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At least 109 records · Page 6Linked to original sources
PubMed1986

Maternal antibodies against fetal cardiac antigens in congenital complete heart block.

An immunologic basis for congenital heart block has been proposed previously. To investigate the association between congenital heart block and maternal antibodies capable of crossing the placenta, we used immunofluorescence to examine serum samples from 41 mothers and 8 affected children, together with serum from controls, for antibodies to fetal cardiac tissue. Twenty-one mothers (51 percent) had IgG antibody reactive with fetal heart tissue, as compared with only 9 of 94 controls (10 percent; P less than 0.001). Three of 8 affected babies, but none of 50 healthy babies, had similar antibodies. The antibodies reacted with all myocardial tissue and were not directed specifically to the conduction system. They also reacted with other fetal tissues and could be distinguished from nuclear and smooth-muscle autoantibodies. We also observed a higher occurrence of antibodies to cytomegalovirus, but not to Epstein-Barr virus, in these mothers. Autopsy specimens from babies with congenital heart block examined by immunoperoxidase staining showed deposition of immunoglobulin and complement components in all cardiac tissues. These findings strengthen the case implicating immune reactivity related to maternal antibody in the development of some but not all cases of congenital heart block.

Antibodies, Antinuclear↗
PubMed1977

Progressive familial heart block--two types.

Two types of heart block which occur extensively in families in the Republic of South Africa are reported. A type I heart block tends to have the pattern of a right bundle-branch block and/or left anterior hemiblock occurring individually or together, and manifesting clinically when complete heart block supervenes, either with syncopal episodes, Stokes-Adams seizures or sudden death. The condition is inherited as an autosomal dominant gene and appears to be progressive in nature; the risk to life appears to be greatest at 3 particular periods:at or soon after birth, during puberty and the early 20s, and again towards middle age. The type II condition also appears to be progressive and is inherited as an autosomal dominant gene. The pattern, however, tends to develop along the lines of a sinus bradycardia with a left posterior hemiblock, again presenting clinically as syncopal episodes. Stokes-Adams seizures or sudden death when complete heart block supervenes. Both conditions are likely to be widely prevalent throughout the Republic of South Africa. The pathogenesis is discussed in relation to the patterns of the conduction disturbances.

Adult↗
PubMed2001

Complete heart block in children at King Chulalongkorn Memorial Hospital.

The etiologies of complete heart block in thirty-one children (mean age 5.5 +/- 5.2 years, range 0-14 years) diagnosed at King Chulalongkorn Memorial Hospital between 1990-2001 were reviewed. Three main groups of patients were identified: 1) patients who presented in utero or in the newborn period (congenital heart block, n = 6), 2) patients who had complete heart block after cardiac surgery (postoperative heart block, n = 10), and 3) children outside the newborn period with a new diagnosis of complete heart block unrelated to cardiac surgery (unknown etiology, n = 15). Among 15 patients in the last group, 5 were asymptomatic (or minimally symptomatic) with complete heart block unexpectedly found. These patients probably had previously undetected congenital heart block. Two patients had complete heart block associated with mild viral illness, but no bradycardia-related symptom. The etiology for heart block in these 2 patients was unknown. Eight patients probably had recent onset heart block because of new bradycardia-related symptoms, or a previously documented normal heart rate. All patients in this group were female (mean age 4.3 +/- 4.3 years, median 3.5 years). All were diagnosed between August and January, and the majority (75%) had a history of non-specific viral illness in the preceding 2 weeks. Seven patients (87.5%) were acutely symptomatic. Syncope and/or seizure were the most common presenting symptoms. Left ventricular systolic dysfunction was found in only one patient. The etiology of complete heart block in these patients probably was an acute viral myocarditis that preferentially affected the conduction system. Two of these eight patients had complete recovery of the atrioventricular conduction. The rest had no improvement or had only partial recovery and subsequently underwent permanent cardiac pacemaker insertion.

Adolescent↗
PubMed1999

First-trimester fetal heart block: a marker for cardiac anomaly.

BACKGROUND: Fetal heart block in the second and third trimesters may be caused by transplacental passage of auto-antibodies or cardiac defects. Little is known about the etiology of first-trimester fetal heart block. MATERIALS AND METHODS: Fetal heart block was diagnosed in four patients (negative antibody serology) referred for first-trimester sonographic evaluation of increased fetal nuchal fold thickness with bradycardia. Two-dimensional echocardiography was complemented by color Doppler flow imaging of the fetal heart. Fetal arrhythmia was verified by M-mode, pulsed wave Doppler and/or color M-mode echocardiography. RESULTS: All fetuses had congenital heart disease, atrioventricular valve regurgitation, heart block and edema. Autopsy confirmed heterotaxy in three cases (left atrial isomerism with atrial septal defect; left isomerism with double-outlet right ventricle, great artery malposition and ventricular septal defect. The third case had dextrocardia with atrioventricular canal defect and the fourth case dextrocardia with great artery transposition. CONCLUSION: First-trimester fetal bradycardia may result from heart block of the type associated with complex congenital heart disease. Accelerated edema formation in this setting may be the basis of nuchal edema formation. First-trimester fetal echocardiography offers the potential for early diagnosis and intervention in these cases with poor prognosis.

Adult↗
PubMed1981

Review article. Congenital complete heart block.

Isolated congenital complete heart block has a heterogenous aetiology. In approximately one-third of the patients in the present material the mothers had symptoms or signs of connective tissue disease. The mortality is highest in the neonatal period, much lower during childhood and adolescence and increases slowly later in life. There are elderly patients who are completely asymptomatic but patients are also encountered with signs and symptoms of more or less severe myocardial damage. Stokes-Adams attacks may occur at any age. About 10% of patients below 15 years of age in this material and about 25% of those above 15 years (mean age 30 years) were paced. In the neonatal period the predominant indication for pacing was heart failure. It is difficult to make a prognosis in the individual patient. Apart from already known risk factors, a fixed or decreasing low ventricular rate neonatally and a prolonged QT time seem to be bad prognostic signs.

Age Factors↗
PubMed2005

Percussion pacing in a three-year-old girl with complete heart block during cardiac catheterization.

Complete heart block frequently requires emergency pacing to restore systemic perfusion. We report the case of a 3-yr-old girl undergoing interventional atrial septal defect closure who suffered from transient complete heart block with circulatory arrest. Transthoracic mechanical pacing for more than 3 min provided temporary support, sustaining an adequate cardiac output until sinus rhythm resumed.

Cardiac Catheterization↗
PubMed2006

Congenital complete heart block and maternal connective tissue disease.

Congenital complete heart block can be isolated or can occur in association with other structural heart diseases. Isolated congenital complete heart block (CCHB) is due to transplacental transfer of autoantibodies from mothers with connective tissue disease. Congenital heart block is usually complete, but incomplete blocks, sinus bradycardia and QTc prolongation are also reported. Anti SS A and Anti SS B antibodies transferred from mothers have inflammatory and arrhythmogenic effects in the fetal conduction system. Cardiac manifestations reported include dilated cardiomyopathy, endocardial fibroelastosis and mitral insufficiency. Low ventricular rate, QT prolongation and arrhythmias on monitoring are high risk features. CCHB has a mortality of 30%, and 60% of infants require pacemaker therapy. Fetal echocardiography is useful in early diagnosis. Prophylactic steroid therapy is controversial. Beta adrenergic agonists were tried in mothers with fetuses having congenital heart block to increase fetal heart rate. Early pacemaker therapy is indicated in patients with symptomatic bradycardia and ventricular dysfunction. The indications for pacing in congenital heart block continue to evolve with advances in techniques and most of these children will ultimately require permanent pacemakers by adulthood.

Autoantibodies↗
PubMed2006

The pathology of the heart conduction system in congenital heart block.

The incidence of congenital complete heart block is estimated in 1 of 2500-20,000 births. Many cases are isolated (found in an otherwise normal heart) and the pathology of the heart conduction system is variable. We report a 51-year-old man with the diagnosis of complete heart block, with a permanent pacemaker. No family history of rhythm disturbances was available. The patient presented and endocarditis after replacement of the pacemaker battery. The prognosis was poor and the patient died three months later. Autopsy examination showed signs of shock, of septic origin. The heart was hypertrophic (450g) and the left ventricle thickened. Histopathological examination of the heart conduction system showed that the sinus and atrioventricular nodes were normal, but the His bundle was interrupted and replaced by fibrous tissue. No inflammatory signs were present. Loss of conducting fibres and their replacement by fibrous tissue is the most common pathological process in complete heart block. In this case His bundle was mostly affected, different to Lev's disease where the process is more distal (branching atrioventricular bundle) and to Lenegre's disease, which shows a diffuse damage in the conducting system.

Autopsy↗
PubMed1998

Intrapartum fetal oxygen saturation monitoring in congenital fetal heart block.

Conventional intrapartum electronic fetal heart rate monitoring is not informative in certain fetal conditions because the electronically-monitored fetal heart rate pattern is uninterpretable in terms of reflecting fetal normoxia. Such fetal conditions include various cardiac dysrrhythmias and some central nervous system abnormalities. Difficulties with intrapartum fetal welfare surveillance in such conditions often lead to operative delivery as a precautionary measure. We report 2 cases of intrapartum fetal oxygen saturation monitoring in the presence of congenital complete heart block (CCHB), using the Nellcor N400/FS14 oxygen saturation monitoring system. Mean intrapartum fetal oxygen saturation (FSpO2) was 32% (SEM +/- 1%) in the first case and 48% (SEM +/- 0.3%) in the second case. In both cases, vaginal delivery of otherwise healthy infants was achieved. Fetal pulse oximetry is a promising new technique which directly measures fetal oxygenation without reference to fetal heart rate patterns. It may assist in the intrapartum fetal welfare assessment in conditions such as complete heart block, thereby helping to avoid otherwise unnecessary operative delivery.

Adult↗