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PubMed2000

Molecular and ionic basis of congenital complete heart block.

Congenital heart block (CHB), detected at or before birth in a structurally normal heart, is strongly associated with autoantibodies reactive with the intracellular soluble ribonucleoproteins 48kD SSB/La, 52kD SSA/Ro, and 60kD SSA/Ro. CHB is presumed to be due to the transplacental passage of autoantibodies from the mother into the fetal circulation. Varying degrees of heart block have been reported. Although second degree block has, on rare occasion, reverted to normal sinus rhythm, complete atrio-ventricular (AV) block is irreversible. CHB carries substantial mortality and morbidity, with > 60% of affected children requiring lifelong pacemakers. The recurrence rate exceeds, by at least twofold, that of the first birth and is likely to influence the decision to have more children. Curiously, the mother's heart is almost never affected (with complete heart block) despite exposure to identical circulating autoantibodies. As part of our continuing effort to understand the complex factors contributing to the pathogenesis of CHB, we have established an animal model of CHB by immunizing female mice with recombinant proteins/antigens, reproduced the human complete AV block in an isolated Langendorff perfused fetal heart, and correlated these findings with L-type Ca channel inhibition by maternal antibodies from mothers of children with CHB. In addition, we established a passive animal model by directly injecting maternal antibodies into pregnant mice and reported significant sinus bradycardia, indicating that the spectrum of conduction abnormalities may extend beyond the AV node. All together, the data provided strong evidence supporting an etiologic role of antibody/Ca channel involvement in the pathogenesis of CHB. However, other yet unknown factors seem necessary to explain the full expression of CHB.

Animals↗
PubMed1987

Beneficial effects of atrioventricular synchrony in dogs with right coronary artery embolization, and complete heart block.

Complete heart block complicating right ventricular infarction frequently is accompanied by shock. Hemodynamic responses to different pacing modes were studied in six anesthetized, closed chest dogs following right coronary artery embolization with mercury and heart block induced by repetitive trans-septal DC shock. Hemodynamics were recorded at control, following right coronary artery embolization, during atrioventricular sequential pacing (DVI) and ventricular pacing (VVI). With respect to the hemodynamics recorded during VVI and DVI pacing; (1) The mean arterial pressure increased by 29.4% during DVI pacing (92.1 +/- 31.3 mm Hg vs 73.4 +/- 28.9 mm Hg p less than 0.005). This increase was primarily due to an augmentation in systolic arterial pressure. (2) The left ventricular end diastolic pressure increased by 35.8% during DVI pacing (16.3 +/- 5.3 mm Hg vs 12.0 +/- 4.3 mm Hg p less than 0.01). (3) Cardiac output improved by 33.8% during DVI pacing (2.34 +/- 0.75 L/min vs 1.76 +/- 0.59 L/min, p less than 0.0005). This was a consistent improvement in cardiac output with a narrow range of 27.1% to 39.0%. (4) There were no significant changes in right atrial, pulmonary, pulmonary capillary wedge pressures or in systemic vascular resistance. In dogs with right coronary artery occlusion and complete heart block DVI pacing is clearly superior to VVI pacing. This is probably because the atrial contribution to ventricular filling, in this model, is critically important to maintain an adequate cardiac output.

Animals↗
PubMed1998

Investigative methods of congenital complete heart block.

Congenital heart block (CHB) has been described for a century and related to the presence of maternal autoimmune disease for three decades, but little is understood about its mechanism. To explore the pathophysiology of CHB, technologies in both basic and clinical electrophysiology are being developed and applied. Human fetal rhythm is currently inferred from cardiac mechanical events by using fetal ultrasound, allowing for the detection of second and third-degree heart block. Fetal electrocardiography is being explored to assess its feasibility as a clinical tool to detect fetal first-degree block in the mid trimester. Sequential composite digital recordings from the maternal abdomen are made every 4 weeks from pregnancies at risk for congenital heart block. Filtering and averaging techniques are used to enhance the fetal signal. So far, these techniques have produced a fetal QRS complex trigger signal for use in three-dimensional fetal echocardiography. Because the human fetus cannot be studied directly, a Langendorff rabbit model of CHB has been developed. With 5-10 mL of human serum in 150-300 mL of Krebs solution, prolongation of the Wenckebach second-degree atrioventricular block cycle length occurred. This was reproduced by using serum from seven of eight CHB mothers as compared with none of six controls mothers.

Animals↗
PubMed1976

Progressive improvement of His-Purkinje conduction during recovery from catheter-induced heart block.

Complete heart block developed during HBE studies in a patient with left bundle branch block, after inadvertent catheter-induced trauma to the right bundle branch. Normal intraventricular conduction (HV interval) was documented during the initial part of the study, and was demonstrated to be markedly prolonged after the appearance of heart block. Conduction through the right bundle branch improved over a short period of time as manifested by steplike shortenings of the HV interval, until the original conduction velocity was re-established. This case strongly supports the concept that the His-Purkinje system is capable of varying its conduction velocity and further demonstrates that, in patients with bundle branch block, a prolonged HV interval indicates disease of the remaining bundle branch.

Bundle of His↗
PubMed1992

Prognosis of acute myocardial infarction complicated by complete heart block (the Worcester Heart Attack Study).

As part of a community-based study of patients hospitalized with acute myocardial infarction (AMI) in the Worcester, Massachusetts, metropolitan area, changes over time in the incidence rates of complete heart block (CHB) complicating AMI, and the prognostic impact of CHB on the in-hospital and long-term survival of these patients were examined. In all, 4,762 patients with validated AMI hospitalized at 16 hospitals in the Worcester metropolitan area during 1975, 1978, 1981, 1984, 1986 and 1988 constituted the study sample. The incidence rates of CHB complicating AMI remained relatively stable at 5.8% over the 13-year (1975 to 1988) period studied. The incidence rates of CHB were approximately twice as high in patients with inferior/posterior wall AMI (7.7%) as in those with anterior wall AMI (3.9%). Use of a multivariate regression analysis to control for factors affecting the incidence rates of CHB revealed that patients were at highest risk for developing CHB during the latter 2 study years (1986 and 1988). Patients with AMI developing CHB had higher in-hospital case fatality rates than did those without CHB overall, as well as during each of the 6 periods studied. The in-hospital survival associated with CHB did not improve over time. After use of a multivariate regression analysis to control for additional prognostic factors, the independent effect of CHB on in-hospital prognosis remained (adjusted risk of dying = 2.10; 95% confidence intervals = 1.37, 3.21). Patients with inferior wall AMI complicated by CHB were at significantly increased risk of dying during hospitalization compared with those without CHB (adjusted risk of dying = 2.71; 95% confidence intervals = 1.60, 4.59).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Complete heart block complicating retrograde left heart catheterization.

Three cases of complete heart block complicating retrograde left heart catheterization are presented. In two of the three cases, electrophysiologic study documented block below the AV (atrial ventricular) node. In the third recurrent complete heart block was fatal. It appears that complete heart block complicating retrograde left sided cardiac catheterization is not simply a pericatheterization event; rather, it appears that there is high risk of recurrent complete heart block and that electrophysiologic study is mandatory.

Aged↗
PubMed2004

Limited Wegener's granulomatosis presenting with complete heart block.

Complete heart block associated with Wegener's granulomatosis (WG) is rare, and has not previously been reported with 'limited' WG. The case of a 36-year-old man who presented with complete heart block due to 'limited' WG [positive cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCA) on indirect immunofluorescence, positive serum antibodies to proteinase-3, and inflammatory sinus disease seen on computerized tomography (CT) without renal or pulmonary involvement] is presented. In addition, a gallium-scan fused with a myocardial perfusion scan and cardiac magnetic resonance imaging (MRI) suggested focal inflammation near the atrioventricular (AV) node.

Adult↗
PubMed2001

Optical mapping of activation patterns in an animal model of congenital heart block.

Congenital heart block (CHB) is associated with high mortality and affects children of mothers with autoantibodies (IgG) to ribonucleoproteins SSB/La and SSA/Ro. IgG from mothers of children with CHB (positive IgG) was used to assess activation patterns in both the right atrium (RA) and right ventricle (RV) of Langendorff-perfused young rabbit hearts. Optical action potentials (AP) were obtained by using a 124-site photodiode array with 4-[-[2-(di-n-butylamino)-6-naphthyl]vinyl]pyridinium. Optical APs were recorded to simultaneously image activation patterns from the RA and RV. Perfusion of positive IgG (800--1,200 micro resulted in sinus bradycardia and varying degrees of heart block. Activation maps revealed marked conduction delay at the sinoatrial junction but only minor changes in overall atrial and ventricular activation patterns. No conduction disturbances were seen in the presence of IgG from mothers with healthy children. In conclusion, besides atrioventricular (AV) block, positive IgG induces sinus bradycardia. These results establish that the sequelae of CHB are associated with impaired intrasinus and/or sinoatrial conduction. The findings raise the possibility that sinus bradycardia in the developing heart may indicate the potential for AV conduction disturbances.

Action Potentials↗
PubMedDate not supplied

Transient non-autoimmune fetal heart block.

OBJECTIVES: Fetal heart block is a rare and irreversible condition associated with structural heart defects or maternal autoantibodies (SS-A/Ro and SS-B/La) resulting in permanent damage of the atrioventricular (AV) node. This is the first report of 4 cases with a transient fetal heart block in structurally normal hearts without maternal autoantibodies. METHODS: A report on 4 patients seen within a 14-year period at one center with fetal heart block without intracardiac abnormalities or maternal autoantibodies. RESULTS: Three patients were referred to our center with a fetal bradycardia (heart rate 70-85 bpm), between 20 and 33 weeks' gestational age, and 1 for a 'triple' test at 16 weeks' gestational age. Echocardiography showed a complete heart block in 2 fetuses, and a second-degree AV block in the other 2. Heart block had completely resolved at all following visits. Postnatal ECG recordings showed normal sinus rhythm in all patients. Echocardiographic evaluation at presentation and follow-up showed normal cardiac anatomy, without signs of hydrops or cardiac decompensation in all patients. All mothers tested negative on SS-A/Ro and SS-B/La autoantibodies. CONCLUSIONS: Fetal heart block can occur in the absence of structural heart defects and maternal autoantibodies to SS-A/Ro and SS-B/La. The origin of such heart block is unknown, but its course seems benign: none of the patients ever showed ventricular heart rates <55 bpm, signs of congestive heart failure or fetal hydrops. Heart block resolved spontaneously in all patients.

Bradycardia↗
PubMed1975

De subitaneis mortibus. X. Familial congential heart block.

Complete heart block was found shortly after birth in a brother and sister (not twins). Both were treated by electronic pacing because of symptoms attributable to inadequate cardiac output and electrical instability of heart. The boy has done well with his artificial pacemaker and is now six years old. His sister died of complications due in part to the large size of her pacemaker and small size of her body. At necropsy special studies of her heart included the centers for normal impulse formation and concuction. The primary abnormalities were at the junction of atrial septum with atrioventricular (A-V) node, and at the origin of the two bundle branches from the His bundle. The A-V node was isolated by collagen at all its margins except its junction with the His bundle. The proximal His bundle was essentially normal, but from that point on through the initial protions of both the left and right bundle branches there was extensive caseous degeneration which interrupted any possible conduction. These findings are discussed in relation to fetal and postnatal development of the human A-V node, and the His bundle and its branches; and in the context of a recently observed mathematical relationship between sinus rate and two forms of experimentally produced A-V junctional escape rhythms.

Atrioventricular Node↗
PubMed1989

Penicillamine-induced polymyositis with complete heart block.

Complete heart block with severe Adams-Stokes attacks and polymyositis was observed in a 69-year-old man following 6 weeks penicillamine treatment for suspected rheumatoid arthritis. After drug withdrawal the muscle enzymes and the cardiac rhythm gradually normalized, only leaving a right bundle branch block. Although this is the first report to show that severe cardiac damage associated with penicillamine-induced polymyositis is a potentially reversible condition, the severity of the three cases reported so far warrants close observation for cardiac involvement in patients with penicillamine-induced polymyositis.

Aged↗