Conduction Velocity Index Research Articles

Clinical study of alprostadil combined with epalrestat and methylcobalamin in the treatment of type 2 diabetic peripheral neuropathy

Objective To study the effect of alprostadil combined with epalrestat and methylcobalamin in the treatment of type 2 diabetic peripheral neuropathy. Methods From January 2014 to June 2016, 120 patients with type 2 diabetic peripheral neuropathy in the First People′s Hospital of Baiyin were randomly divided into two groups according to the random number table method.64 patients of the observation group were given the treatment of alprostadil, epalrestat combined with methylcobalamin.56 patients of the control group were given the treatment of alprostadil and methylcobalamin.And the two groups were treated for 4 weeks.The blood glucose, clinical symptoms, adverse reaction, nerve conduction velocity index were compared between the two groups before and after treatment. Results The fasting blood glucose and 2-hour postprandial blood glucose of the two groups after treatment were significantly decreased(t=18.20, 17.61, 15.75, 23.69, all P 0.05). Conclusion Alprostadil combined with epalrestat and methylcobalamin in the treatment of type 2 diabetic peripheral neuropathy has good effect. Key words: Diabetic neuropathies; Alprostadil; Epalrestat; Methylcobalamin

Arrhythmogenic anatomical isthmuses identified by electroanatomical mapping are the substrate for ventricular tachycardia in repaired Tetralogy of Fallot.

Aims The majority of ventricular tachycardias (VTs) in repaired tetralogy of Fallot (rTOF) are related to anatomically defined isthmuses. We aimed to identify specific electroanatomical characteristics of anatomical isthmuses (AI) related to VT which may allow for individualized risk stratification and tailored ablation. Methods and results Seventy-four consecutive rTOF patients (40 ± 16 years, 63% male) underwent VT induction and right ventricular electroanatomical voltage and activation mapping during sinus rhythm (SR) to identify the presence and characteristics of AI (isthmus width, length and conduction velocity index [CVi]). Twenty-eight patients were inducible for 41 VTs. All 74 patients had at least one AI. However, AI in patients with VT were longer (22 ± 7 vs. 16 ± 7 mm, P = 0.001), narrower (20 ± 8 vs. 28 ± 11 mm, P < 0.001) and had lower CVi (0.36 ± 0.34 vs. 0.78 ± 0.24 m/s, P < 0.001). Thirty-seven VTs in 24 patients were mapped (pace-, entrainment mapping, and/or VT termination by ablation) to 28 AI. All 28 AI related to VT had a CVi < 0.5 m/s (slow conducting AI (SCAI)). In contrast, 87 of 89 AI of the 46 patients without VT had CVi ≥ 0.5 m/s. Sixty-two patients were discharged without the presence of an SCAI (44 had no SCAI at baseline, 18 underwent ablation of the SCAI) and 10 still had an SCAI (no/failed ablation). During follow-up (50 ± 22 months), no patient without SCAI had any VT, which occurred in 5/10 patients with SCAI ( P < 0.001). Conclusion In rTOF, slow conducting anatomical isthmuses identified by electroanatomical mapping during SR are the dominant substrate for VT allowing individualized risk stratification and preventive ablation.

003 Gap junctional uncoupling with carbenoxolone slows conduction and increases vulnerability to ventricular arrhythmias in structurally normal hearts: an optical mapping study

<h3>Background</h3> Gap junctional uncoupling is thought to contribute to arrhythmogenesis through its effects on conduction slowing and creation of heterogeneities, often in the context of action potential or structural abnormalities. However, it is uncertain as to whether moderate conduction slowing through gap junctional uncoupling on its own, in the absence of action potential or structural changes, is sufficient to be pro-arrhythmic. We used optical mapping: (1) to study the effects of carbenoxolone, a gap junction uncoupler, on conduction velocity and action potential duration, and (2) to assess the effects of moderate conduction slowing and gap junctional uncoupling on arrhythmia vulnerability in structurally normal hearts. <h3>Methods</h3> Normal rat hearts (n=12) were isolated and perfused with Krebs-Henseleit solution, then loaded with a voltage-sensitive dye (RH237) and perfused with an excitation-contraction uncoupler (10 μM blebbistatin) to eliminate motion artefact. Transmembrane voltage (V_m) transients were recorded using a 256-photodiode array and epicardial activation was mapped across the anterolateral left ventricle during ventricular pacing (stimulus 1 mA, cycle length 180 ms). Hearts were then perfused with 30 μM carbenoxolone (CBX; n=6) or control (n=6) for 30 min and epicardial activation mapped every 2 min. Subsequently, hearts were subjected to programmed ventricular stimulation with up to three extrastimuli and assigned an Inducibility Quotient depending on ease of arrhythmia inducibility. <h3>Results</h3> Carbenoxolone significantly slowed conduction across the left ventricular epicardial surface (Conduction velocity index: Baseline 100%, CBX 70% ± 2%, p&lt;0.01) whereas there was no change in conduction velocity in control hearts after 30 min (Baseline 100%, Controls 98%±3%, p=NS). Carbenoxolone did not affect action potential duration (Baseline: APD50: 52±2 ms, APD75: 70±3 ms, APD90: 90±3 ms; CBX: APD50: 54±4 ms; APD75: 74±6 ms; APD90: 94±5 ms; all p=NS). Inducibility of ventricular arrhythmias was significantly increased in CBX hearts compared with control hearts during programmed stimulation (Inducibility quotient: CBX: 5.0±1.0; Control: 2.5±1.0; p&lt;0.05). <h3>Conclusions</h3> Gap junctional uncoupling with carbenoxolone produced a 30% reduction in conduction velocity without changes in action potential duration, and resulted in increased arrhythmia vulnerability in structurally normal hearts. These results suggest that moderate conduction slowing produced by gap junctional uncoupling in isolation, that is, in the absence of changes in action potential duration or structural abnormalities, is sufficient to increase susceptibility to ventricular arrhythmias, and therefore highlight the importance of gap junctional uncoupling in ventricular arrhythmogenesis.

Dynamic effects of intravenous procainamide infusion on the electrophysiological properties during atrial fibrillation.

Although the mechanism of atrial fibrillation (AF) is still controversial, multiple wandering reentry is considered the primary mechanism in most AF. It has been suggested that prolongation of the wavelength would make it impossible for the reentry to continue and would lead to the termination of the AF. In the present study a dynamic fluctuation in the electrophysiological properties was observed with procainamide infusion during AF. In 12 patients, both the local electrogram and monophasic action potentials (MAP) during AF were recorded from the right atrium before, during and after infusion of procainamide (10 mg/kg). The minimum AF cyclelength (CLmin), MAP duration at 90% repolarization (MAPD90) and widths of the intraatrial potentials (WAP) were measured with custom-made computer software. The conduction velocity index (CVI) was determined from the WAP. The wavelength index (WLI=CVIxCLmin) and postrepolarization refractoriness (PRR= CLmin-MAPD90) were calculated. In 6 patients, AF was terminated by procainamide infusion (group A), but not in the other 6 patients (group B). Group A patients showed a biphasic change in the parameters following procainamide infusion. In phase I, the CLmin, MAPD90 and PRR increased, while the CVI decreased, and the WLI remained unchanged. In phase II, the PRR, CVI and WLI increased and the AF was terminated. No restoration of the CVI nor increase in the WLI were observed in group B. The biphasic fluctuation in the CVI and the remarkable increase of the PRR and WLI were observed before termination of AF by procainamide infusion.