Complete Atrioventricular Conduction Block Research Articles

Strategy and technique for surgical treatment of Ebstein's anomaly.

Ebstein's anomaly (EA) is a rare and complex congenital heart anomaly, and the effect of surgical treatment is not ideal. This study aims to introduce our experience in management strategies, surgical techniques, and operative indications for patients with Ebstein's anomaly. A retrospective study of 258 operations was performed in 253 patients by the same cardiac surgeon in The First Hospital of Tsinghua University between March 2004 and January 2020. 32 patients had previously received cardiac surgery in other hospitals. The clinical data including diagnosis, operative indications, techniques, pathological changes, and survival rates were collected and analyzed. Anatomical correction was performed in 203 (78.7%) operations, 1½ ventricle repair in 38 (14.7%) operations, tricuspid valve repair only in four operations (1.6%), tricuspid valve replacement in ten (3.9%), total cavopulmonary connection (TCPC) in two (0.8%), and Glenn operation in one operation (0.4%). Reoperation was performed in five patients (2.0%) during hospitalization. Among them, tricuspid valve replacement was performed in one patient, 1½ ventricle repair in two patients, and tricuspid valve annulus reinforcement in two patients. Five patients died with an early mortality rate of 2.0%. Complete atrioventricular conduction block was complicated in one patient (0.4%). A total of 244 patients was followed up (four in the 253 patients lost) with a duration of 3.0-168.0 (87.6 ± 38.4) months. Cardiac function of 244 patients improved significantly with mean New York Heart Association (NYHA) functional class recovery from 3.5 to 1.1. The mean grade of tricuspid valve regurgitation improved from 3.6 to 1.5. Three late deaths (1.2%) occurred. The survival rates at five and ten years after surgery were 98.6% and 98.2%, respectively. Reoperation was performed in five patients (2.0%) during the follow-up period. Based on our management strategies and operative principles and techniques, anatomical correction of EA is capable of achieving excellent long-term results, and low rates of TCPC, 1½ ventricle repair and valvular replacement.

Percutaneous Transcatheter Closure of Congenital Ventricular Septal Defects.

Ventricular septal defects (VSDs) are the most common kind of congenital heart disease and, if indicated, surgical closure has been accepted as a gold-standard treatment. However, as less-invasive methods are preferred, percutaneous device closure has been developed. After the first VSD closure was performed percutaneously by Lock in 1988, both techniques and devices have developed consistently. A perventricular approach for closure of muscular VSD in small patients and the closure of perimembranous VSD using off-label devices are key remarkable developments. Even though the Amplatzer membranous VSD occluder (Abbott) could not be approved for use due to the high complete atrioventricular conduction block rate, other new devices have shown good results for closure of perimembranous VSDs. However, the transcatheter technique is slightly complicated to perform, and concerns about conduction problems after VSD closure with devices remain. There have been a few reports demonstrating successful closure of subarterial-type VSDs with Amplatzer devices, but long-term issues involving aortic valve damage have not been explored yet. In conclusion, transcatheter VSD closure should be accepted as being as effective and safe as surgery but should only be performed by experienced persons and in specialized institutes because the procedure is complex and requires different techniques. To avoid serious complications, identifying appropriate patient candidates for device closure before the procedure is very important.

The acute toxic effects of platinum nanoparticles on ion channels, transmembrane potentials of cardiomyocytes in vitro and heart rhythm in vivo in mice.

BackgroundPlatinum nanoparticles (PtNPs) have been considered a nontoxic nanomaterial and been clinically used in cancer chemotherapy. PtNPs can also be vehicle exhausts and environmental pollutants. These situations increase the possibility of human exposure to PtNPs. However, the potential biotoxicities of PtNPs including that on cardiac electrophysiology have been poorly understood.MethodsIon channel currents of cardiomyocytes were recorded by patch clamp. Heart rhythm was monitored by electrocardiogram recording. Morphology and characteristics of PtNPs were examined by transmission electron microscopy, dynamic light scattering and electrophoretic light scattering analyses.ResultsIn cultured neonatal mice ventricular cardiomyocytes, PtNPs with diameters 5 nm (PtNP-5) and 70 nm (PtNP-70) concentration-dependently (10–9 – 10–5 g/mL) depolarized the resting potentials, suppressed the depolarization of action potentials and delayed the repolarization of action potentials. At the ion channel level, PtNPs decreased the current densities of INa, IK1 and Ito channels, but did not affect the channel activity kinetics. In vivo, PtNP-5 and PtNP-70 dose-dependently (3–10 mg/kg, i.v.) decreased the heart rate and induced complete atrioventricular conduction block (AVB) at higher doses. Both PtNP-5 and PtNP-70 (10–9 – 10–5 g/mL) did not significantly increase the generation of ROS and leak of lactate dehydrogenase (LDH) from cardiomyocytes within 5 mins after exposure except that only very high PtNP-5 (10–5 g/mL) slightly increased LDH leak. The internalization of PtNP-5 and PtNP-70 did not occur within 5 mins but occurred 1 hr after exposure.ConclusionPtNP-5 and PtNP-70 have similar acute toxic effects on cardiac electrophysiology and can induce threatening cardiac conduction block. These acute electrophysiological toxicities of PtNPs are most likely caused by a nanoscale interference of PtNPs on ion channels at the extracellular side, rather than by oxidative damage or other slower biological processes.

Atrioventricular conduction disturbance during pulmonary vein isolation using the second-generation cryoballoon — Vagal impact of cryoballoon ablation

BackgroundVagal reactions of the sinus node during pulmonary vein isolation (PVI) have been reported, however, data on intra-procedural atrioventricular conduction disturbances have been sparse. The present study aimed to investigate the clinical characteristics of atrioventricular conduction block (AVB) during PVI using second-generation cryoballoons. MethodsA total of 2252 PVs among 568 consecutive atrial fibrillation patients undergoing PVI with 28-mm cryoballoons were analyzed. In 44 patients, left superior PVs (LSPVs) were initially targeted (initial-LSPV-group). In the remaining 524 patients, LSPVs were targeted following right superior PVs (RSPVs) (initial-RSPV-group). ResultsMarked sinus arrests/bradycardia occurred in 14 patients only in the initial-LSPV-group, and the incidence was significantly higher in the initial-LSPV than initial-RSPV-group (14/44 vs. 0/524, p < 0.001). Intra-procedural AVB with 3.6 [1.9–8.2] second maximal RR intervals appeared in 12 patients during freezing (n = 1) or after balloon deflation following freezing (n = 11). The targeted PVs were the LSPV, left common PV, right inferior PV, and RSPV in 8, 1, 2, and 1 patients, respectively. The incidence was similar between the initial-LSPV and initial-RSPV-groups (1/44 vs. 11/524, p = 0.938). Four patients exhibited complete AVB with more than a 6 s maximal RR interval. Three patients experienced AVB during atrial fibrillation. AVB was observed a median of 23.0 [15.0–70.0] seconds after balloon deflation and 76.0 [60.0–125.0] seconds after freezing termination. AVB persisted for 56.0 [36.0–110.0] seconds, and all recovered spontaneously with or without requiring back-up pacing. ConclusionsA marked transient AV conduction disturbance could occur after balloon deflation, especially during LSPV ablation, regardless of the order of targeted PVs.

Time course and interrelationship of dysrhythmias in patients with surgically repaired atrial septal defect

Atrial fibrillation (AF) and other supraventricular tachycardias (SVTs) are known complications after surgical repair of atrial septal defect (ASD), but sinus node dysfunction (SND) and complete atrioventricular conduction block (cAVB) may also occur. The aim of this study was to examine time course and interrelationship of various dysrhythmias in patients with ASD. Adult patients (N = 95) with surgically repaired secundum ASD (n = 40), partial atrioventricular septal defect (n = 37) or sinus venosus defect (n = 18), and documented SND, cAVB, AF, and/or other SVT were included. The median age at repair was 13 years (interquartile range [IQR] 6-45 years), and patients were followed for 26 years (IQR 15-37 years) after ASD repair. SND was observed in 34 patients (36%), cAVB in 14 (14%), AF in 48 (49%), and SVT in 44 (45%); 37 patients (39%) had ≥2 dysrhythmias. All dysrhythmias presented most often after ASD repair (P < .01), with a median duration of 12 years (IQR 17days - 32 years) to 16 years (IQR 4 - 28 years) between repair and onset. Development of SND and cAVB late after ASD repair was not related to a redo procedure in 100% and 60% of patients, respectively. SND preceded atrial tachyarrhythmias in 50% (P=.31) and SVT preceded AF in 68% (P = .09) of patients with both dysrhythmias. A substantial number of dysrhythmias presented (very) late after ASD repair. In most patients, development of late SND and cAVB was not related to redo procedures. In patients with multiple dysrhythmias, a specific order of appearance was not observed.

The acute toxic effects of silver nanoparticles on myocardial transmembrane potential, INa and IK1 channels and heart rhythm in mice

This study focused on the potential toxicity of silver nanoparticles (AgNPs) on cardiac electrophysiology which is rarely investigated. We found that AgNPs (10−9–10−6 g/ml) concentration-dependently depolarized the resting potential, diminished the action potential, and finally led to loss of excitability in mice cardiac papillary muscle cells in vitro. In cultured neonatal mice cardiomyocytes, AgNPs (10−9–10−7 g/ml) concentration-dependently decreased the Na+ currents (INa), accelerated the activation, and delayed the inactivation and recovery of Na+ channels from inactivation within 5 min. AgNPs at 10−8 g/ml also rapidly decreased the inwardly rectifying K+ currents (IK1) and delayed the activation of IK1 channels. Intravenous injection of AgNPs at 3 mg/kg only decreased the heart rate, while at ≥4 mg/kg sequentially induced sinus bradycardia, complete atrio-ventricular conduction block, and cardiac asystole. AgNPs at 10−10–10−6 g/ml did not increase reactive oxygen species (ROS) generation and only at 10−6 g/ml mildly induced lactate dehydrogenase (LDH) release in the cardiomyocytes within 5 min. Endocytosis of AgNPs by cardiomyocytes was not observed within 5 min, but was observed 1 h after exposing to AgNPs. Comparative Ag+ (≤0.02% of the AgNPs) could not induce above toxicities. We conclude that AgNPs exert rapid toxic effects on myocardial electrophysiology and induce lethal bradyarrhythmias. These acute toxicities are likely due to direct effects of AgNPs on ion channels at the nano-scale level, but not caused by Ag+, ROS, and membrane injury. These findings provide warning to the nanomedical practice using AgNPs.

GW24-e2342 Normal QRS escape rhythm occurred after transit artificial complete heart block in a patient with dilated cardiomyopathy and complete left bundle branch block

ObjectivesNormal QRS Escape Rhythm Occurred after Transit Artificial Complete Heart Block in a Patient with Dilated Cardiomyopathy and Complete Left Bundle Branch BlockMethodsA male with 65 years old was admitted...

Patent foramen ovale and ventricular septal defect closure

Despite the growing recognition of the patent foramen ovale (PFO), particularly when associated with an atrial septal aneurysm, as risk factor for several disease manifestations (above all paradoxical embolism), the...

Plasma levels of B-type natriuretic peptide in children and adolescents with high degree atrioventricular block

B-type natriuretic peptide (BNP) was measured in 43 children and adolescents with high-grade second degree or complete atrioventricular conduction block. BNP plasma level was significantly higher ( p < 0.01) in patients without pacemaker ( n = 21) than in patients with permanent pacemaker ( n = 26). In all four patients with measurement of BNP both before and after placement of a permanent pacemaker, individual plasma BNP decreased. Additionally, patients with dual-chamber pacing had significantly lower BNP values compared to those with single chamber ventricular pacing ( p < 0.05). Conclusively, high degree atrioventricular block can induce elevated plasma BNP levels and the loss of atrioventricular synchrony induce a further increase of plasma BNP.

Delayed isolated hemothorax caused by temporary pacemaker: A case report

An 81-year-old male was admitted to our hospital with dysarthria. Electrocardiogram revealed complete atrioventricular conduction block and then temporary pacemaker was performed. Nine days later, massive hemothorax was presented, but not pericardial effusion existed by echocardiography and chest computer tomography findings. Being a rare complication of transvenous temporary pacemaker insertion, we discussed the delayed hemothorax without associated pericardial effusion.

Invited commentary

Invited commentary

Cardiac Conduction through Engineered Tissue

In children, interruption of cardiac atrioventricular (AV) electrical conduction can result from congenital defects, surgical interventions, and maternal autoimmune diseases during pregnancy. Complete AV conduction block is typically treated by implanting an electronic pacemaker device, although long-term pacing therapy in pediatric patients has significant complications. As a first step toward developing a substitute treatment, we implanted engineered tissue constructs in rat hearts to create an alternative AV conduction pathway. We found that skeletal muscle-derived cells in the constructs exhibited sustained electrical coupling through persistent expression and function of gap junction proteins. Using fluorescence in situ hybridization and polymerase chain reaction analyses, myogenic cells in the constructs were shown to survive in the AV groove of implanted hearts for the duration of the animal's natural life. Perfusion of hearts with fluorescently labeled lec-tin demonstrated that implanted tissues became vascularized and immunostaining verified the presence of proteins important in electromechanical integration of myogenic cells with surrounding re-cipient rat cardiomyocytes. Finally, using optical mapping and electrophysiological analyses, we provide evidence of permanent AV conduction through the implant in one-third of recipient animals. Our experiments provide a proof-of-principle that engineered tissue constructs can function as an electrical conduit and, ultimately, may offer a substitute treatment to conventional pacing therapy.

Childhood‐onset autosomal‐dominant limb‐girdle muscular dystrophy with cardiac conduction block

We report childhood-onset autosomal-dominant limb-girdle muscular dystrophy (LGMD) in a Chinese family with complete atrioventricular conduction block in the adult members. Six patients, including 5 men and 1 woman with an age of onset from 3 to 7 years, were affected. The grandfather had exercise intolerance since childhood and complete heart block with pace-maker placement at age 52. Three siblings had proximal muscle weakness and/or wasting since age 5 and heart block in their 40s. Two grandsons at the ages 7 and 3 showed exercise intolerance, and proximal muscle weakness and wasting. Sinus bradycardia was present in the elder grandson. Muscle enzymes were elevated in 3, particularly in childhood. Muscle biopsies from the proband showed myopathic changes with fatty degeneration, whorled fibers, and rimmed vacuoles. In adult patients, muscle magnetic resonance imaging scans disclosed atrophic changes and fatty degeneration in the gluteal, quadriceps, adductors, hamstrings, gastrocnemius, and soleus muscles, while in child probands the early atrophic changes were seen in the gluteal and hamstrings muscles. We conclude that this distinct family is characterized by childhood-onset autosomal-dominant LGMD with heart block and that prevention of sudden death in these patients is important. © 1997 John Wiley & Sons, Inc. Muscle Nerve, 20, 286–292, 1997.

A Case of Cardiac Amyloidosis with Complete Atrioventricular Conduction Block Treated by Permanent Pacemaker

A Case of Cardiac Amyloidosis with Complete Atrioventricular Conduction Block Treated by Permanent Pacemaker

Clinical significance of antibodies against neutrophils in patients with inflammatory bowel disease and primary sclerosing cholangitis.

The presence of perinuclear antibodies against neutrophils (pANCA) has been detected recently in sera of patients with inflammatory bowel disease and primary sclerosing cholangitis. In order to evaluate their clinical significance, sera from 126 patients with inflammatory bowel disease (80 Crohn's disease and 46 ulcerative colitis and 22 patients with primary sclerosing cholangitis were examined for pANCA by indirect immunofluorescence on liver sections and cytocentrifuge slides of neutrophils and by immunoblot. Perinuclear antibodies against neutrophils were found in 83% of patients with ulcerative colitis in 88% of patients with primary sclerosing cholangitis and inflammatory bowel disease, in 40% of patients with primary sclerosing cholangitis but without inflammatory bowel disease, and in 25% of patients with Crohn's disease using the immunofluorescence test. Titres of pANCA ranged from 1:10 to 1:1000 in ulcerative colitis and primary sclerosing cholangitis (median 1:100), whereas in Crohn's disease only four patients had titres of more than 1:10. The occurrence of pANCA did not correlate with clinical activity of Crohn's disease and primary sclerosing cholangitis whereas in ulcerative colitis high titres of pANCA were found mainly in active disease. Using an immunoblot system with sonified neutrophils as antigen, 82% of sera from patients with primary sclerosing cholangitis reacted with up to five different determinants, whereas only 12% of sera from patients with Crohn's disease and 11% of sera with ulcerative colitis detected one of the determinants, suggesting different antigens involved in pANCA reaction.

Termination of digitalis-induced ventricular tachycardias by clonidine involves central alpha 2-adrenoceptors in cats.

1. Effects of intravenous (i.v.) and intravertebral arterial (i.a.) administration of the alpha 2-adrenoceptor agonist, clonidine (Clon) and its antagonist, yohimbine (Yoh, 0.5 mg kg-1, i.v.; 0.05 mg kg-1, i.a.), on ventricular tachycardia (VT) induced by intravenous acetylstrophanthidin (AS) were studied in cats anaesthetized with intraperitoneal chloralose. 2. AS dose-dependently produced cardiac arrhythmias including complete atrioventricular conduction block (118 +/- 14 micrograms kg-1, i.v.), junctional tachycardia (128 +/- 20 micrograms kg-1, i.v.), multiform ventricular premature beats (157 +/- 21 micrograms kg-1, i.v.) and sustained VT (220 +/- 23 micrograms kg-1, i.v.). 3. Doses of Clon (i.v.) required for termination of VT following i.v. Yoh (62.9 +/- 5.2 micrograms kg-1) or i.a. Yoh (88.5 +/- 16.3 micrograms kg-1) were higher than those for termination of VT without Yoh administration (28.3 +/- 6.2 micrograms kg-1). Doses of Clon (i.a.) required for termination of VT without or with i.a. Yoh administration were 5.8 +/- 1.0 or 14.8 +/- 3.7 micrograms kg-1, respectively, and they were significantly different. 4. These experiments demonstrate that either i.v. or i.a. Yoh antagonizes the antiarrhythmic effect of Clon on AS-induced VT. Since small doses of Clon administered i.a. act predominantly on the central nervous system, we suggest that its antiarrhythmic effect is likely to be on central alpha 2-adrenoceptors in the central nervous system.

Acceleration of idioventricular rhythms by histamine in guinea pig heart: mediation by H2 receptors.

To evaluate the ability of histamine to induce ventricular arrhythmias, we studied the effects of histamine on ventricular rhythmicity in the isolated guinea pig heart with complete atrioventricular conduction block. As a function of dose (0.1-30 microgram), histamine enhanced the idioventricular rate by increasing the rate of firing of the original pacemaker and also by causing the sudden appearance of faster idioventricular rhythms that coincided with changes in pacemaker site. Anaphylaxis in the isolated guinea pig heart with complete atrioventricular conduction block caused histamine release and acceleration of idioventricular rate. The effects of histamine on idioventricular rhythmicity were not attenuated by the histamine H1 receptor antagonist chlorpheniramine, but were antagonized by the H2 receptor antagonist cimetidine. Moreover, the selective H2 agonist 4-methylhistamine (4MeH) accelerated the idioventricular rate, whereas 2-(2-thiazolyl) ethylamine (ThEA), at doses selective for H1 receptor activation, did not. The effects of histamine on idioventricular rhythmicity were not modified by the beta-adrenergic blocker pindolol. The mechanism by which histamine increases idioventricular rate probably involves two components: (1) an enhancement in automaticity of the original pacemaker, and (2) the induction of faster rhythms via reentry and/or afterdepolarizations. Whatever the mechanism, both components of the ventricular chronotropic action of histamine appear to involve exclusively histamine receptors of the H2 type. Thus, our results suggest that H2 receptor antagonists may have a role as specific antiarrhythmic agents in the treatment of cardiac dysfunctions caused by histamine release.