A novel ECG algorithm to differentiate between ventricular arrhythmia from right versus left ventricular outflow tract.

AIM: The aim of this study was to evaluate the accuracy of the diagnostic criteria for determining the origin of outflow tract ventricular arrhythmia (OTVA) and develop an ECG algorithm to predict its origin. METHOD: We analyzed the ECGs of 100 patients with OTVA who underwent successful ablation. The QRS complex was measured during sinus rhythm and ventricular arrhythmia. After the ECG algorithm was developed, it was validated in an additional 100 patients from two different hospitals. RESULTS: In this retrospective study, among the parameters without restrictions in the transition lead, the V2S/V3R index (AUC = 0.96) was significantly better in predicting ventricular arrhythmia originating from the right ventricular outflow tract (RVOT). Further, the larger initial r wave surface area (ISA) in V1 and V2 (AUC = 0.06) was significantly better in predicting ventricular arrhythmias originating from the left ventricular outflow tract (LVOT). Among the parameters with the transition lead in V3, the V2S/V3R index (AUC = 0.82) was significantly better in predicting VAs originating from the RVOT. On the contrary, the V3 R-wave deflection interval (AUC = 0.19) was significantly better in predicting ventricular arrhythmias originating from the LVOT. The algorithm combining the V2S/V3R index and the larger ISA in V1 and V2 could predict OTVA origin with an accuracy of 95.00%, a sensitivity of 87.18%, a specificity of 100.00%, a positive predictive value (PPV) of 100.00%, and a negative predictive value (NPV) of 92.42%. In the validation study, the algorithm exhibited excellent accuracy (95.00%) and AUC (AUC = 0.95), with a sensitivity of 94.12%, a specificity of 95.45%, a PPV of 91.43%, and an NPV of 96.92%. CONCLUSION: Our developed algorithm can reliably predict OTVA origin without restrictions in the transition lead.

A specific notation for contrast medium and dehydrated ethanol injection into the vein of Marshall during mitral isthmus ablation-A case report.

BACKGROUND: Ablation of the vein of Marshall (VOM) by dehydrated ethanol (DE) is an important method for completely blocking the mitral isthmus (MI). Before DE ablation of the VOM, Marshall angiography should be performed so that the contrast medium is inevitably exposed to DE. METHOD: We present a case of DE ablation of the VOM. When iodixanol was exposed to DE, some floccule embolized the lumen of the over-the-wire (OTW) balloon dilatation catheter and led to the impossibility of DE ablation. Then, we performed in vitro experiments: iodixanol, not iomeprol, produced many stable white floccules when it encountered DE. CONCLUSION: Iodixanol is not an appropriate contrast for DE ablation of the VOM. However, if there is no other alternative contrast, the following methods might be used to address the problem: ⑴ diluted iodixanol (iodixanol:normal saline 1:1) could be used for VOM ablation; or ⑵ the lumen of the OTW could be flushed by NS after VOM angiography, and then DE injection could be performed.

Effect of evolocumab on the progression and stability of atherosclerotic plaques as evaluated by grayscale and iMAP-IVUS.

BACKGROUND: Evolocumab inhibits the proprotein convertase subtilisin/kexin type 9 protein and is a potent cholesterol-lowering drug. However, the relationship between evolocumab and inflammation, and the effects of evolocumab on the stability of atherosclerotic plaques remain unknown. METHODS: Twenty-seven purebred New Zealand rabbits were fed with an atherogenic diet for 2 weeks. The abdominal aortic endothelium was balloon-injured. The rabbits were divided into the atorvastatin (2 mg/kg/day; Ato), evolocumab (7 mg/kg/2 weeks, Evo) and control groups. Intravascular ultrasound (IVUS) images of the abdominal artery were analyzed at 10 and 18 weeks. Additionally, the serum levels of the biomarkers were measured at baseline, and at 10 and 18 weeks. RESULTS: The serum levels of triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and monocyte chemoattractant protein-1 (MCP-1) increased after 10 weeks of administration of the proatherosclerotic diet, while the levels of high-density lipoprotein cholesterol (HDL-C) and transforming growth factor-ß (TGF-ß) decreased. The reduction in the serum levels of triglycerides, total cholesterol, LDL-C, MCP-1, TGF-ß, and toll-like receptor 4 (TLR4) following treatment with evolocumab was higher than that of atorvastatin. Both evolocumab and atorvastatin reduced the percent atheroma volume. Evolocumab increased the fibrotic% and decreased the necrotic%. Correlation analysis revealed that the levels of triglycerides, total cholesterol, LDL-C, MCP-1, TGF-ß, and TLR4 were negatively correlated with the fibrotic%, but were positively correlated with the necrotic%. Multivariate linear regression analysis revealed that treatment with atorvastatin, and especially evolocumab, was a consistent predictor of the percent atheroma volume, and fibrotic and necrotic composition. CONCLUSIONS: Proprotein convertase subtilisin/kexin type 9 regulates the serum levels of lipid and cholesterol may via inflammatory pathways. The results also indicate that evolocumab is more potent than atorvastatin in suppressing the progression and stability of atherosclerotic plaque in rabbits.

Influence of remote ischemic conditioning on radial artery occlusion.

This study aimed to explore the influence of remote ischemic conditioning (RIC) on radial artery occlusion (RAO) and distinguish the risk factors for RAO. A total of 640 consecutive patients who prospectively underwent transradial artery coronary angiography (TRACA) (322 patients received RIC before TRACA) were enrolled. RIC was not performed in 318 patients. RAO was estimated using Doppler ultrasonography after the procedure. Patients were divided into two groups according to the protocol of RIC: RIC and non-RIC. The rate of RAO was significantly lower in the RIC group than in the non-RIC group. Patients were divided into two groups according to the patency of radial artery: radial artery patency (RAP) and RAO. The radial artery diameter was significantly narrower in the RAO group (2.31 ± 0.53) than in the RAP group (2.59 ± 0.47). The rate of applying ß-blocker was significantly higher in the RAP group (69%) than in the RAO group (41%). The rate of applying trimetazidine was significantly higher in the RAP group (49.1%) than in the RAO group (17.6%). The multiple logistic regression analysis using radial artery diameter, RIC, ß-blocker, and trimetazidine treatments revealed that small radial artery diameter, lack of ß-blockers, and RIC were independent predictors of RAO. RIC might help in improving the rate of RAO. The multiple logistic regression analysis showed that the lack of ß-blockers, RIC, and small radial artery diameter were independent predictors of RAO.

Efficacy and safety of proprotein convertase subtilisin/kexin type 9 monoclonal antibody in adults with familial hypercholesterolemia.

Proprotein convertase-subtilisin/kexin type 9 (PCSK9) monoclonal antibody is a new therapy to reduce low-density lipoprotein cholesterol (LDL-C) level in patients with familial hypercholesterolemia (FH). This pooled analysis aimed to estimate the efficacy and safety of PCSK9 antibody therapy in FH. Reports of randomized controlled trials (RCTs) comparing PCSK9 antibody to placebo were retrieved by a search of MEDLINE via PubMed, EMBASE, the Cochrane Library databases, ClinicalTrials.gov and Clinical Trial Results (up to November 30, 2015) with no language restriction. Data were abstracted by a standardized protocol. We found eight RCTs (1,879 patients with FH) for the pooled analysis. As compared with placebo, PCSK9 antibody therapy remarkably reduced LDL-C level (mean reduction: -48.54 %, 95 % CI: -53.19 to -43.88), total cholesterol (mean reduction: -31.08%, 95 % CI: -35.20 to -26.95), lipoprotein (a) (mean reduction: -20.44%, 95 % CI: -25.21 to -15.66), and apolipoprotein B (mean reduction: -36.32%, 95 % CI: -40.75 to -31.90) and elevated the level of high-density lipoprotein cholesterol (mean change: 6.29 %, 95 % CI: 5.12 to 7.46) and apolipoprotein A1(mean change: 4.86%, 95 % CI: 3.77 to 5.95). Therapy with and without PCSK9 antibodies did not differ in rate of adverse events (pooled rate: 50.86 % vs. 48.63%; RR: 1.03; 95 % CI: 0.92 to 1.15; P = 0.64; heterogeneity P = 0.13; I2= 40%) or serious adverse events (pooled rate: 7.14% vs. 6.74%; RR: 1.05; 95 % CI: 0.70 to 1.58; P = 0.80; heterogeneity P = 0.69; I2= 0%). PCSK9 antibody may be an effective and safe treatment for FH.

Effect of microRNA-208a on mitochondrial apoptosis of cardiomyocytes of neonatal rats.

OBJECTIVE: To explore the effect and mechanism of microRNA-208a (miR-208a) in the mitochondrial apoptosis of cardiomyocytes of neonatal rats. METHODS: The primary cultured cardiomyocytes of neonatal rats were added into the hypoxia incubator for the hypoxia induction. The overexpression system for miR-208a of cardiomyocytes of neonatal rats was built. The flow cytometry assay was employed to detect the incidence of apoptosis in the over-expressed miR-208a. The mitochondrial staining technique was used to detect the change in the mitochondrial morphology of over-expressed miR-208a. The bioinformatic analysis was chosen to analyze and predict the target gene of miR-208a. RESULTS: Firstly, the primary culture system of cardiomyocytes of neonatal rats was successfully built. The miR-208a was over-expressed in cardiomyocytes of neonatal rats by miR-208a Mimics. Results of flow cytometry assay showed that the over-expressed miR-208a could significantly reduce the incidence of apoptosis; while results of mitochondrial staining indicated the change in the mitochondrial morphology of over-expressed miR-208a and the mitochondrial fission process was inhibited. In conclusion, it was supposed that miR-208a could inhibit the activation of mitochondrial fission process to keep the cardiomyocytes from apoptosis. CONCLUSIONS: The over-expressed miR-208a can reduce the incidence of apoptosis in the cardiomyocytes of neonatal rats, significantly change the mitochondrial morphology and inhibit the mitochondrial fission process.