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Aim:Small GTPase Rac1 is a member of the Ras superfamily, which plays important roles in regulation of cytoskeleton reorganization, cell growth, proliferation, migration, etc. The aim of this study was to determine how a constitutively active Rac1b regulated cell proliferation and to investigate the effects of the Rac1b inhibitor sanguinarine.Methods:Three HEK293T cell lines stably overexpressing GFP, Rac1-GFP or Rac1b-GFP were constructed by lentiviral infection. The cells were treated with sanguinarine (1 μmol/L) or its analogue berberine (1 μmol/L) for 4 d. Cell proliferation was evaluated by counting cell numbers and with a BrdU incorporation assay. The levels of cleaved PARP-89 (an apoptosis marker) and cyclin-D1 (a proliferative index) were measured using Western blotting.Results:In 10% serum-containing media, overexpressing either Rac1 or Rac1b did not significantly change the cell proliferation. In the serum-starved media, however, the survival rate of Rac1b cells was significantly increased, whereas that of Rac1 cells was moderately increased. The level of cleaved PARP-89 was significantly increased in serum-starved Rac1 cells, but markedly reduced in serum-starved Rac1b cells. The level of cyclin-D1 was significantly increased in both serum-starved Rac1 and Rac1b cells. Treatment with sanguinarine, but not berberine, inhibited the proliferation of Rac1b cells, which was accompanied by significantly increased the level of PARP-89, and decreased both the level of cyclin-D1 and the percentage of BrdU positive cells.Conclusion:Rac1b enhances the cell proliferation under a growth-limiting condition via both anti-apoptotic and pro-proliferative mechanisms. Sanguinarine, as the specific inhibitor of Rac1b, is a potential therapeutic agent for malignant tumors with up-regulated Rac1b. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) is estimated to affect nearly 3 million people around the world. It is the most common arrhythmia and its incidence increases with age. Catheter ablation is an interventional procedure performed to reduce the patient's AF burden when pharmacotherapy did not succeed in relieving the patient's symptoms. The ablation is most effective in paroxysmal AF; however, many techniques are being developed to make this procedure more eligible for patients with persistent arrhythmia. The most common AF ablation technique involves separating electric activity of the pulmonary veins from the left atrium. Over recent years, many novel and promising techniques were developed (e.g., balloon cryoablation, circular catheter ablation, laser ablation, robotic navigation, etc.), which may further improve AF ablation efficacy. [ABSTRACT FROM AUTHOR]

Dysfunction of endothelial progenitor cells ( EPC) contribute to diabetic vascular disease. Micro RNAs (mi RNAs) are key regulators of diverse cellular processes, including angiogenesis. We recently reported that downregulated miR-130a in patients with Type 2 diabetes mellitus ( DM) results in EPC dysfunction, including increased apoptosis, likely via its target runt-related transcription factor 3 (Runx3). However, whether miR-130a affects the autophagy of EPC is unknown. The aim of the present study was to explore the effects of miR-130a on the autophagy and cell death of EPC, as well as their expression of Beclin 1 ( BECN1; an initiator of autophagosome formation) and the anti-apoptotic protein Bcl2 (which binds to and inactivates BECN1), and the role of Runx3 in mediating these effects. The EPC were cultured from peripheral blood mononuclear cells of diabetic patients and non-diabetic controls. Cells were transfected with an miR-130a inhibitor, or mimic- miR-130a or mimic- miR-130a plus lentiviral vector expressing Runx3 to manipulate miR-130a and/or Runx3 levels. The number of autophagosomes was counted under transmission electron microscopy and cell death was examined by flow cytometry. The mRNA expression of Beclin1 was measured by real-time polymerase chain reaction and the protein expression of Beclin1 and Bcl2 was determined by western blotting. Both the number of autophagosomes and Beclin1 expression were increased in EPC from patients with DM. Inhibition of miR-130a increased the number of autophagosomes and Beclin1 expression, but attenuated Bcl2 expression. Overexpression of miR-130a decreased the number of autophagosomes, cell death and Beclin1 expression, but promoted Bcl2 expression; these effects were mediated by Runx3. In conclusion, miR-130a is important for maintaining normal autophagy levels and promoting the survival of EPC via regulation of Bcl-2 and Beclin1 expression, via Runx3. MiR-130a may be a regulator linking apoptosis and the autophagy of EPC. [ABSTRACT FROM AUTHOR]

It has been shown that the elevated concentrations of oxidized low-density lipoprotein (Ox-LDL) or high-sensitivity C-reactive protein (hs-CRP) are predictive of future cardiovascular events for acute coronary syndrome (ACS) patients. But, the combined value of Ox-LDL and hs-CRP for predicting cardiovascular events is still unknown. Serum concentrations of Ox-LDL, hs-CRP, and cTnT were measured in a prospective cohort of 425 selective ACS patients followed 3-5 years for the occurrence of acute myocardial infarction (AMI) or death (AMI/death). Among 425 enrolled patients, 124 patients demonstrated AMI/death. Baseline levels of Ox-LDL, hs-CRP, and cTnT were significantly higher in AMI/death group than the event-free survival group. Kaplan-Meier survival analyses supported that elevations in Ox-LDL or hs-CRP predicted increased cardiovascular events risks. However, the strongest risk prediction was achieved by assessing Ox-LDL and hs-CRP together. Patients with high levels of Ox-LDL and hs-CRP were more likely to experience AMI or death than those with either Ox-LDL or hs-CRP elevated. Receiver-operating characteristic curves showed that Ox-LDL and hs-CRP have higher sensitivity and specificity than those of cTnT for predicting AMI or death. This was reflected by the AUC values for Ox-LDL, hs-CRP, and cTnT, which were 0.891, 0.834, and 0.626, respectively. The combined use of Ox-LDL and hs-CRP may improve prognosis after ACS with high-sensitivity and specificity. [ABSTRACT FROM AUTHOR]

Aim:To investigate whether resveratrol suppressed oxidative stress-induced arrhythmogenic activity and Ca2+ overload in ventricular myocytes and to explore the underlying mechanisms.Methods:Hydrogen peroxide (H2O2, 200 μmol/L)) was used to induce oxidative stress in rabbit ventricular myocytes. Cell shortening and calcium transients were simultaneously recorded to detect arrhythmogenic activity and to measure intracellular Ca2+ ([Ca2+]i). Ca2+/calmodulin-dependent protein kinases II (CaMKII) activity was measured using a CaMKII kit or Western blotting analysis. Voltage-activated Na+ and Ca2+ currents were examined using whole-cell recording in myocytes.Results:H2O2 markedly prolonged Ca2+ transient duration (CaTD), and induced early afterdepolarization (EAD)-like and delayed afterdepolarization (DAD)-like arrhythmogenic activity in myocytes paced at 0.16 Hz or 0.5 Hz. Application of resveratrol (30 or 50 μmol/L) dose-dependently suppressed H2O2-induced EAD-like arrhythmogenic activity and attenuated CaTD prolongation. Co-treatment with resveratrol (50 μmol/L) effectively prevented both EAD-like and DAD-like arrhythmogenic activity induced by H2O2. In addition, resveratrol markedly blunted H2O2-induced diastolic [Ca2+]i accumulation and prevented the myocytes from developing hypercontracture. In whole-cell recording studies, H2O2 significantly enhanced the late Na+ current (INa,L) and L-type Ca2+ current (ICa,L) in myocytes, which were dramatically suppressed or prevented by resveratrol. Furthermore, H2O2-induced ROS production and CaMKII activation were significantly prevented by resveratrol.Conclusion:Resveratrol protects ventricular myocytes against oxidative stress-induced arrhythmogenic activity and Ca2+ overload through inhibition of INa,L/ICa,L, reduction of ROS generation, and prevention of CaMKII activation. [ABSTRACT FROM AUTHOR]

The expression of the chemorepellent Sema3a is inversely related to sympathetic innervation. We investigated whether overexpression of Sema3a in the myocardial infarction ( MI) border zone could attenuate sympathetic hyper-innervation and decrease the vulnerability to malignant ventricular tachyarrhythmia ( VT) in rats. Survived MI rats were randomized to phosphate buffered saline ( PBS, n = 12); mock lentivirus ( MLV, n = 13) and lentivirus-mediated overexpression of Sema3a ( SLV, n = 13) groups. Sham-operated rats served as control group ( CON, n = 20). Cardiac function and electrophysiological study ( PES) were performed at 1 week later. Blood and tissue samples were collected for histological analysis, epinephrine ( EPI), growth-associated factor 43 ( GAP43) and tyrosine hydroxylase ( TH) measurements. QTc intervals were significantly shorter in SLV group than in PBS and MLV groups (168.6 ± 7.8 vs. 178.1 ± 9.5 and 180.9 ± 8.2 ms, all P < 0.01). Inducibility of VT by PES was significantly lower in the SLV group [30.8% (4/13)] than in PBS [66.7% (8/12)] and MLV [61.5% (8/13)] groups ( P < 0.05). mRNA and protein expressions of Sema3a were significantly higher and the protein expression of GAP43 and TH was significantly lower at 7 days after transduction in SLV group compared with PBS, MLV and CON groups. Myocardial EPI in the border zone was also significantly lower in SLV group than in PBS and MLV group (8.73 ± 1.30 vs. 11.94 ± 1.71 and 12.24 ± 1.54 μg/g protein, P < 0.001). Overexpression of Sema3a in MI border zone could reduce the inducibility of ventricular arrhythmias by reducing sympathetic hyper-reinnervation after infarction. [ABSTRACT FROM AUTHOR]

The impact of angiotensin II receptor blockers (ARBs) on electrical remodelling after myocardial infarction (MI) remains unclear. The purpose of the present study was to evaluate the effect of valsartan on incidence of ventricular arrhythmia induced by programmed electrical stimulation (PES) and potential link to changes of myocardial connexins (Cx) 43 expression and distribution in MI rats. Fifty-nine rats were randomly divided into three groups: Sham ( n = 20), MI ( n = 20) and MI + Val (20 mg/kg/day per gavage, n = 19). After eight weeks, the incidence of PES-induced ventricular tachycardia (VT) and fibrillation (VF) was compared among groups. mRNA and protein expressions of Cx43, angiotensin II type 1 receptor (AT1R) in the LV border zone (BZ) and non-infarct zone (NIZ) were determined by real-time PCR and Western blot, respectively. Connexins 43 protein and collagen distribution were examined by immunohistochemistry in BZ and NIZ sections from MI hearts. Valsartan effectively improved the cardiac function, reduced the prolonged QTc (163.7 ± 3.7 msec. versus 177.8 ± 4.5 msec., P < 0.05) after MI and the incidence of VT or VF evoked by PES (21.1% versus 55%, P < 0.05). Angiotensin II type 1 receptor expression was significantly increased in BZ and NIZ sections after MI, which was down-regulated by valsartan. The mRNA and protein expressions of Cx43 in BZ were significantly reduced after MI and up-regulated by valsartan. Increased collagen deposition and reduced Cx43 expression in BZ after MI could be partly attenuated by Valsartan. Valsartan reduced the incidence of PES-induced ventricular arrhythmia, this effect was possibly through modulating the myocardial AT1R and Cx43 expression. [ABSTRACT FROM AUTHOR]

1. Inflammation is central to the pathogenesis of acute coronary syndrome ( ACS) and is associated with adverse clinical outcomes after percutaneous coronary intervention ( PCI). Recent in vitro work has demonstrated the anti-inflammatory effect of berberine, a primary component of the traditional Chinese medicine 'umbellatine'. In the present study, we further tested whether berberine had any beneficial effects on ACS patients following PCI. 2.In all, 130 ACS patients undergoing PCI were recruited to the present study. Sixty-one patients were treated with berberine (300 mg, t.i.d., for 30 days) in addition to standard therapy, whereas the remaining patients received standard therapy alone. Circulating inflammatory markers were measured by ELISA, whereas serum lipid profiles were measured by routine chemical assays. 3.In the berberine-treated group, matrix metalloproteinase ( MMP)-9, intercellular adhesion molecule ( ICAM)-1, vascular cell adhesion molecule ( VCAM)-1, C-reactive protein, interleukin-6 and monocyte chemoattractant protein-1 were significantly reduced relative to baseline values. Furthermore, the changes in MMP-9, ICAM-1 and VCAM-1 from baseline to after 1 month of treatment differed significantly between the two patient groups. There was a tendency for berberine to induce a slightly greater reduction in low-density lipoprotein cholesterol and triglycerides than standard therapy alone, without affecting high-density lipoprotein cholesterol, but the differences failed to reach statistical significance. No severe adverse effects of berberine were observed. 4.The results of the present study provide the first clinical evidence of the anti-inflammatory action of berberine in ACS patients following PCI. Berberine may become adjunct therapy to further improve clinical outcomes via its anti-inflammatory effect in ACS patients. [ABSTRACT FROM AUTHOR]

Aims: Bronchi or pulmonary arteries (PAs) could be injured during atrial fibrillation (AF) ablation. Therefore, the aim of the present study was to evaluate the spatial relationship between left atrial roof or superior pulmonary veins (PVs) and neighbouring structures of AF patients and provide anatomic guidance for AF ablation to avoid injuring bronchi or PAs. Methods and Results: A dual-source computed tomography (DSCT) scan was used to depict the left atrium (LA), PVs, and nearby structures including bronchi and PAs in 58 patients with drug-refractory AF (mean age, 64 ± 9 years). The distance between LA roof or superior PVs (SPVs) and bronchi or PAs was measured. The average minimal distances from the left, middle, and right points of the LA roof to the principal bronchi were 17.0 ± 6.4, 23.7 ± 5.1, and 23.2 ± 7.7 mm, respectively. The LA roof was closer to the right PA (RPA) than the left PA (LPA) for more than 90% of patients. The average minimal distances from the left, middle, and right points of the LA roof to the PAs were 8.3 ± 5.0, 5.9 ± 3.1, and 6.0 ± 2.8 mm, respectively. The average minimal distances between the left superior pulmonary vein and bronchi or LPA were 0.32 ± 0.79 or 0.4 ± 1.0 mm, respectively. The average minimal distances between the right superior pulmonary vein and bronchi or RPA were 0.27 ± 0.94 and 0.0 ± 0.1 mm, respectively. Both of the root parts of SPVs of most patients were in direct contact with branches of trachea and PAs. Conclusion: Dual-source computed tomography provides important imaging information for determining the relationship between LA, PVs, and neighbouring structures. Use of pre-procedural cardiac CT scans may help avoid ablation-induced injury of bronchi and PAs. [ABSTRACT FROM AUTHOR]

Abstract: Genetic predisposition may be underlying the prevalence of acquired atrial fibrillation (AF). We investigated the association between polymorphism in angiotensinogen (AGT) and angiotensin-converting enzyme gene and risk of acquired AF in a pair-matched case-control study conducted in Chinese Hans. We selected 9 single nucleotide polymorphisms (SNPs) in the AGT gene and 3 SNPs in the angiotensin-converting enzyme gene using a tagging-SNP strategy. We observed significant association between tagging-SNP rs699 (M235T), located in exon 2 of the AGT gene, and AF. The AA genotype of rs699 increased the risk of AF by 70% (95% confidence interval, 1.01-2.85; P = .044) under a recessive model (AA vs AG + GG). The significance remained after controlling for covariates age, smoking, body mass index, hypertension, diabetes, and left atrial dimension, with an increased risk of AF by 90% (95% confidence interval, 1.04-3.46; P = .036). We provide evidence that polymorphism in AGT gene may confer predisposition to acquired atrial fibrillation in Chinese Hans. [Copyright &y& Elsevier]

Abstract: The arrhythmogenic effect of intracardiac skeletal myoblast (SKM) transplantation may be related to the differentiation state of SKMs. We tested the hypothesis that lentivirus mediated siRNA against the loop region of miRNA-181a could upregulate the SKMs differentiation repressor homeobox protein A11 (Hox-A11) and reduce the arrhythmias post SKM transplantation into ischemic myocardium of rats. Primary cultured SKMs were transfected with Lenti-siR-miR-181 (recombined lentivirus expressing the unique siRNA against miR-181a, LV group). Real-time PCR showed that miRNA-181a level was significantly decreased and Hox-A11 protein level significantly increased in LV group than in control group at days 5 and days 7 post Lentivirus transfection. Knockdown of miRNA-181a significantly promoted SKMs'' growth and attenuated the connexin43 downregulation in SKMs in vitro. Seven days after left coronary artery ligation, rats were randomized to receive intramyocardial injection of either 5×106 SKMs transfected with Lenti-siR-miR-181 (MI-SKMLV), 5×106 Lenti-siLUC SKMs (MI-SKM) or PBS (MI-PBS). Systolic function was significantly improved in both MI-SKM and MI-SKMLV groups fourteen days after injection. Incidence of inducible self-terminating ventricular tachycardia was significantly lower in MI-SKMLV than that in MI-SKM group. Engraftments of SKMs with knockdowned miRNA-181a similarly improved cardiac function as SKM transplantation but significantly decreased the arrhythmogenic effect of SKM transplantation in rats with experimental myocardial infarction. [Copyright &y& Elsevier]

Introduction: Nonfamiliar atrial fibrillation (AF) is usually associated with acquired structural heart disease, including valvular heart disease, coronary artery disease, and hypertension. Suggestive evidence indicates that these forms of acquired AF are more likely to occur in individuals with a genetic predisposition. We investigated the effect of the potassium channel voltage-gated subfamily member 2 ( KCNH2) gene on the prevalence of acquired AF in a Chinese population. Methods: In a pair-matched, hospital-based case control study (297 vs 297) conducted in Chinese Hans, we investigated 4 tagging single nucleotide polymorphisms (tSNPs), rs1805120, rs1036145, rs3807375, and rs2968857 in the KCNH2 gene, and determined their association with AF acquired from structural heart diseases. Results: We did not observe the association of rs1036145, rs3807375, and rs2968857 with AF. However, we determined that the tSNP, rs1805120, in exon 6 confers the risk of AF in Chinese Hans. Both genotype and allele frequencies of rs1805120 were distributed differently in cases and controls (P = 0.0289 and P = 0.0172, respectively). The most significant association was observed under a recessive model for the minor GG genotype with a 1.45-fold risk of developing AF (95% confidence interval 1.09–1.93, P = 0.012). The significance remained after controlling for the covariates of age, smoking, BMI, hypertension, and diabetes. Conclusion: We report a new genetic variation (rs1805120) in the KCNH2 gene that predisposes Chinese Han individuals to the risk of acquired AF. Further genetic and functional studies are required to identify the etiological variants in linkage disequilibrium with this polymorphism. [ABSTRACT FROM AUTHOR]

Background: Few data are available to define the circuits in ventricular tachycardia (VT) after myocardial infarction and the conduction time (CT) through the zone of slow conduction (SCZ). This study assessed the CT of the SCZ and identified different reentrant circuits. Methods: During VTs, concealed entrainment (CE) was attempted. The SCZ was identified by a difference between postpacing interval (PPI) and VT cycle length (VTcl) ≤30 ms. Since the CT in the normally conducting part of the VT circuit is constant during VT and CE, a CE site within the reentrant circuit with (S-QRS)/PPI ≥ 50% was classified as an inner reentry in which the entire circuit was within the scar, and a CE site with (S-QRS)/PPI < 50% as a common reentry in which part of the circuit was within the scar and part out of the scar. Results: CE was achieved in 20 VTs (12 patients). Six VTs (30%) with a (S-QRS)/PPI ≥50% were classified as inner reentry and 14 VTs (70%) with a (S-QRS)/PPI <50% during CE mapping as common reentry. The EG-QRS interval (308 ± 73 ms vs 109 ± 59 ms, P < 0.0001) was significantly longer and the incidence of systolic potentials higher (4/6 vs 0/12, P < 0.001) in the inner reentry group. For the 14 VTs with a common reetry, the CT of the SCZ was 348 ± 73 ms, while the CT in the normal area was 135 ± 50 ms. Conclusion: According to the proposed classification, 30% of VTs after myocardial infarction had an entire reentrant circuit within the scar. In VTs with a common reentrant circuit, the CT of the SCZ is approximately four times longer than the CT in the normal area, accounting for more than 70% of VTcl. [ABSTRACT FROM AUTHOR]

Ablation of Ventricular Fibrillation. It has been demonstrated that idiopathic ventricular fibrillation (VF) can be triggered by ventricular premature beats (VPBs) arising from the Purkinje fibers. Eliminating these VPBs by radiofrequency catheter ablation prevented VF recurrences. Whether the same pathophysiology and the same treatment option exist in patients with structural heart disease is unknown. Recurrent VF was observed in a 17-year-old patient after aortic valve repair of a perforated noncoronary cusp with resulting severe aortic regurgitation. VF recurred despite therapy with various antiarrhythmic drugs. A maximum of 14 external defibrillations was necessary during a 24-hour period to stabilize the patient. Due to increasing hemodynamic instability as a result of this electrical storm, the patient was referred for invasive diagnostics. During electrophysiologic study, frequent short runs of VF initiated by VPB with a narrow QRS complex were observed. After extensive mapping of the right and left ventricles, two distinct sources of VPBs originating from anteroseptal and inferoseptal areas of the left ventricle could be successfully ablated. VPBs were preceded by distinct Purkinje potentials with intervals from the Purkinje potential to QRS onset of VPB of 68 ms and 30 ms at effective sites, respectively. During short-term follow-up of 2 months, there was no VF recurrence. VPB originating from the Purkinje system may be one possibility for VF initiation in patients with structural heart disease. Eliminating these sources of VPBs by catheter ablation can prevent recurrent VF in such patients. (J Cardiovasc Electrophysiol, Vol. 15, pp. 90-93, January 2004) [ABSTRACT FROM AUTHOR]

Background: Critical sites within reentry circuits of postinfarction ventricular tachycardia (VT) were identified during sinus rhythm (SR) and VT to determine whether electrogram characteristics during SR may be helpful in identifying successful ablation sites. Methods: In 33 patients (mean age 67 ± 11 yrs) with prior infarction, mapping and radiofrequency (RF) catheter ablation of 57 hemodynamically-tolerated VT's (cycle length 478 ± 96) were performed. The morphologies of electrograms (EGM) at sites of concealed entrainment (CE) were compared during SR and VT. RF energy was delivered at 94 sites (51 successful and 43 unsuccessful ablation sites). Results: During SR, isolated potentials (IP), but not late potentials (LP) recorded via the mapping catheter, were associated with successful ablation. At 29/39 sites with an IP during sinus rhythm, an isolated diastolic potential (IDP) also was present during VT, whereas at 4 sites IP's were present only during SR ( p < 0.001). At 11/29 sites where isolated potentials were present during SR and VT, the morphology of the isolated potential during VT and SR was similar; and all but one of these sites were successful ablation sites ( p = 0.01). The EGM amplitude during VT correlated with the amplitude during SR ( R = 0.9, p < 0.001). An identical pacemap was present during SR at 33/94 sites; this was not associated with successful ablation. Conclusion: SR mapping may be helpful in identifying critical sites of reentry in postinfarction VT. At sites within the reentry circuit, characteristics of sinus rhythm EGM's that are associated with successful ablation include the presence of IP's, but not the presence of LP's. [ABSTRACT FROM AUTHOR]

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Objective: The mechanism by which pacing terminates ventricular tachycardia (VT) may depend on the location of the pacing site relative to the reentry circuit. The purpose of this study was to compare the mechanisms by which pacing terminates VT at left ventricular (LV) sites with and without concealed entrainment (CE) in patients with prior myocardial infarction. Methods and Results: LV mapping was performed in 29 patients (26 men, 3 women, mean age 67±11 years, ejection fraction 0.28±0.11) with 55 hemodynamically-tolerated VTs (mean cycle length 478±92 msec). A total of 408 pacing trains were delivered at 102 sites with CE. Radiofrequency catheter ablation was successful in 41 of 55 VT's. At sites with concealed entrainment, VT was terminated by pacing at 17/41 (41%) successful and at 4/61 (7%) unsuccessful ablation sites (p<0.01). Termination without global ventricular capture was the most frequent termination mode (10/21), followed by termination with orthodromic (4/21) and non-orthodromic capture (7/21). Conclusion: In patients with prior myocardial infarction, pacing at sites of CE during VT usually terminates VT either without global capture or by orthodromic capture. Termination of VT by pacing without global capture or with orthodromic capture at sites of CE suggests that the site is within a critical area of the reentry circuit. [ABSTRACT FROM AUTHOR]

Background: Recently, left bundle branch area pacing (LBBAP) has been shown to be feasible. However, the right ventricular (RV) implantation site for LBBAP remains elusive. We believe that the RV implantation site should be located at the posteromedial basal septum, and in this paper, we propose a new method to help guide lead implantation. The aim of this study is to demonstrate the feasibility of the proposed method.Methods: The RV implantation site was positioned by a combination of a nine-grid system on fluoroscopy and the use of intracardiac echocardiogram (ICE) and then verified by ICE.Results: Fifteen patients were enrolled for LBBAP using our method. The acute success rate was 86.7% (13/15), which demonstrated that our method is useful for assisting with lead implantation. According to ICE, the distance between the implantation site and apex (the front) and the distance between the implantation site and tricuspid annulus (the back) were 44.9 ± 10.7 and 33.2 ± 10.4 mm, respectively, and the ratio of the front and the back was 1.57 ± 0.80. The distance between the implantation site and the front junction point of the left-right ventricle (the upper) and the distance between the implantation site and the back junction point (the lower) were 33.4 ± 10.6 and 24.5 ± 10.2 mm, respectively. The ratio of the upper to the lower was 1.76 ± 1.36. These results suggest that the implantation site was at the posteromedial basal septum. The width of the QRS duration increased from 110.4 ± 33.1 ms at baseline to 114.1 ± 16.1 ms post LBBAP (P > 0.05). The operation time was 133 ± 32.9 min. The time of X-ray fluoroscopy was 21.2 ± 5.9 min. The mean time for lead positioning during LBBAP was 33.8 ± 16.6 min. During a follow-up of 3 months, the LBB capture threshold remained stable in 12 patients, except for one patient who had an increase in the LBB capture threshold to 3.0 v/0.4 ms.Conclusions: Our preliminary results indicate that the posteromedial basal septum could be seen as the implantation site for LBBAP. As a technique for LBBAP, ICE is a useful method for assisting with lead implantation. It is feasible and safe to use a nine-grid system combined with ICE for LBBAP. [ABSTRACT FROM AUTHOR]