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At least 19 recordsLinked to original sources
PubMed1997

[Classification and pitfalls of atrioventricular blocks].

Atrioventricular blocks may be classified according to their degree, their site and their aetiology. Assessing the degree of block is not always easy when the P waves are poorly visible and/or masked by the ventricular complexes. Affirmation that a 2nd degree block is a Mobitz II block requires examination of the ECG to differentiate it from "false" Mobitz II due to variable PP intervals or concealed hisian extrasystoles. Complete atrioventricular block is easy to define on the ECG but not always synonymous with totally blocked conduction and should be interpreted taking into account the frequency of escape beats. Determining the site of block is important as it has therapeutic implications; the type of block evaluated from the surface ECG also provides useful but not always decisive information. The investigation of the aetiology of the block is valuable for differentiating acute, transient blocks from chronic (permanent or paroxysmal) blocks, the former sometimes requiring temporary but rarely permanent cardiac pacing.

Body Surface Potential Mapping↗
PubMed1997

Atrioventricular nodal reentrant tachycardia with atrioventricular block.

Atrioventricular block (AVB) during atrioventricular nodal reentrant tachycardia (AVNRT) has been well documented, although it is not a common phenomenon. The mechanism for the initiation and resolution of AVB during AVNRT have been postulated. However, the site of AVB and its implication on the reentrant circuit in AVNRT is not clear. We illustrate two examples of AVNRT with AVB and offer further clarification on the site and mechanism of AVB.

Adult↗
PubMed1991

Role of aminophylline in atropine resistant atrioventricular block.

Atrioventricular (AV) block may be induced by ischaemia as a result of production of adenosine, a metabolite that accumulates during hypoxia and ischaemia. Adenosine antagonism has been shown to reverse experimental AV node block in dogs. Recently, theophylline has been shown to be highly effective in diminishing the frequency and severity of bradycardia in newborn infants with apnoea-bradycardia spells. We report here a case of acute inferior wall myocardial infarction who developed atropine resistant AV block which was reversed by aminophylline, a competitive, antagonist of adenosine.

Aminophylline↗
PubMed1978

His bundle recordings in atrioventricular nodal alternating Wenchebach periods ending in 5:1 atrioventricular block coexisting with paroxysmal atrioventricular nodal block.

Atrioventricular nodal alternating Wenckebach periods ending in 5:1 atrioventricular block occurring during rapid atrial rhythms were explained by postulating the presence of block in three levels of the atrioventricular node. This pattern of conduction occurred in ten of 11 patients who either had received ouabain or verapamil (nine patients) or who had organic atrioventricular nodal disease (two patients). In contrast, this pattern of conduction occurred in only one of eight nonmedicated patients without organic atrioventricular nodal disease. The frequent association of this pattern with paroxysmal, tachycardia-dependent atrioventtricular nodal block suggested a similar, but not necessarily identical, mechanism. In conclusion, atrioventricular nodal alternating Wenckebach periods ending in 5:1 atrioventricular block, as well as paroxysmal atrioventricular nodal block, were only rarely the result of rapid atrial rates per se their occurrence indicating organic or pharmacologic effects on the atrioventricular node. Since both can be produced by carotid sinus pressure, further studies appear to be necessary to determine the role that vagal effects can have in their genesis.

Bundle of His↗
PubMed1983

[Binodal disease: diseased sinus node and atrioventricular block].

Atrioventricular (AV) conduction disturbances in patients (pts) with sick sinus syndrome (SSS) are well known, but sinus node function (SNF) in AV block is not well documented. We therefore performed electrophysiological tests to evaluate SNF in 30 pts with high-degree AV block (group 1) and AV conduction in 15 pts with SSS (group 1). These measurements were repeated after vagolysis with atropine in group 2. In group 1 ergometry was performed if the electrophysiological SNF tests were abnormal. Results (mean +/- 1 SD) for group 1 were: sinus node recovery time (SNRT) 1184 +/- 473 ms, corrected SNRT (cSNRT) 337 +/- 394 ms. In 3 pts SNRT or cSNRT was abnormal. In these 3 pts the response of sinus rate to exercise was insufficient. In group 2 SNRT before and after atropine was 2345 +/- 822 ms and 1558 +/- 815 ms respectively (p less than 0.05), cSNRT 1285 +/- 965 ms and 954 +/- 832 ms (n.s.), sinoatrial conduction time 319 +/- 283 ms and 150 +/- 149 ms (n.s.), and Wenckebach point 532 +/- 178 ms and 383 +/- 68 ms (p less than 0.01). His-ventricle time was 48 +/- 5.8 ms. In 6 of these 15 pts impaired AV-conduction was present (defined as Wenckebach point below 500 ms), but normalized in 4 pts after atropine. We postulate that persistence of abnormal SNF and AV conduction after vagolysis is an argument for organic binodal disease. This occurs with equal frequency in both groups in about 10% of patients. Increased vagal tone is common in SSS and uncommon in AV block. In patients with SSS the frequent additional AV conduction delay must be taken into consideration when atrial pacing is considered.

Adult↗
PubMed2003

Atrioventricular block during atrioventricular nodal reentrant tachycardia is not always benign.

A 70-year-old Japanese woman was admitted to our hospital because of transient second degree atrioventricular (AV) block. An electrophysiologic study (EPS) was performed, and Mobitz type II infra-Hisian block during atrial pacing at a rate of 130/min was noted. An AV nodal reentrant tachycardia (AVNRT) was induced by ventricular pacing at a rate of 180/min, and 2:1-3:1 infra-Hisian block during AVNRT was observed. The AV block and AVNRT rarely occurred in the clinical setting, and the patient did not complain of any symptoms related to these arrhythmias. Therefore, the patient refused permanent pacemaker implantation, although she continued to be followed in our outpatient clinic. However, the patient was re-admitted one year later because of palpitations and dyspnea upon exertion related to the AV block. The 12-lead ECG showed high degree AV block with narrow QRS complexes. The patient underwent pacemaker implantation during the subsequent hospitalization, and her symptoms improved postoperation. AV block during AVNRT is sometimes observed, and it has been considered as a functional AV block. In the present case, a pathologic conduction disturbance in the His-Purkinje system caused the high degree AV block during AVNRT. The high degree AV block during AVNRT may indicate the existence of a conduction disturbance in the His-Purkinje system in some of these types of cases.

Aged↗
PubMed1996

2:1 atrioventricular block during atrioventricular node reentrant tachycardia.

OBJECTIVES: The purpose of this study was to determine the incidence and to clarify the mechanism of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophysiology laboratory. BACKGROUND: In patients with 2:1 AV block during AV node reentrant tachycardia, the absence of a His bundle potential in the blocked beats has been considered evidence of intranodal, lower common pathway block. METHODS: In consecutive patients with AV node reentrant tachycardia, the incidence of 2:1 AV block and the response to atropine and a single ventricular extrastimulus was observed. RESULTS: Persistent 2:1 AV block occurred in 13 of 139 patients with AV node reentrant tachycardia. A His bundle deflection was present in the blocked beats in eight patients and absent in five. Patients with 2:1 AV block had a shorter tachycardia cycle length than did patients without such block (mean +/- SD 312 +/- 32 vs. 353 +/- 55 ms, p < 0.01). Atropine did not alter the 2:1 block in any patient. In every patient, a single ventricular extrastimulus introduced during the tachycardia converted the 2:1 block to 1:1 conduction. CONCLUSIONS: The incidence of induced 2:1 AV block during AV node reentrant tachycardia is approximately 10%. The lack of a response to atropine and the consistent conversion of 2:1 block to 1:1 conduction by a ventricular extrastimulus indicate that, regardless of the presence or absence of a His bundle potential in blocked beats, 2:1 block during AV node reentrant tachycardia is due to functional infranodal block.

Adult↗
PubMed1985

Disopyramide induced second and third degree atrioventricular block in patients with bifascicular block. An acute stress test to predict atrioventricular block progression.

Syncopal attacks in patients with bifascicular block may be due to both ventricular tachyarrhythmias and intermittent atrioventricular block in addition to non-cardiac causes and lead to antiarrhythmic treatment with drugs or pacemaker or both. The acute electrophysiological effect of intravenous disopyramide 2 mg/kg body weight given over five minutes on the His-Purkinje system was assessed in 27 patients with chronic bifascicular block undergoing evaluation for permanent pacemaker treatment. The predictive value of this pharmacological stress test as regards the development of atrioventricular block during follow up was analysed. The HV interval increased (mean 43%) and the QRS duration was prolonged (mean 24%). Intrahisian or infrahisian second or third degree atrioventricular block occurred in 14 patients after disopyramide administration, requiring temporary pacing in four of them. Before the electrophysiological study 15 of the 27 patients had had at least two syncopal attacks of suspected cardiac origin but no evidence of second or third degree atrioventricular block. Second or third degree atrioventricular block was subsequently recorded in five of these 15 patients during a mean of two years follow up. The sensitivity, specificity, and predictive value of second or third degree atrioventricular block produced by disopyramide administration including subsequent atrial pacing--a positive disopyramide test--as regards later development of atrioventricular block were 80%, 90%, and 80% respectively. Intravenous administration of disopyramide to patients with bifascicular block and syncopal attacks of suspected cardiac origin may provoke atrioventricular block and asystole requiring immediate temporary pacing. Furthermore, a positive disopyramide test seems to have a significant value in predicting the later development of atrioventricular block.

Adult↗
PubMed1999

[Congenital atrioventricular block].

Congenital atrioventricular block is defined (Yater) as a documented conduction defect in a young subject with unquestionable bradycardia in the absence of a history of infection which might have caused the condition after birth. It is a rare condition (1 out of 20,000 births) and may be isolated or associated with another congenital malformation. Four cardiac malformations are classically associated: endomyocardial fibrosis, morphological abnormalities close to the conduction system: corrected transposition, left isomerism; patent ductus arteriosus and atrial septal defect apparently unrelated but the most common; the association of mitral regurgitation in adults, although the significance is not very clear. Isolated block is often observed in patients with mothers suffering from autoimmune disease, often clinically latent. Anti Ro/SS-A and La/SS-B antibodies cross into the foetal circulation and cause inflammation of the conduction tissues but the causal mechanism is not known. The diagnosis of the conduction defect is sometimes made during foetal life by echocardiography. After birth, the diagnosis is made by electrocardiography but the block is not always complete or permanent, its degree often increasing with time. In addition, in advanced degrees of block, the escape rhythm tends to slow down. Long-term follow-up studies have revised the previously considered good prognosis of isolated congenital atrioventricular block but advances in cardiac pacing provide satisfactory treatment. In the foetus, isolated atrioventricular block is usually associated with an escape rhythm > 60/min and enables normal vaginal delivery; a low heart rate < 55/min and anasarca carry a poor prognosis. In the neonate, pacing is indicated in babies with cardiac failure and a heart rate < 55/min. Follow-up by Holter monitoring, exercise testing and echocardiography is justified in children and adolescents; the patients may become symptomatic at any age. Pacing is essential in symptomatic cases (malaise, ventricular dysfunction) and useful in cases with long QT intervals, frequent ventricular extrasystoles and wide ventriculogrammes. Pacing is not always easy in children. Epicardial pacing by thoracotomy or an epigastric approach is possible but endocavitary pacing is to be preferred using thin pacing catheters introduced via the subclavian vein and small pacemakers implanted in a sub or prepectoral site. A pacing mode which restores the normal atrioventricular sequence is theoretically superior to single ventricular pacing even if rate responsive frequency.

Adult↗
PubMed2001

[Complete congenital atrioventricular block].

Congenital atrioventricular block is defined (Yater) as a documented conduction defect in a young subject with unquestionable bradycardia in the absence of a history of infection which might have caused the condition. This condition may be isolated or associated with structural cardiac disease. Isolated block is often observed in patients with mothers suffering from autoimmune disease, often clinically latent. Anti-Ro/SS-A and La/SS-B antibodies cross into the fetal circulation and cause inflammation of the fetal conduction system. The diagnosis of the conduction defect is sometimes made during fetal life by echocardiography. Echocardiography assesses fetal hemodynamic status and may detect signs of fetal deterioration. Long-term follow-up studies have revised the previously considered good prognosis of isolated congenital atrioventricular block but advances in cardiac pacing provide satisfactory treatment. Follow-up by Holter monitoring, exercise testing and echocardiography is justified in children and adolescents; the patients may become symptomatic at any age. Indications for permanent pacing in pediatric patients have been difficult to determine due to the lack of data from controlled studies and multicenter trials. Pacing is not always easy in children. Epicardial pacing is advocated in small patients (< 5 years of age or 30 kg in weight). A pacing mode which restores the normal atrioventricular sequence is theoretically superior to single ventricular pacing even with rate responsive frequency.

Adolescent↗