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At least 19 recordsLinked to original sources
PubMed1993

Neonatal lupus erythematosus syndrome: late detection of isolated heart block.

Heart block in neonatal lupus erythematosus is typically complete and detected in utero or in the neonatal period. We describe a child diagnosed with incomplete heart block at 9 years of age whose mother was diagnosed with Sjögren's syndrome and anti-Ro(SSA) 2 years after diagnosis of heart block in her child. This is the first case of late detection of incomplete heart block in a child felt to be causally related to the presence of anti-Ro(SSA) in the mother.

Autoantigens↗
PubMed2003

Complete heart block during central venous catheter placement in a patient with pre-existing left bundle branch block.

Heart block and arrhythmia are complications of pulmonary artery and cardiac catheterization. Injury to the conducting system of the heart often involves the right bundle causing right bundle branch block (RBBB). If patients already have left bundle branch block (LBBB), complete heart block (CHB) may result. After trauma, impairment of the right bundle is usually transient with recovery in hours, but complete heart block can lead to symptoms requiring invasive treatment. Similar complications are rare with insertion of central venous catheters, as they should not enter the heart. Injury to the right bundle during central venous catheter insertion can be by trauma from the guide wire or from the catheter itself. The function of the AV node and bundle of His in these patients has not been studied before. We report a patient with LBBB who developed CHB during insertion of a central venous cannula. Conduction through the AV node and His-Purkinje system was intact, showing that the transient RBBB was caused by traumatic injury rather than by other disease of the conduction system.

Bundle-Branch Block↗
PubMed1994

Exercise-induced complete heart block in a patient with chronic bifascicular block.

Heart block induced by exercise or associated with symptomatic, chronic bifascicular block can progress to high-grade atrioventricular (AV) block and sudden death. The authors describe a case of exercise-induced AV block in a patient with chronic bifascicular block. Thirty seconds of ventricular asystole were observed during exercise treadmill testing. Myocardial ischemia was ruled out, and the cause was determined to be distal AV nodal block. The pathophysiology, diagnosis, and treatment of distal AV nodal block are reviewed. The role of exercise treadmill testing and electrophysiologic studies in distal AV block are outlined in a diagnostic and therapeutic strategy.

Aged↗
PubMed1989

Risk of right bundle-branch block and complete heart block during pulmonary artery catheterization.

The need for the prophylactic insertion of a pacemaker before pulmonary artery catheterization in patients with pre-existing left bundle-branch block (LBBB) is controversial. To determine the incidence of new right bundle-branch block (RBBB) and complete heart block during bedside pulmonary artery catheterization, 293 patients undergoing 307 pulmonary artery catheterizations were prospectively studied. Nine patients had pacemaker rhythms and 19 patients had an RBBB on their precatheterization ECGs and therefore were excluded from analysis. In the remaining 279 pulmonary artery catheterizations, eight (3%) were associated with the development of a new RBBB. None of the 14 patients with a pre-existing LBBB developed complete heart block. The incidence of complete heart block during pulmonary artery catheterization of patients with previous LBBB was not higher than the incidence of RBBB in patients without underlying conduction defects. Because of the rare but grave consequences of RBBB in patients with pre-existing LBBB, we recommend the use of standby external pacemakers and equipment for transvenous pacemaker insertion in these patients during pulmonary artery catheterization. We do not recommend prophylactic pacemaker insertion.

Bundle-Branch Block↗
PubMed2006

Decrease in density of INa is in the common final pathway to heart block in murine hearts overexpressing calcineurin.

Overexpression of calcineurin in transgenic mouse heart results in massive cardiac hypertrophy followed by sudden death. Sudden deaths are caused by abrupt transitions from sinus rhythm to heart block (asystole) in calcineurin-overexpressing (CN) mice. Preliminary studies showed decreased maximum change in potential over time (dV/dt(max)) of phase 0 of the action potential. Accordingly, the hypothesis was tested that decreased activity of the sodium channel contributes to heart block. Profound decreases in activity of sodium currents (I(Na)) paralleled the changes in action potential characteristics. Progressive age-dependent decreases were observed such that at 42-50 days of life little sodium channel function existed. However, this was not paralleled by decreased protein expression as assessed by immunocytochemistry or by Western blot. Since calcineurin can interact with the ryanodine receptor, we assessed whether chronic in vitro treatment with BAPTA-AM, thapsigargin, and ryanodine could rescue the decrease of I(Na). All of these treatments rescued I(Na) to levels indistinguishable from wild type. The nonspecific PKC inhibitor bisindolylmaleimide I also rescued the decrease of I(Na). To assess whether decreased sodium channel activity contributes to sudden death in vivo, the response to encainide (20 mg/kg) was assessed: 6 of 10 young CN mice died because of asystole, whereas 0 of 10 wild-type mice died (P < 0.01). Moreover, encainide produced exaggerated prolongation of the QRS width in sinus beats before the heart block. Catecholamine tone appears necessary to support life in older CN mice because propranolol (1 mg/kg) triggered asystolic death in five of six CN mice. We conclude that decrease in sodium channel activity is in the common final pathway to asystole in CN mice.

Action Potentials↗
PubMed1981

Hyperkalemia-induced bundle branch block and complete heart block.

Hyperkalemia was associated with complete heart block in one patient that resolved by first showing right anterior hemiblock). Then the right bundle branch block resolved, leaving the marked left axis deviation that was present before the hyperkalemic episode. Another patient with hyperkalemia had right bundle branch block with marked left axis deviation, both of which disappeared with correction of the hyperkalemia. These findings suggest that hyperkalemia can depress conduction in the His-Purkinje system and raise the possibility that hyperkalemia may induce complete heart block distal to the atrioventricular junction.

Aged↗
PubMed1996

Neonatal lupus erythematosus with congenital heart block and severe heart failure due to myocarditis and endocardititis of the mitral valve.

We report a case of neonatal lupus erythematosus (NLE) with congenital heart block and severe myocardial failure, which was followed from the 25th week of gestation because of fetal bradycardia. The child was delivered at the 37th week of gestation by elective cesarean section because of echocardiographically documented heart enlargement, pericardial effusion and moderate insufficiency of the mitral and tricuspid valves. In spite of immediate pacing, intubation and supportive treatment, the newborn developed progressive heart failure. Echocardiography showed endocarditis of the mitral valve and diffuse myocarditis. The heart failure resolved under steroid treatment. Our experience supports the early use of steroids in treating myocarditis due to NLE. Intrauterine steroid treatment in the presence of fetal hydrops and congenital heart block is discussed.

Adult↗
PubMed1993

Isolated congenital heart block: fetal and infant outcome and familial incidence of heart block.

OBJECTIVE: To determine the 1-year outcome of infants with isolated congenital heart block, the risk of fetal loss in mothers of affected infants, and the risk of recurrence of congenital heart block. METHODS: The outcomes of 34 infants with isolated congenital heart block and of the 109 pregnancies in the 32 mothers of these infants were analyzed retrospectively. A control group consisted of 170 pregnancies in 64 women individually matched for age, parity, and socioeconomic status. RESULTS: Five (15%) of the 34 infants with isolated congenital heart block died before 1 year of age. The relative risk for fetal loss in mothers of affected children, after the exclusion of a mother with 16 spontaneous abortions, was 1.9 (95% confidence interval 0.9-3.8; P = .094). The prevalence of congenital heart block in all siblings of children with congenital heart block was 4% (two of 45). The risk of having a child with congenital heart block after a previous birth of an affected child was 8% (two of 26). CONCLUSIONS: Infant mortality in isolated congenital heart block is considerable, and mothers of affected children tend to have an increased risk of fetal loss. However, the risk of recurrence of congenital heart block is low.

Abortion, Spontaneous↗
PubMed2005

Ro/SSA autoantibodies directly bind cardiomyocytes, disturb calcium homeostasis, and mediate congenital heart block.

Congenital heart block develops in fetuses after placental transfer of Ro/SSA autoantibodies from rheumatic mothers. The condition is often fatal and the majority of live-born children require a pacemaker at an early age. The specific antibody that induces the heart block and the mechanism by which it mediates the pathogenic effect have not been elucidated. In this study, we define the cellular mechanism leading to the disease and show that maternal autoantibodies directed to a specific epitope within the leucine zipper amino acid sequence 200-239 (p200) of the Ro52 protein correlate with prolongation of fetal atrioventricular (AV) time and heart block. This finding was further confirmed experimentally in that pups born to rats immunized with p200 peptide developed AV block. p200-specific autoantibodies cloned from patients bound cultured cardiomyocytes and severely affected Ca2+ oscillations, leading to accumulating levels and overload of intracellular Ca2+ levels with subsequent loss of contractility and ultimately apoptosis. These findings suggest that passive transfer of maternal p200 autoantibodies causes congenital heart block by dysregulating Ca2+ homeostasis and inducing death in affected cells.

Amino Acid Sequence↗
PubMed2006

Natural history of postoperative heart block in congenital heart disease: implications for pacing intervention.

After half a century of major progress in congenital heart disease management, atrioventricular conduction block continues to complicate 1-3% of surgical procedures. Unless treated with an implanted pacemaker, permanent postoperative heart block is associated with 28-100% mortality. Postoperative heart block often proves to be transient, typically resolving within 10 days of onset. The duration of postoperative heart block is widely used as a key determinant for permanent pacemaker implantation. Current professional pacemaker implantation guidelines are largely based on this criterion. However, available natural history data suggest that other factors, such as residual conduction system injury, likely play a role in increasingly recognized cases of very late postoperative mortality and morbidity in patients who have experienced transient postoperative heart block. As growing numbers of congenital heart disease patients survive into adulthood, and artificial pacemaking capabilities continue to improve, it might be necessary to reconsider and refine currently accepted pacing indications for postoperative heart block.

Cardiac Pacing, Artificial↗