Definitions and Pitfalls in the Diagnosis of Atrioventricular Block.

The widespread use of disparate definitions of atrioventricular block has created important diagnostic problems. Adherence to the correct definitions provides a logical and simple framework for clinical evaluation. This review focuses on the clinical importance of the definitions in the diagnosis of the various types of atrioventricular (AV) block and the associated diagnostic pitfalls.

Five cases of complete atrioventricular block induced by bending forward: unusual but not unique.

AIMS: We describe five patients with syncope caused by a complete atrioventricular block (AVB) while they were bending forward, not rising after bending, and aim to describe the occurrence and the association between bending forward and AVB. METHODS AND RESULTS: In two patients, bending forward was the exclusive trigger for syncope, while in the remaining three, other postural changes (sitting down, standing up, and exertion) could also provoke syncope. Complete AVB as the cause of syncope was documented using ECG monitoring in two cases and an implantable loop recorder in the other three. Ectopic beats without preceding sinus slowing occurred before syncope in four cases. Two cases had a left bundle branch block. All patients responded favourably to cardiac pacing. CONCLUSION: This is the first case series on complete AVB provoked by bending forward. Syncope during bending forward should suggest a search for an AVB. Arguments in favour of a vagal mechanism were syncope triggered by bending forward, and that other triggers could also evoke syncope. However, the absence of sinus slowing before syncope in some cases and the fact that bending forward did not seem to provoke reflex syncope without AVB, cast doubts on a reflex mechanism. There were also arguments favouring conduction disorder: i.e. ectopic beats before syncope and pre-existing conduction disturbances in two cases. The cases are reminiscent of paroxysmal AVB. Discrimination between paroxysmal AVB and vagal AVB is important because a pacemaker is warranted in arrhythmic complete AVB, while the benefit is limited or absent in reflex AVB.

Atrioventricular block precipitated by isoproterenol.

An isoproterenol infusion was administered during an electrophysiologic study (EPS) in a patient with a history of near syncope, left bundle branch block, and no documented atrioventricular (AV) block. Isoproterenol precipitated classic 2:1 Infra-Hisian AV block most probably proximal to the site of recording a His-Purkinje potential consistent with right bundle branch activity. Paroxysmal AV block also occurred during isoproterenol washout at a different site located distal to the presumed right bundle branch potential. Isoproterenol may be valuable diagnostically in an occasional patient suspected of AV block in whom an EPS is unrevealing and a drug challenge is negative.

Second-degree atrioventricular block induced by electrical stimulation of transcranial motor-evoked potential: a case report.

BACKGROUND: Although several complications of transcranial motor-evoked potentials (Tc-MEPs) have been reported, reports of arrhythmias during Tc-MEP are very rare. CASE PRESENTATION: A 71-year-old woman underwent transforaminal lumbar interbody fusion under general anesthesia, with intraoperative Tc-MEP monitoring. Preoperative electrocardiography showed an incomplete right bundle branch block but no cardiovascular events in her life. After induction of anesthesia, Tc-MEP was recorded prior to the surgery. During the Tc-MEP monitoring, electrocardiography and arterial blood pressure showed a second-degree atrioventricular block, but it improved rapidly at the end of the stimulation, and the patient was hemodynamically stable. Tc-MEP was recorded seven times during surgery; the incidence of P waves without QRS complexes was significantly higher than before stimulation. The surgery was uneventful, and she was discharged eight days postoperatively without complications. CONCLUSIONS: Our case suggests that electrical stimulation for Tc-MEP can cause arrhythmia. Electrocardiography and blood pressure must be closely monitored during Tc-MEP monitoring.

Paroxysmal atrioventricular block induced during paroxysmal intra-atrial reentrant tachycardia.

Paroxysmal atrio-ventricular (AV) block is a relatively rare form of bradyarrhythmia that may be caused by vagal reflex, intrinsic His-Prukinje system (HPS) disorder, or idiopathic mechanisms. We report a case with paroxysmal AV block and syncopal episodes that appeared only during intra-atrial reentrant tachycardia (IART) after an ablation procedure. Syncope did not occur under sinus rhythm with stable 1:1 AV conduction. An HPS disorder was proven in an electrophysiological study. It was suggested that paroxysmal AV block was induced via a tachycardia-dependent mechanism with an exacerbation of latent HPS disorder. The occurrence of the IART was only transient, and there was no recurrent syncope during one-year follow-up. Pacemaker implantation could be avoided. .

The Longer the Block, the Harder You Fall: Extrinsic Idiopathic Atrioventricular Block Masquerading as Seizures.

History and physical examination are the diagnostic cornerstones of transient loss of consciousness (TLOC). However, details can be scarce and examination unrevealing, thus making the diagnosis elusive. In a case of convulsive TLOC, the initial diagnosis was incorrect, but a fortuitously captured event on telemetry yielded the diagnosis: extrinsic idiopathic atrioventricular block. (Level of Difficulty: Beginner.).

A case of paroxysmal atrioventricular block with atrial pacemaker shift during ventricular arrest.

We present a case of paroxysmal atrioventricular block with atrial pacemaker shift, focusing on the change of P-wave morphology.

Clinical and electrophysiological characteristics of patients with paroxysmal intra-His block with narrow QRS complexes.

BACKGROUND: Atrioventricular (AV) block is usually due to infranodal disease and associated with a wide QRS complex; such patients often progress to complete AV block and pacemaker dependency. Uncommonly, infranodal AV block can occur within the His bundle with a narrow QRS complex. OBJECTIVES: The aims of this study were to define clinical/echocardiographic characteristics of patients with AV block within the His bundle and report progression to pacemaker dependency. METHODS: We retrospectively identified patients with narrow QRS complexes and documented intra-His delay or block at electrophysiology study (group A) or with electrocardiogram-documented Mobitz II AV block/paroxysmal AV block (group B). Clinical, electrophysiological, and echocardiographic variables at presentation and pacemaker parameters at the last follow-up visit were evaluated. RESULTS: Twenty-seven patients (19 women) were identified (mean age 64 ± 13 years; range, 38-85 years). Four patients who had <1 month of follow-up were excluded. There were 12 patients in group A and 11 in group B; 21 of 23 presented with syncope/presyncope. All patients received pacemakers: 8 single chamber and 15 dual chamber. After a median follow-up of 6.4 years, the median percentage of ventricular pacing was 1% (interquartile range 0%-4.66%). One patient developed true pacemaker dependency. Aortic and/or mitral annular calcification was present in 13 of 22 patients with available echocardiograms. CONCLUSION: Patients who present with syncope and narrow QRS complexes with intra-His delay or Mobitz II paroxysmal AV block with narrow QRS complexes rarely progress to pacemaker dependency and require infrequent pacing. This entity is more common in women, with a higher prevalence of aortic and/or mitral annular calcification. If confirmed by additional studies, single-chamber pacemaker may be sufficient.

Syncope and paroxysmal atrioventricular block.

Current literature reveals three types of paroxysmal atrioventricular block (AVB) that can cause syncope: Intrinsic paroxysmal atrioventricular block is due to an intrinsic disease of the AV conduction system; this type of "cardiac syncope" is also called Stokes-Adams attack; Extrinsic vagal paroxysmal atrioventricular block is linked to the effect of the parasympathetic nervous system on cardiac conduction and is one of the mechanisms involved in "reflex syncope." Extrinsic idiopathic paroxysmal atrioventricular block is associated with low levels of endogenous adenosine and is supposed to be one of the mechanisms involved in "low-adenosine syncope." These three types of paroxysmal AVB present different clinical and electrocardiographic features. Additionally, the efficacy of cardiac pacing and theophylline therapy to prevent syncopal recurrences is also different for these three types of AVB.

Perservative paroxysmal atrioventricular block : Cardiac syncope misdiagnosed as anxiety for more than 20 years.

A 42-year-old woman was referred for cardiac diagnostic work-up of loss of recurrent consciousness over the past 25 years. She received medication with an anxiolytic, an antidepressant, and a neuroleptic drug. After a normal resting ECG, there were 112 episodes of paroxysmal atrioventricular block III° in her 24 h Holter recording with asystole for up to 27 s. The patient was symptomatic only once with dizziness due to an asystole of 8.8 s while she was awake in the early morning. After DDDR pacemaker implantation, the patient was asymptomatic during the following 2 years. This case illustrates the complex and not fully understood problem of paroxysmal AV block, in this instance neither intrinsic, nor phase 4 or vagally induced. It further reminds us to carefully clarify the cause of loss of consciousness consistently which may render prolonged ECG monitoring necessary also in patients without heart disease.

A proposal of clinical ECG index "vagal score" for determining the mechanism of paroxysmal atrioventricular block.

BACKGROUND: Paroxysmal atrioventricular block (P-AVB) is a well-known cause of syncope; however, its underlying mechanism is difficult to determine. This study aimed to evaluate a new ECG index, the "vagal score (VS)," to determine the mechanism of P-AVB. METHODS: We evaluated the VS in 20 patients with P-AVB (13 men, 7 women; aged 25-78 years [mean, 59.3 years]). The VS was developed by assigning 1 point each for the following: (1) no AVB or intraventricular conduction disturbance on the baseline ECG, (2) PR prolongation immediately before P-AVB, (3) sinus slowing immediately before P-AVB, (4) initiation of P-AVB by PP prolongation, (5) sinus slowing during ventricular asystole, and (6) resumption of AV conduction with PP shortening, and by assigning -1 point each for (7) the initiation of P-AVB by a premature beat, and (8) resumption of AV conduction by an escape beat. Based on the clinical situations and electrophysiologic findings, we considered the mechanism of P-AVB as vagally mediated or intrinsic conduction disease (ICD). RESULTS: The VS ranged from 5 to -2 points for each patient. Five patients with a definite vagally mediated P-AVB had high VSs (3-5 points). We observed characteristic ECG findings of ICD consisting of changes in AV conduction by an extrasystole and/or escape beat in only 5 of the 6 patients (83%) with a low VS (1 to -2). CONCLUSIONS: The VS is simple and potentially useful for determining the mechanism of P-AVB. P-AVB with a VS ≥3 strongly suggested a vagally mediated mechanism.