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The article presents a case study of a 44-year-old male patient with repeated syncope for 5 years referred to our hospital. An electrophysiological study was performed. In addition, increasing the output from the proximal CS region may alter the atrial inputs by penetrating the AV node at more than one input. This phenomenon of treatment can be explained as vagal response caused by adjacent vagus ganglion capture.

Background: Previous studies have demonstrated that WenXin KeLi (WXKL), a traditional Chinese medicine, can exert antiarrhythmic properties through complex multichannel inhibition, but its pharmacologic effect remains to be elucidated, especially in the cardiac conductive system.Objective: To explore the antiarrhythmic property of WXKL in cardiac Purkinje cells (PCs).Methods: PCs were isolated from rabbit hearts and action potentials (APs) and ion currents were recorded by whole-cell patch clamp technique. Anemonia toxin II (ATX-II) and isoproterenol (ISO) were used to induce early or delayed afterdepolarizations (EADs, DADs) or triggered activities (TAs).Results: WXKL (1 g/L and 5 g/L) significantly abbreviated the action potential duration (APD) of PCs in a dose- and rate-dependent manner. Treatment of PCs with ATX-II (2 nM) prolonged APD and induced EADs, which were significantly suppressed by WXKL. WXKL (1, 5 g/L) also inhibited ISO-induced EADs, DADs, and TAs. To reveal the ionic mechanisms, we studied the effects of WXKL on late sodium current (I(NaL)), peak sodium current (I(NaP)), and L-type calcium currents (ICaL) in PCs. WXKL-attenuated ATX-II (5 nM) induced I(NaL) augmentation and blocked I(NaL) with an IC50 of 4.3 ± 0.5 g/L, which is 3- to 4-fold more selective than that of I(NaP) (13.3 ± 0.9 g/L) and ICaL (17.6 ± 1.4 g/L). Moreover, WXKL exerted significantly less use-dependent block of I(NaP) than that of flecainide, indicating its lower proarrhythmic effect.Conclusions: WXKL exhibits antiarrhythmic properties in cardiac PCs via selective inhibition of I(NaL). [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]

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]

ISRAEL, C.W., et al.: Immediate Reinitiation of Atrial Tachyarrhythmias after Spontaneous Restoration of Sinus Rhythm in Patients with an Implanted Monitoring Device. --> Immediate reinitiation of atrial tachyarrhythmia (IRAT) has been observed after cardioversion. After spontaneous restoration of sinus rhythm (SR), incidence and characteristics of IRAT have not been described. Therefore, in patients with atrial tachyarrhythmias (ATs) and bradycardia, a pacemaker with dedicated memory functions was implanted. Devices were interrogated after 1 month and stored episodes of AT were analyzed: incidence of IRAT, duration and rate of the preceding episode, sinus rate before AT, coupling interval of atrial premature beats (APBs) initiating AT, and incidence of repetitive APBs. A potential association with IRAT was assessed for clinical characteristics. In 36 of 68 patients, stored electrograms confirmed correct detection of AT onset and termination in 545 episodes. IRAT was present in 212 (39%, 24 patients) episodes of AT. Episodes of AT preceding IRAT were longer than those before non‐IRAT (156 vs 46 s,P < 0.001), and occurred during a higher atrial rate before onset of AT (cycle length775 ± 111vs856 ±133 ms, P < 0.001). The coupling interval of APBs initiating IRAT was shorter (502 ± 83vs538 ± 89  ms; P < 0.001) while the percentage of episodes with repetitive APBs before AT onset and the median atrial cycle length of the preceding AT were not different. On stepwise logistic regression analysis, none of the clinical factors evaluated independently predicted IRAT. In conclusion, IRAT is frequent after spontaneous restoration of SR. Changes of atrial electrophysiological properties promoting IRAT may already develop during AT of short duration. (PACE 2003; 26:1317–1325) [ABSTRACT FROM AUTHOR]

Introduction: Atrial fibrillation (AF) is associated with significant morbidity and mortality that may be related to hemodynamic Impairment thromboembolic events, or enhanced electrical instability of the ventricular myocardium. There is, however, a lack of data concerning the association of AF and ventricular tachyarrhythmias. Methods and Results: Consecutive patients with Indication for an implantable cardioverter deft' brillator (lCD) were classified for the presence or absence of persistent Al at the time of device implantation. Incidence of device therapy, stored electrograms, and clinical events during follow-up were evaluated prospectively. Two hundred fifty patients were included. During follow-up (20 ± 14 months), patients in Al experienced appropriate device therapy for recurrent ventricular arrhythmitts more frequently compared with patients in sinus rhythm (SR) (63% vs 38%, P = 0.01). On multivariate analysis, AF was an independent predictor of appropriate LCD therapy (relative risk 1.8; 95% confidence Interval [CI] 1.2 to 2.9) and Inappropriate device therapy (relative risk 23; 95% CI 1.2 to 4.5). Predefined clinical events (cluster endpoint: death, syncope, and hospitalizations) were observed more frequently in Al than In SR patients (55% vs 31%, p = 0.01). Analysis of device-stored electrograms revealed a higher incidence of short-long-short cycles preceding ventricular arrhythmias in AF compared with SR patients (50% vs 16%, P = 0.002). Baseline heart rate preceding ventricular arrhythmias did not differ between the two groups. Conclusion: AF is an Independent predictor of recurrent ventricular arrhythmias In lCD recipients. The underlying electrophysiologic mechanism seems to be irregular rather than rapid ventricular activation, with a high incidence of short-long-short sequences preceding ventricular tachyarrhythmias in A F patients. [ABSTRACT FROM AUTHOR]

Introduction Ischemia causes myocardial infarction and arrhythmias. Up-regulation of cardiac CLC-3 chloride channels is important for ischemic preconditioning-induced second-window protection against myocardial infarction. But its consequences in ischemia-induced electrical remodeling are still unknown. Methods The recently-characterized heart-specific overexpression of human short CLC-3 isoform ( hsCLC-3 OE ) mice was used to study the effects of CLC-3 up-regulation on cardiac electrophysiology under ischemia/reperfusion conditions. In vivo surface electrocardiography (ECG) and intracardiac electrophysiology (ICEP) were used to compare the electrophysiological properties of age-matched wild-type ( Clcn3 +/+ ) and hsCLC-3 OE mice under control and myocardial ischemia–reperfusion conditions. Results QT and QTc intervals of hsCLC-3 OE mice were significantly shorter than those of Clcn3 +/+ mice under control, ischemia and reperfusion conditions. In the ICEP, ventricular effective refractory period (VERP) of hsCLC-3 OE mice (26.7 ± 1.7 ms, n = 6) was significantly shorter than that of Clcn3 +/+ mice (36.9 ± 2.8 ms, n = 8, P < 0.05). Under ischemia condition, both VERP (19.8 ± 1.3 ms) and atrial effective refractory period (AERP, 34.8 ± 2.5 ms) of hsCLC-3 OE mice were significantly shorter than those of Clcn3 +/+ mice (35.2 ± 3.0 ms and 45.8 ± 1.6 ms, P < 0.01, respectively). Wenckebach atrioventricular nodal block point (AVBP, 91.13 ± 4.08 ms) and 2:1 AVBP (71.3 ± 3.8 ms) of hsCLC-3 OE mice were significantly shorter than those of Clcn3 +/+ mice (102.0 ± 2.0 ms and 84.1 ± 2.8 ms, P < 0.05, respectively). However, no differences of ICEP parameters between hsCLC-3 OE and Clcn3 +/+ mice were observed under reperfusion conditions. Conclusion Heart-specific overexpression of hsCLC-3 limited the ischemia-induced QT and ERP prolongation and postponed the advancements of Wenckebach and 2:1 AVBP. CLC-3 up-regulation may serve as an important adaptive mechanism against myocardial ischemia. [ABSTRACT FROM AUTHOR]