decreases myocardial fibrosis and LVH, and then improves the pathological symptoms of DCM in rats.

Application of percutaneous balloon mitral valvuloplasty in patients of rheumatic heart disease mitral stenosis combined with tricuspid regurgitation.

BACKGROUND: Tricuspid regurgitation (TR) is frequently associated with severe mitral stenosis (MS), the importance of significant TR was often neglected. However, TR influences the outcome of patients. The aim of this study was to investigate the efficacy and safety of percutaneous balloon mitral valvuloplasty (PBMV) procedure in rheumatic heart disease patients with mitral valve (MV) stenosis and tricuspid valve regurgitation. METHODS: Two hundred and twenty patients were enrolled in this study due to rheumatic heart disease with MS combined with TR. Mitral balloon catheter made in China was used to expand MV. The following parameters were measured before and after PBMV: MV area (MVA), TR area (TRA), atrial pressure and diameter, and pulmonary artery pressure (PAP). The patients were followed for 6 months to 9 years. RESULTS: After PBMV, the MVAs increased significantly (1.7 ± 0.3 cm 2 vs. 0.9 ± 0.3 cm 2 , P < 0.01); TRA significantly decreased (6.3 ± 1.7 cm 2 vs. 14.2 ± 6.5 cm 2 , P < 0.01), right atrial area (RAA) decreased significantly (21.5 ± 4.5 cm 2 vs. 25.4 ± 4.3 cm 2 , P < 0.05), TRA/RAA (%) decreased significantly (29.3 ± 3.2% vs. 44.2 ± 3.6%, P < 0.01). TR velocity (TRV) and TR continue time (TRT) as well as TRV × TRT decreased significantly (183.4 ± 9.4 cm/s vs. 254.5 ± 10.7 cm/s, P < 0.01; 185.7 ± 13.6 ms vs. 238.6 ± 11.3 ms, P < 0.01; 34.2 ± 5.6 cm vs. 60.7 ± 8.5 cm, P < 0.01, respectively). The postoperative left atrial diameter (LAD) significantly reduced (41.3 ± 6.2 mm vs. 49.8 ± 6.8 mm, P < 0.01) and the postoperative right atrial diameter (RAD) significantly reduced (28.7 ± 5.6 mm vs. 46.5 ± 6.3 mm, P < 0.01); the postoperative left atrium pressure significantly reduced (15.6 ± 6.1 mmHg vs. 26.5 ± 6.6 mmHg, P < 0.01), the postoperative right atrial pressure decreased significantly (13.2 ± 2.4 mmHg vs. 18.5 ± 4.3 mmHg, P < 0.01). The pulmonary arterial pressure decreased significantly after PBMV (48.2 ± 10.3 mmHg vs. 60.6 ± 15.5 mmHg, P < 0.01). The symptom of chest tightness and short of breath obviously alleviated. All cases followed-up for 6 months to 9 years (average 75 ± 32 months), 2 patients with severe regurgitation died (1 case of massive cerebral infarction, and 1 case of heart failure after 6 years and 8 years, respectively), 2 cases lost access. At the end of follow-up, MVA has been reduced compared with the postoperative (1.4 ± 0.4 cm 2 vs. 1.7 ± 0.3 cm 2 , P < 0.05); LAD slightly increased compared with the postoperative (45.2 ± 5.7 mm vs. 41.4 ± 6.3 mm, P < 0.05), RAD slightly also increased compared with the postoperative (36.1 ± 6.3 mm vs. 28.6 ± 5.5 mm, P < 0.05), but did not recover to the preoperative level. TRA slightly increased compared with the postoperative, but the difference was not statistically significant (P > 0.05). The PAP and left ventricular ejection fraction appeared no statistical difference compared with the postoperative (P > 0.05), the remaining patients without serious complications. CONCLUSIONS: PBMV is a safe and effective procedure for MS combined with TR in patients of rheumatic heart disease. It can alleviate the symptoms and reduce the size of TR. It can also improve the quality-of-life and prognosis. Its recent and mid-term efficacy is certain. While its long-term efficacy remains to be observed.

Application of peripheral-blood-derived endothelial progenitor cell for treating ischemia-reperfusion injury and infarction: a preclinical study in rat models.

BACKGROUND: Our aim was to explore the therapeutic effects of peripheral blood-derived endothelial progenitor cells (PB-EPC) in cardiac ischemia-reperfusion infarction models in rats and in in vitro culture systems. METHODS: Rat models of ischemia reperfusion and myocardial infarction were developed using male, Sprague-Dawley rats. Cardiomyocyte and endothelial cell cultures were also established. Therapeutic effects of PB-EPCs were examined in vivo and in vitro in both models. Rats underwent either cardiac ischemia-reperfusion (n = 40) or infarction (n = 56) surgeries and were transplanted with genetically modified EPCs. Treatment efficacy in the ischemia-reperfusion group was measured by infarct size, myocardial contraction velocity, and myeloperoxidase activity after transplantation. Cardiomyocyte survival and endothelial cell apoptosis were investigated in vitro. Vascular growth-associated protein expression and cardiac function were evaluated in the myocardial infarction group by western blot and echocardiography, respectively. RESULTS: Infarct size and myeloperoxidase activity were significantly decreased in the ischemia-reperfusion group, whereas myocardial contractility was significantly increased in the EPC and Tß4 groups compared with that in the control group. In contrast, no differences were found between EPC + shRNA Tß4 and control groups. Rates of cardiomyocyte survival and endothelial cell apoptosis were significantly higher and lower, respectively, in the EPC and Tß4 groups than in the control group, whereas no differences were found between the EPC + shRNA Tß4 and control group. Four weeks after myocardial infarction, cardiac function was significantly better in the EPC group than in the control group. Expressions of PDGF, VEGF, and Flk-1 were significantly higher in EPC group than in control group. CONCLUSIONS: Study findings suggest that PB-EPCs are able to protect cardiomyocytes from ischemia-reperfusion or infarction-induced damage via a Tß4-mediated mechanism. EPCs may also provide protection through increased expression of proteins involved in mediating vascular growth. Autologous peripheral-blood-derived EPCs are readily available for efficient therapeutic use without the concerns of graft rejection.

[Radiofrequency catheter ablation for ventricular premature beats of left coronary cusp under the guidance of 3-dimensional mapping system].

OBJECTIVE: To explore the efficacy and safety of radiofrequency catheter ablation (RCA) for ventricular premature beats originating from left coronary sinus under the guidance of 3-dimensional mapping system (CARTO). METHODS: A total of 15 patients with premature ventricular contractions (PVCs) originating from left coronary sinus underwent CARTO-guided RCA. Anatomical structures were constructed and three-dimension (3D) electrical activation sequence was plotted for left ventricle and aortic sinus. The distance of earliest activation point of PVCs and origin of left coronary artery were surveyed after left coronary arteriography. RESULTS: The electrocardiogram (ECG) results showed that R-wave was upward in leads II, III and avF, QRS waves in lead I was mainly of rS, rs and rsr types, QS type in lead avL, RS, Rs and rS type in lead V(1), RS type in lead V(3) and absence of S wave in lead V(5)/V(6). Intraoperative mapping detected the earliest activation point on the posterior-inferior origin of left coronary artery (LMCA) ostium (n = 7), on the anterio-inferior of LMCA ostium (n = 3) and on the inferior of LMCA ostium (n = 5). The earliest activation point (local activation time) was shorter 86 - 120 ms than surface electrocardiogram QRS wave, discharge melting on the earliest activation point and nearby succeeded. PVCs disappeared, PVCs failed to be induced under similar preoperative conditions (aleudrin intravenous) and no complication occurred intraoperatively and postoperatively. CONCLUSION: The CARTO-guided RCA is a safe and effective in the treatment of PVCs originating from left coronary sinus.

[Comparative study of interventricular electrical and mechanical synchrony at different cardiac pacing sites].

OBJECTIVE: To compare the different impacts of right ventricular apex, right ventricular outflow tract septum and left ventricular outflow tract septum region on interventricular electro-mechanical synchronization and assess the ideal pacing sites for maintaining the interventricular electro-mechanical synchronization. METHODS: A total of 30 patients without organic heart disease were operated with radiofrequency ablation at our hospital. The mapping electrodes were implanted post-operatively on the left ventricular posterior wall (LVPLW) and right ventricular anterior lateral wall (RVALW) respectively. And the ablation electrodes were placed subsequently in right ventricular apex, right ventricular outflow tract septum region and left ventricular outflow tract septum. The difference values were measured between transmission time from pacemaker to LVPLW, from pacemaker to RVALW and between aortic pre-ejection interval (APEI) and pulmonary artery pre-ejection interval (PPEI). Then their correlations were compared. RESULTS: When pacing at right ventricular apex, the difference value between transmission time from pacemaker to LVPLW and from pacemaker to RVALW was (34 ± 7) ms. And it was (18 ± 4) ms while pacing at right ventricular outflow tract septum region and (12 ± 4) ms at left ventricular outflow tract septum region. There was significant difference (P < 0.01). The absolute value of APEI-PPEI was (25 ± 5) ms at right ventricular apex, (13 ± 4) ms at right ventricular outflow tract septum region and (11 ± 3) ms at left ventricular outflow tract septum region. And there was significant difference (P < 0.01). The absolute value of APEI-PPEI was positively correlated with the change of LVPLW-RVALW (r = 0.993, P < 0.01). Left ventricular outflow tract septum pacing showed ABp and left ventricle end-systolic pressure significantly increased [(127 ± 23) mm Hg, (142 ± 22) mm Hg, P < 0.05], left ventricular end-diastolic pressure was significantly lower [(9 ± 3) mm Hg, P < 0.05]. CONCLUSION: Compared with right ventricular apical pacing and right ventricular outflow tract ventricular septal pacing, left ventricular outflow tract septum has a smaller impact on the electro-mechanical synchronization. It conforms more closely to the physiological pacing so that there is a higher synchronization of electrical and mechanical ventricular contractions.

[Percutaneous coronary intervention of patients with complex small coronary artery lesion unsuitable for coronary artery bypass graft].

OBJECTIVE: To investigate the safety and efficacy of percutaneous coronary intervention (PCI) in patients with low left ventricular ejection fraction (LVEF) and complex small coronary artery lesions. METHODS: Complete or partial post-PCI revascularization of coronary artery was employed in 16 patients with a low LVEF and complex small coronary artery lesions who were unsuitable for CABG (coronary artery bypass grafting). All cases were observed with regards to immediate success rate of operation, complication, hospitalization duration, improvement of cardiac function and LVEF and major adverse cardiac events (including cardiac death, myocardial infarction and target lesion revascularization) at 12 months post-operation. RESULTS: All cases were successfully treated without death and severe complications while the hospitalization duration was (11 +/- 5) days. The follow-up survey at 12 months post-operation showed that no major adverse cardiac event occurred, the post-operative improvement of cardiac function was from III - IV grade to I - II grade, the improvement of LVEF was from 25% - 45% [(29 +/- 8)%] to 32% - 48% [(37 +/- 7)%], left ventricular end diastolic diameter (LVDd) was shortened from 52 - 79 (66 +/- 11) mm to 49 - 68 (58 +/- 8) mm. The reexamination of 14 cases by coronary angiography at 12 months post-operation showed that there was no intra-stent thrombosis while 20% - 40% intra-stent restenosis occurred in 2 cases. CONCLUSION: For patients with a low LVEF and complex small coronary artery lesions, PCI is a safe and effective method to lower the mortality rate of CHD patients with heart failure and improve the long-term patient prognosis.