The electrophysiological hallmark of cells and tissues isolated from failing hearts is prolongation of action potential duration (APD) and conduction slowing. In human studies and a number of animal models of heart failure, functional downregulation of K currents and alterations in depolarizing Na and Ca currents and transporters are demonstrated. Alterations in intercellular ion channels and matrix contribute to heterogeneity of APD and conduction slowing. The changes in cellular and tissue function are regionally heterogenous particularly in the heart failure with dyssynchronous LV contraction (DHF). Furthermore, β-adrenergic signaling and modulation of ionic currents is blunted in heart failure. Cardiac resynchronization therapy (CRT) partially reversed the DHF-induced downregulation of K current and improved Na channel gating. CRT significantly improved Ca homeostasis especially in myocytes from late-activated, lateral wall, and restores the DHF-induced blunted β-adrenergic receptor responsiveness. CRT abbreviated DHF-induced prolongation of APD in the lateral wall myocytes and reduced the LV regional gradient of APD, and suppressed development of early afterdepolarizations. In conclusion, CRT partially restores DHF-induced ion channel remodeling, abnormal Ca homeostasis, blunted β-adrenergic response and regional heterogeneity of APD, thus may suppress ventricular arrhythmias and contribute to the mortality benefit of CRT as well as improve mechanical performance of the heart.
Background: The pacing lead system is electrically evaluated by a pacing system analyzer (PSA) during device implantation. However, it remains unknown whether measured data vary according to the PSA or the implantable device. We estimated differences in lead impedance measured by different PSAs and devices using a laboratory model. Methods: Five pacing and 3 defibrillation leads were used. We fixed the lead tip to a piece of meat immersed in physiologic saline and measured lead impedance using 4 PSA and 13 implantable device models. Results: The mean impedance of the 5 pacing leads as measured by PSAs was 735 to 611 ohms and the difference between the maximum and minimum values was 126 ohm. The maximum difference according to PSAs was 222 ohm. The mean impedance of the 5 pacing leads as measured by the implantable generators was 770 to 606 ohms, the difference was 175 ohms and the maximum difference was 309 ohms. The 3 defibrillation lead impedances varied from 427 to 1091 ohms and the mean impedance was 706 to 557 ohms. The differences were 149 ohm as measured by the PSAs and 157 ohms by the implantable cardioverter defibrillator (ICD) generators. The maximum differences were 241 ohms by the PSAs and 281 ohms by the ICD generators. Conclusion: Lead impedance varied according to analyzing systems.
Aim: The aim of this study was to assess the frequency and characteristics of complications in patients on anticoagulant therapy who were to undergo invasive procedure. Methods and Results: We sent a questionnaire to 2758 doctors who were on the mailing list of the Japanese Society of Cardiac Pacing and Electrophysiology in August 2004. We received 614 questionnaires (response rate, 22.3%). Out of the 614 doctors, 19 (3.1%) reported that their patients had embolic events upon the interruption of warfarin therapy during dental extraction. In patients undergoing invasive procedures such as surgery, endoscopy, pacemaker implantation, and catheterization, 168 (27.4%) of the 614 doctors reported embolic events after the interruption of warfarin therapy. Further, 255 (41.5%) of the 614 doctors reported bleeding episodes when warfarin therapy was continued during the invasive procedures. Conclusion: Several complications of different types were reported to occur in patients receiving warfarin therapy who underwent elective invasive procedures, regardless of whether warfarin administration was interrupted or continued at the time of the invasive procedure. Therefore, it is necessary to make careful decisions about the management of patients on warfarin therapy who will be undergoing invasive procedures.
Introduction: We examined whether the additional use of amiodarone (AMD) under implantable cardioverter-defibrillator (ICD) therapy may have beneficial effects in patients at risk for lethal ventricular arrhythmias with structural heart diseases. Methods: Sixty patients (47 males, mean age, 62±13 years) with structural heart disease who underwent ICD implantation were retrospectively analyzed. There were 2 groups: one group (AMD group) was treated with AMD (n=33) and the other group (non-AMD group) was treated without AMD (n=27). We compared the incidence and appropriateness of ICD shock therapy between two groups. Results: During a mean follow-up of 28±17 months, we identified a total of 62 episodes in 18 patients (30%) who received ICD shock therapy. ICD shock episodes were significantly less frequent in AMD group than in non-AMD group (15% versus 48%, P<0.01), while inappropriate shock episodes were greater in non-AMD group than in AMD group (49% versus 4%, P=0.03). In cumulative probability of shock events, the risk of events was significantly lower in AMD group (P=0.007). Of 4 patients who died in AMD group, we observed one fatal pulmonary fibrosis. Conclusions: Additional AMD therapy in patients with an ICD may be effective in reducing the risk of shock discharge.
Background: The neurohypophyseal hormones oxytocin (OT) and [Arg8]-vasopressin (AVP) have recently been implicated in cardiac function. This study was designed to investigate actions of OT and AVP on regulation of the voltage-gated Ca2+ channel in cardiomyocytes. Methods and Results: Cultured neonatal rat cardiomyocytes were stimulated with OT or AVP (10−8 M to 10−6 M) for 24–72 h, followed by real-time PCR and patch clamp studies. Although OT did not exert any modulatory effect on L-type Ca2+ channel current, as a short-term effect, stimulation of cardiomyocytes with OT but not AVP decreased the expression of CaV1.2 mRNA with a reduced L-type Ca2+ channel current. A transcription factor CREB mRNA expression was down-regulated by OT treatment, although T-type Ca2+ channels (CaV3.1, CaV3.2) were unaffected by OT or AVP. Conclusion: OT but not AVP down-regulates L-type Ca2+ channel expression through the inhibition of CREB transcriptional, suggesting a novel mechanism of OT action in the cardiac electrophysiology.
Introduction: It has become clear that the onset of heart failure is closely linked to right apex pacing, which lengthens the QRS duration and evokes discoordinate contraction of the left ventricle (LV). Currently, it is thought that the site inducing the shortest QRS duration is optimal for pacing. Objectives: The purpose of this study was to ascertain the pacing site inducing the shortest QRS duration and to examine the configuration of the 12-lead electrocardiogram and heart function while pacing at this site. Methods: Nine patients with normal heart function were enrolled. Pacing at right ventricular outflow, mid-interventricular septum (MS), and right ventricular apex was performed. QRS duration was measured and the configuration of the 12-lead electrocardiogram changed by pacing was studied. Output and LV dp/dt were calculated at each pacing site. Results: QRS duration became shorter with MS pacing and the pacing lead situated at the periphery of the coronary sinus and turned in a posterior direction. The configuration of the 12-lead electrocardiogram showed an Rs or rS pattern with II, III, and aVF leads. Output and LV dp/dt showed a tendency to increase with MS pacing. Conclusion: It is thought that mid-interventricular septum pacing shortens the QRS duration.
Background: Early repolarization, which was regarded as benign, has recently been associated with malignant arrhythmia. Despite the newly emerged importance of early repolarization, little is known about prevalence and QT interval of early repolarization. Methods: Early repolarization (defined as an elevation at the junction between QRS complex and ST segment ≥0.1 mV in at least 2 leads) was assessed in database containing 308,391 ECGs consisting of 102,065 patients (52,779 males and 49,286 females). Results: A total of 1,775 patients (mean age, 49±30 years) with early repolarization were chosen (1.7% of total population). The prevalence of early repolarization was about 11-times higher in male patients (n=1,623) than in female patients (n=152). The prevalence of early repolarization was 1.4% at the age of 0–9 years, peaked (5.0%) at the age of 10–19 years, and progressively decreased with advancing age from 20 to 79 years (3.3, 2.1, 1.6, 0.9, 0.5, and 0.3% at the age of 20–29, 30–39, 40–49, 50–59, 60–69, and 70–79 years, respectively). Bazett’s QTc interval of patients with early repolarization did not significantly differ among groups of each decade and between genders. Conclusion: The prevalence of early repolarization was both age- and gender-dependent in a hospital-based population. Yet, there was no association between QTc interval and age and between QTc interval and gender.
A 75-year-old male presented with palpitation on exertion. He suffered from frequent tachycardia attacks. His 12-leads electrocardiogram showed irregular cycle lengths (400–550 ms) of tachycardia with occasional 2:1 atrioventricular conduction (thus AV reentry was excluded). He had a complex anatomy of persistent left superior vena cava (PLSVC)/enlarged coronary sinus (CS). The activation map in a 3-dimensional CARTO system (Biosense-Webster, USA) was merged with the multi-detector computed tomography image and revealed that the tachycardia spread centrifugally from the junction between the PLSVC and enlarged CS. However, delivery of radio frequency (RF) energy to the earliest atrial activation site did not affect the tachycardia. Finally, the tachycardia was diagnosed as a fast/slow type atrioventricular nodal reentrant tachycardia (AVNRT) because the tachycardia was cured only after the anterograde/retrograde AV conduction was disturbed by the application of RF energy to the posteroseptal perimitral area, possibly due to the injury to the AV node.
We report a case involving a patient with ischemic cardiomyopathy who developed polymorphic ventricular tachycardia (PVT) and ventricular fibrillation storm after coronary artery bypass graft. Because PVT was initiated by various right bundle branch type premature ventricular contractions (PVCs), we assessed the relatively monomorphic ventricular tachycardia (MVT) during PVT. Electroanatomical mapping revealed that the earliest ventricular activation of the MVT was located in the scar border zone at the posterior septum of the left ventricle. Stable potentials which preceded the MVT were observed. Catheter ablation for the preceding potential suppressed the maintenance of the PVT, although triggered PVCs appeared frequently. Catheter ablation was effective as a bailout therapy in a patient with PVT-induced cardiomyopathy after cardiac operation.