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PubMed1999

[Atrioventricular block secondary to topical ophthalmic beta blockers].

It is known that ophthalmic beta-blockers can induce atrioventricular block. In our series of 243 patients with atrioventricular block, 12 were treated with topic ophthalmic timolol. None of them recognized the eye-drops as a treatment. In 7 cases the sinus rhythm was recovered and in 5 a pacemaker was implanted. There is a significant percentage of atrioventricular blocks produced by the ophthalmic beta-blockers that the patient does not recognize as treatment, and 60% of them are reversible. It is important to ask about the use of eye-drops in patients with bradycardia or atrioventricular block.

Adrenergic beta-Antagonists↗
PubMed2002

Optimal ventricular pacing rate in fetal lambs with complete atrioventricular block.

OBJECTIVE: This study was undertaken to determine the optimum ventricular pacing rate at which the optimal cardiac function can be attained in fetal lambs with complete atrioventricular block. STUDY DESIGN: Complete atrioventricular block was created by cryosurgery in 12 fetal lambs, and the ventricle was paced randomly at rates of 60, 90, 120, 150, 180, 210, 240, and 270 beats/min. The aortic pressure, central venous pressure, and right ventricular cardiac output were measured before cryosurgery and during ventricular pacing. RESULTS: Complete atrioventricular block was created in 9 of 12 fetal lambs. Systolic aortic pressure significantly decreased at pacing rates of 60, 90 and 240 beats/min (P <.01), and central venous pressure was increased significantly at a pacing rate of 60 beats/min (P <.01) compared with the control. Right ventricular cardiac output significantly decreased at pacing rates of 60, 90, 120, 180, 210, 240, and 270 beats/min (P <.01), although no significant difference was found at the pacing rate of 150 beats/min compared with control. CONCLUSION: Ventricular pacing at a rate of 150 beats/min gave the highest aortic pressure, the lowest central venous pressure, and the highest right ventricular cardiac output in fetal lambs with complete atrioventricular block.

Animals↗
PubMed1976

Pseudo second degree atrioventricular block with bradycardia. Successful treatment with quinidine.

Pseudo second degree atrioventricular block resulting from blocked His premature beats was successfully treated with quinidine. The diagnosis was proved by His bundle electrogam which showed both blocked and conducted His premature beats. The blocked His prematures produced second degree atrioventricular block by making the atrioventricular junction refractory. Quinidine abolished both conducted and blocked His extrasystoles. There has been no recurrence of arrhythmia during a one-year follow-up.

Bradycardia↗
PubMed2006

[Permanent His-bundle pacing in patients with infra-Hisian atrioventricular block].

INTRODUCTION AND OBJECTIVES: Permanent His-bundle pacing is effective in patients with supra-Hisian atrioventricular block. We report our experience in patients with infra-Hisian atrioventricular block. METHODS: The study involved selected patients referred for syncope and intraventricular conduction disturbance, infra-Hisian atrioventricular block, with left ventricular dyssynchrony and no coronary sinus access. All patients underwent electrophysiological study to evaluate infra-Hisian atrioventricular conduction, both at baseline and after flecainide administration. We selected patients with an indication for permanent pacing in whom His-bundle pacing produced a narrow QRS complex. Leads were implanted in the right atrium, in the bundle of His, and at the apex of the right ventricle, and connected to the atrial, left ventricular, and right ventricular terminals, respectively, of a biventricular pacemaker generator. All pacemakers were programmed in DDD mode with a left ventricle-right ventricle interval of 80 ms. RESULTS: Between February and December 2004, seven patients met the study's inclusion criteria. The His-bundle lead was implanted successfully in five. The His-bundle pacing threshold remained stable in two patients, whereas it increased in three. During follow-up, at between 2 and 12 months, no lead dislodgement or failure to capture was observed. Echocardiography did not disclose any deterioration in ventricular function, or any worsening of or new valvular incompetence, but showed that ventricular dyssynchrony had disappeared in previously affected patients. CONCLUSIONS: His-bundle pacing is the only pacing mode capable of inducing a physiologically normal ventricular contraction. It can be used in some patients with infra-Hisian atrioventricular block.

Bundle of His↗
PubMed2002

Location and clinical implications of high-degree atrioventricular block during dipyridamole infusion: a case report.

We describe a patient with bifascicular block, who developed transient high-degree atrioventricular block during dipyridamole infusion. This patient was subsequently found to have significant His-Purkinje disease at electrophysiology study, and underwent permanent pacemaker implantation. Spontaneous atrioventricular block was documented during follow-up. This case report raises the issue of dipyridamole safety in patients with intraventricular conduction defects, and contributes an additional mechanism to the possible explanation of dipyridamole-induced atrioventricular block.

Aged↗
PubMed1976

Congenital complete atrioventricular block and prolapsing mitral valve.

Congenital complete atrioventricular block and prolapsing mitral valve are described in a 41-year-old woman who exhibited ventricular arrhythmias and symptoms initially attributed to her atrioventricular block. The importance of physical examination to elicit clues in the diagnosis of prolapsing mitral valve is emphasized.

Adult↗
PubMed1995

Third degree atrioventricular block and acquired myasthenia gravis in four dogs.

Third degree atrioventricular block was diagnosed in 4 dogs with acquired myasthenia gravis (serum acetylcholine receptor antibody titer > 0.6 nmol/L). All 4 dogs had megaesophagus. Two dogs also had mediastinal thymomas, which were resected. One dog with thymoma received a permanent pacemaker at the same time that it underwent thymectomy; the other did not develop third degree atrioventricular block until 3 months after thymectomy. Both dogs with thymoma died of severe aspiration pneumonitis within 3 months after surgery. The third dog received a permanent pacemaker and was treated with pyridostigmine bromide, but also died of aspiration pneumonitis 1 month after the pacemaker was implanted. The fourth dog was treated with prednisolone and pyridostigmine bromide and improved, but did not become clinically normal. Because third degree atrioventricular block as well as myasthenia gravis can cause signs of weakness, acquired myasthenia gravis should be considered in dogs with idiopathic cardiac conduction disturbances. Likewise, an ECG should be evaluated in dogs with acquired myasthenia gravis.

Animals↗
PubMed1996

Congenital complete atrioventricular block: asymptomatic at 38 years.

Congenital complete atrioventricular block is quite rare, with usually a benign clinical evolution. However, because the first manifestation can be sudden death, it is important to evaluate patients and to establish clear prognostic criteria. A case of complete congenital atrioventricular block in a 38-year-old woman is presented to illustrate these criteria.

Adult↗
PubMedDate not supplied

Primary cardiac lymphoma with infiltration of the atrioventricular node: remission with reversal of the atrioventricular block induced by chemotherapy.

We describe a rare case of primary cardiac lymphoma associated with complete atrioventricular block, with recovery following systemic chemotherapy. A 61 year-old woman was admitted because of a massive pericardial effusion and complete atrioventricular block. Echocardiography disclosed several polypoid masses in the right atrium. A diagnosis of primary cardiac lymphoma was made. After three cycles of chemotherapy, the patient achieved a complete remission, the ECG showed first-degree atrioventricular block, and echocardiography revealed disappearance of the right atrial masses. This is the first report of a patient recovering from primary cardiac lymphoma and complete atrioventricular block following systemic chemotherapy. We conclude that aggressive treatment of this malignancy can improve cardiac function and the patient's prognosis.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1982

Anatomic substrate for congenital atrioventricular block in middle-aged adults.

Congenital atrioventricular block is usually a benign disorder not necessitating pacing. In some patients slowing of rate and/or mortality have been noted with aging. However an anatomic substrate has not been established for the progressive slowing of the escape rate. In this study we report an anatomic substrate in two such patients who were dying in congestive heart failure, ages 49 and 42, respectively. Multiple pre-mortem ECG's in both cases revealed wide QRS escape rhythms, and escape rates of approximately 35 and 28 beats/minute, respectively. Conduction system examination by serial section in both cases revealed lack of connection between the atrial septum with the peripheral conduction system with total replacement by fat of the AV nodal approaches and AV node, and advanced sclerosis of the summit of the ventricular septum which was more marked on the right side. In addition, the His bundle showed marked septation in case one and fragmentation in case two. Sclerosis of the summit of the ventricular septum involved the branching bundle and the bundle branches in both cases. In conclusion, both patients had the characteristic lesions of congenital atrioventricular block, namely replacement of the AV node and AV nodal approaches by fat, with lack of connection to the peripheral conduction system, and one also had a fragmented His bundle. In addition premature aging of the summit of the ventricular septum may have reflected the long-standing hemodynamic stresses of chronic bradycardia. This in turn resulted in trifascicular involvement of the conduction system leading to a shifting of the escape rhythm distally eventuating in a slower idioventricular escape rhythm.

Adult↗
PubMed2005

[Duration of complete atrioventricular block complicating inferior wall infarction treated with fibrinolysis].

INTRODUCTION AND OBJECTIVES: The aim of this study was to determine the duration of complete atrioventricular block complicating inferior wall acute myocardial infarction after the administration of fibrinolytic therapy. PATIENTS AND METHOD: From 1 January 1992 to 31 January 2002 a total of 449 patients were admitted directly to our hospital with inferior wall acute myocardial infarction in the first 6 hours; 282 of them (64%) received fibrinolytic therapy. Complete atrioventricular block appeared in 39 of these 282 patients (13.8%, group A). Of the 167 patients who did not receive thrombolytic therapy, complete atrioventricular block appeared in 13 (8%, control group). We compared the two groups by analyzing the duration of heart block, time to appearance, hemodynamic repercussion, and treatment required. RESULTS: On admission, 38% of the patients in group A and 61% (P=NS) of those in the control group had complete atrioventricular block. Median duration of the block was 75 minutes (10 minutes to 48 hours) in group A and 24 hours (15 minutes to 9 days) in the control group (P=.004). After fibrinolytic therapy was administered, median duration of the block was 45 minutes (5 minutes to 48 hours). A temporary pacemaker was implanted in 43% of the group A patients and 84.6% of the control group patients (P=.01). CONCLUSION: Complete atrioventricular block appears as a complication of inferior myocardial infarction within the first hours after the event. Duration of the block seems to be shorter in patients treated with fibrinolytic therapy.

Aged↗
PubMed1990

Prognostic significance of complete atrioventricular block in patients with acute inferior myocardial infarction with and without right ventricular involvement.

Data were obtained and analyzed in 243 patients with acute inferior myocardial infarction who were admitted to the coronary care unit during the years 1987 and 1988. One hundred and ninety-eight patients had no signs of right ventricular involvement (group I), whereas 45 patients had inferior myocardial infarction with right ventricular infarction (group II). Patients were divided into groups depending on the presence or absence of complete atrioventricular block during hospital stay (groups Ia and IIa without block and groups Ib and IIb with block). Selected clinical and laboratory variables were compared for each group. We found that patients with inferior myocardial infarction and complete atrioventricular block had significantly higher mortality rates only in the presence of right ventricular infarction: 41% mortality rate in group IIb versus 11% mortality rate in group Ib (p less than 0.05). Patients with right ventricular infarction but without complete atrioventricular block (group IIa) had a mortality rate similar to that found in patients with inferior myocardial infarction and no atrioventricular block (group Ia): 14% versus 11% (p = NS). In patients with inferior myocardial infarction without right ventricular involvement (group I), complete atrioventricular block did not influence survival: 14% mortality rate in group Ib versus 11% mortality rate in group Ia (p = NS). The excessively high mortality rate in patients who have inferior myocardial infarction with right ventricular involvement and complete atrioventricular block could be the consequence of greater infarct size, but the synergistic influence of right ventricular infarction and complete atrioventricular block could be the other factor that influences outcome.

Cause of Death↗
PubMed1994

Atrial natriuretic peptide release from the ventricles in response to exercise in dogs with atrioventricular block.

The purpose of this study was to examine atrial natriuretic peptide (ANP) secretion at rest and in response to moderate treadmill exercise (10 min, 4 km/h, 26% slope) in control dogs (n = 17) and in dogs (n = 14) with complete atrioventricular block produced by electrocauterization of the His bundle. Atrial rates were similar in both groups (103 +/- 13 vs. 102 +/- 9 beats/min at rest and 162 +/- 10 vs. 160 +/- 17 beats/min at exercise in control dogs and in dogs with atrioventricular block, respectively; mean +/- SE), but ventricular rate was markedly lower in dogs with atrioventricular block (47 +/- 9 and 61 +/- 10 beats/min at rest and exercise, respectively). The lower ventricular rate was associated with an increased cardiac preload, as evidenced by the higher right atrial pressure in dogs with atrioventricular block at rest (2.2 +/- 1.4 vs. 1.1 +/- 0.9 mmHg; p < 0.05) and exercise (7.6 +/- 3.1 vs. 4.2 +/- 1.7 mmHg; p < 0.05). Arterial plasma ANP concentrations were markedly higher at rest (151 +/- 21 vs. 36 +/- 10 pg/mL; p < 0.05) and exercise (353 +/- 31 vs. 72 +/- 17 pg/mL; p < 0.05) in dogs with atrioventricular block. This observation supports the hypothesis that atrial wall stretching is a major stimulus for ANP release at rest and exercise. Ventricular release of ANP could also contribute to the higher plasma ANP concentrations observed both at rest and during exercise in dogs with complete atrioventricular block. Indeed, a large ANP concentration gradient was measured between the aorta and the distal part of the coronary sinus in these dogs at rest (227 +/- 55 pg/mL) and exercise (240 +/- 57 pg/mL) but not in control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Theophylline for the treatment of atrioventricular block after myocardial infarction.

OBJECTIVE: To show that second- or third-degree atrioventricular block occurring as an early complication of acute inferior myocardial infarction is mediated by adenosine. SETTING: Cardiac care unit. DESIGN: Uncontrolled, observational, hypothesis-driven study. PATIENTS: Patients who developed clinically significant atrioventricular nodal blockade within 4 hours of admission for acute inferior myocardial infarction. INTERVENTION: Theophylline, 100 mg/min intravenously to a maximum of 250 mg. MEASUREMENTS: Continuous multilead electrocardiographic monitoring before and after administration of theophylline. RESULTS: During a 6-month period, eight men who had had acute inferior myocardial infarction developed clinically significant atrioventricular block. Three had third-degree block, and five had high-grade second-degree block. In all patients, 1:1 atrioventricular nodal conduction was restored and normal sinus rhythm reappeared within 3 minutes of the administration of theophylline. All patients remained free of arrhythmia for at least 24 hours. CONCLUSIONS: Adenosine produced by the ischemic myocardium may induce atrioventricular nodal block. In our patients, atrioventricular nodal block was resistant to conventional therapy such as atropine, but it responded to the adenosine antagonist theophylline.

Adenosine↗
PubMed1977

Second-degree atrioventricular block in the His-Purkinje system following acute myocardial infarction. Clinical observations on its evolution.

The evolution of second-degree atrioventricular block in the His-Purkinje system was studied in four patients with acute myocardial infarction, utilizing continuous electrocardiographic monitoring and serial His bundle recordings. Three patients had anterior wall infarction; all developed acute right bundle-branch block and two also showed a left anterior hemiblock one to four hours prior to onset of second-degree atrioventricular block. The fourth patient had an old anteroseptal infarction and chronic right bundle-branch block and left anterior hemiblock; he developed second-degree atrioventricular block following an acute lateroposterior infarction. His bundle electrograms were obtained during the insertion of a temporary ventricular pacemaker within the first 24 hours of onset of chest pain. A second His bundle electrogram was obtained during removal of the temporary paceemaker 7 to 14 days after the first recording. In all cases the block was localized in the His-Purkinje system. In three patients the first His bundle recording showed second-degree atrioventricular block with minimal increment of delay in conduction (3 to 10 msec) prior to the blocked beat (equivalent of Mobitz type 2 block). The second His bundle electrogram showed the development of significant increment of delay in conduction (35 to 210 msec) prior to block (equivalent of Wenckebach conduction). The fourth patient illustrated the reverse order of the observations seen in the other three. Three patients showed resumption of 1:1 atrioventricular conduction; however, when one patient was challenged with rapid atrial pacing, he developed repetitive block in the His-Purkinje system.

Aged↗
PubMed1997

Hypertrophic cardiomyopathy presenting with 3rd-degree atrioventricular block.

A 15-year-old boy presented with exercise intolerance and near syncope. Electrocardiography showed 3rd-degree atrioventricular block. He was treated emergently with temporary transvenous ventricular pacing. Two-dimensional echocardiography revealed hypertrophic cardiomyopathy. Subsequently, a permanent, transvenous, dual-chamber pacemaker was implanted. Hypertrophic cardiomyopathy rarely causes complete atrioventricular block. It is particularly unusual for the presenting symptoms of hypertrophic cardiomyopathy to be caused by atrioventricular block. The case report is followed by a review of the pediatric literature on hypertrophic cardiomyopathy with atrioventricular block.

Adolescent↗
PubMed1998

Effect of multiple doses of oral isradipine on atrioventricular conduction in patients with first-degree atrioventricular block.

The purpose of this study was to investigate the effect of multiple doses of orally administered isradipine on atrioventricular nodal conduction in patients with first-degree atrioventricular block. Forty-eight patients with a P-R interval > or =0.22 seconds on a surface electrocardiogram (ECG) (first-degree atrioventricular block) with or without a bundle-branch block were randomized to one of four groups for 6 weeks of treatment with either placebo or 5.0 mg/d, 7.5 mg/d, or 10.0 mg/d isradipine. P-R interval prolongation was assessed at baseline and posttreatment using resting 12-lead ECGs and 24-hour Holter monitoring. The effect of isradipine on the following parameters were assessed: systolic and diastolic blood pressures, heart rate, respiration rate, oral temperature, and weight. Neither isradipine nor placebo treatment had a statistically significant treatment effect on the change from baseline in P-R interval, QRS duration, Q-T interval (uncorrected), or sinus heart rate at week 7 as measured by 12-lead ECG. All treatment groups, however, had small, statistically insignificant decreases from baseline in the mean P-R interval. The largest decrease (from 0.26 seconds at baseline to 0.22 seconds at week 7) was recorded for the 7.5 mg/d isradipine group, which also had the greatest posttreatment decreases in QRS duration, sinus heart rate, and systolic and diastolic blood pressures. The treatment groups did not differ significantly with respect to the change from baseline to study end in P-R interval prolongation or degree of atrioventricular block (as measured by 24-hour Holter monitoring), radial pulse rate, respiration rate, weight, or oral temperature. In this study, isradipine did not have a negative dromotropic effect on the atrioventricular node. The trend toward a posttreatment decrease in P-R interval suggests that isradipine may actually improve atrioventricular nodal conduction in patients with first-degree atrioventricular block and thus may be used safely in this population.

Administration, Oral↗