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At least 91 records · Page 5Linked to original sources
PubMed1975

Hemodynamic changes during ventricular pacing in patients with complete heart block and aortic and mitral valvular heart disease.

Increasing the heart rate to near normal in patients with complete heart block (CHB) and slow ventricular rates may lead to greater improvement in ventricular function than when the heart rate is increased from normal to more rapid heart rates. Improvement in ventricular function is usually manifested by a decrease in left ventricular end-diastolic pressure (LVEDP) and volume and by an increase in contractility. In patients with both CHB and valvular heart disease improvement in ventricular function during pacing may be modified by the nature of the valvular disease. Hemodynamic data from six patients with both valvular heart disease and CHB were compared with those from ten patients with CHB and normal cardiac valves. Hemodynamic studies were performed at slow or idioventricular rates and again after increasing the heart rate to more nearly normal levels by ventricular pacing. When obstruction to left ventricular inflow (mitral stenosis) co-existed with CHB, increasing the heart rate resulted in a reduction of an elevated LVEDP to normal. This resulted in only a small increase in left atrial pressure in spite of a striking increase in the mean left atrial-ventricular gradient. When obstruction to left ventricular outflow prevailed (aortic stenosis), improvement in cardiac function was manifested mainly by a decrease in LVEDP and was accompanied by a decrease in left ventricular stroke work. When a large regurgitant volume (aortic insufficiency) was added to a ventricle which has enlarged subsequent to CHB, there was striking elevation in ventricular filling pressures which returned to more nearly normal levels when the heart rate was increased. This was accompanied by a reduction in regurgitant stroke volume in the patient in whom it was measured. Thus, an increase in heart rate may be especially beneficial to those patients with CHB who also have valvular lesions which contribute to an increase in LVEDP and end-diastolic volume. Careful hemodynamic evaluation is helpful in determining appropriate therapy in these patients.

Aged↗
PubMed2000

A case report on the perinatal management of a 30-week preterm baby with congenital complete heart block.

INTRODUCTION: Congenital complete heart block is an uncommon condition in the newborn, but is known to occur with maternal systemic lupus erythematosus. CLINICAL PICTURE: This paper presents one such baby with complete heart block who was born premature (after a gestation of 30 weeks) and weighing 759 g. TREATMENT: Continuous isoprnaline infusion was initially used to support the baby while her other neonatal problems were treated. A Medtronics VV1 pacemaker was subsequently inserted to maintain a heart rate that would be more physiologically acceptable for the patient. OUTCOME: This baby is currently thriving well, having been followed up for one year. CONCLUSIONS: The management issues, encompassing maternal and neonatal problems, and a review of current literature on this condition are discussed.

Adult↗
PubMedDate not supplied

Congenital complete heart block.

Congenital complete heart blocks (CCHB) are mostly related to the neonatal lupus syndrome. The purpose of this paper was to assess the clinical spectrum of CCHB in our hospital. Nine patients were retrospectively enrolled between 1994 and 1999. The birth history, electrocardiography, 24-hour Holter monitoring, pacemaker insertion and its complications, maternal disease, and maternal and infant autoantibody levels were studied. All nine cases were diagnosed prenatally. Hydrops fetalis was noted in five (55.6%). Six cases were live births and the other three were terminated. No anatomical heart defects were noted. Initial electrocardiography revealed the atrial rates ranged from 150 to 166 beats per minute. The minimal ventricular rates ranged from 46 to 80 beats per minute. VVI mode pacemakers were inserted through xyphoid approach in all live-birth infants. Complications were noted in three of them (50%). Antinuclear antibody and anti-SSA/Ro antibody were positive in all 8 mothers (100%). The anti-SSB/La antibody was positive in 6 of the eight mothers (75%). Five infants tested positive for anti-SSA/Ro antibody. None of the infants tested positive for anti-SSB/La antibody. In conclusion, all CCHBs in our series were associated with maternal autoantibodies. Because of high complication rate of permanent pacemaker insertion during the neonatal period, it should be restricted in certain conditions.

Antibodies, Antinuclear↗
PubMed1997

Anti-Ro (SSA) and anti-La (SSB) antibodies and complete congenital heart block.

Complete congenital heart block (CCHB) is the most severe manifestation of neonatal lupus syndrome, associated with a mortality rate of up to 31%. It is caused by irreversible damage to the cardiac conduction system due to the transplacental passage of maternal antibodies to the fetus. Anti-Ro (SSA) and anti-La (SSB) antibodies are usually detected in sera of mothers of children with prenatally diagnosed CCHB and in cardiac tissues of affected newborns. Their pathogeneic role in the development of CCHB has been established in several studies. When CCHB is detected during pregnancy, careful monitoring and delivery are needed before heart failure is developed. Treatment strategies are debatable and may include prophylactic therapy for high-risk pregnant women and a combination of intrauterine plasmapheresis with plasma exchange or with corticosteroids. Pacemaker insertion is required in most infants during the first three months of life. Assays for anti-Ro (SSA) and anti-La (SSB) antibodies should be performed on sera of pregnant women with SLE and newborns with CCHB.

Antibodies↗
PubMed2001

Direct inhibition of expressed cardiac l- and t-type calcium channels by igg from mothers whose children have congenital heart block.

BACKGROUND: Congenital heart block (CHB) is a disease that affects the offspring of mothers with autoimmune diseases. We recently reported that maternal sera containing antibodies against SSA/Ro and SSB/La ribonucleoproteins (positive IgG) inhibited L-type Ca current in isolated cardiac myocytes and induced sinus bradycardia in a murine model of CHB. The direct interaction of positive IgG with L-type Ca channel proteins and the possible inhibition of T-type Ca current that could account for the sinus bradycardia remain unknown. METHODS AND RESULTS: The 2-electrode voltage-clamp technique was used to record currents via L-type (I(Ba)-alpha(1C) or I(Ba)-alpha(1C)+beta(2a)+alpha(2)/delta) and T-type (I(Ba)-alpha(1H)) Ca channels, Na channels (I(Na)-hH1), and K channels (I(Ks)-minK+KvLQT1) expressed in Xenopus oocytes. Positive IgG (350 microgram/mL) inhibited I(Ba)-alpha(1C) by 50.6+/-4.7% (P<0.01) and I(Ba)-alpha(1C)+beta(2a)+alpha(2)/delta by 50.9+/-4.2% (P<0.01); I(Ba)-alpha(1H) was reduced by 18.9+/-1.0% (P<0.01). Immunoblot data show cross-reactivity of positive IgG with alpha(1C) subunit. Pretreatment of oocytes with atropine (1 micromol/L) or acetylcholine (10 micromol/L) did not affect the inhibitory effect of IgG on I(Ba)-alpha(1C) and I(Ba)-alpha(1C)+beta(2a)+alpha(2)/delta (P<0.05). Positive IgG had no effect, however, on either I(Na)-hH1 or I(Ks)-minK+KvLQT1. CONCLUSIONS: Positive IgG inhibited expressed L-type I:(Ba) and cross-reacted with the alpha(1C) subunit in Xenopus oocytes, providing strong evidence that maternal antibodies interact directly with the pore-forming alpha(1)-subunit of Ca channels. In addition, we show for the first time that positive IgG also inhibited T-type I(Ba) but not I(Na)-hH1 or I(Ks)-minK+KvLQT1. This could provide, in part, the ionic basis of sinus bradycardia reported in animal models of CHB and clinically in humans.

Adult↗
PubMed1991

Cardiac changes implicated in chronic heart block.

Fifteen cases of chronic heart block were studied. Eight of them could be designated as idiopathic or primary heart block; the others were associated with hypertension, diabetes and ischaemic heart disease, either singly or in various combinations. In six cases, the whole heart was available for histopathological study of the conduction system. In the other 9 cases, only a portion of the heart muscle was available for examination. A V nodal fibrosis extending upto the proximal bundle of His was seen in all the six whole heart autopsy materials. Fibrosis of the adjacent myocardium was seen in five cases. In three cases, conducting system fibrosis was associated with atherosclerotic (1 case) or diabetic changes (3 cases) of the intramural vessels. In the 9 partial autopsy studies, myocardial fibrosis was seen in two cases, diabetic microangiopathy in one and atherosclerotic changes in two including an old thrombus in one. Thus, diabetic microangiopathy was seen in total four cases. These changes may be responsible for the cardiomegaly and cardiac failure associated with conduction defects observed in diabetes. In the idiopathic group also, heart block could be considered as a significant facet of a primary myocardial degenerative process.

Chronic Disease↗
PubMed1983

Connective-tissue disease, antibodies to ribonucleoprotein, and congenital heart block.

The relation between congenital heart block and maternal connective-tissue disease was studied by antibody screening of serum samples obtained in connection with 45 cases of isolated congenital complete heart block. Serum was available from 41 mothers (17 who had connective-tissue disease and 24 who were healthy) and 21 children. Thirty-four mothers had antibody to a soluble tissue ribonucleoprotein antigen called Ro(SS-A), which was identified by immunodiffusion. Anti-Ro(SS-A) was found in seven of eight serum samples collected from affected children when they were less than three months old but in none of 13 samples obtained when these children were older. It appears that maternal anti-Ro(SS-A) antibody crosses the placenta and is a marker for risk of congenital complete heart block; its absence from maternal serum suggests that a child is unlikely to be affected. Anti-Ro(SS-A) or a related antibody is probably involved in the pathogenesis of congenital complete heart block.

Autoantibodies↗
PubMed1976

Heart block complicating acute inferior wall myocardial infarction.

Heart block was noted in 60 (35 complete and 25 second-degree) of 410 patients with acute inferior wall myocardial infarction. This group with heart block was compared to a control group of 30 patients with acute inferior wall infarction without heart block. The incidences of prior myocardial infarction and hypertension, in addition to the highest level of serum creatine phosphokinase and a maximum degree of ST-segment elevation in the inferior leads, were all greater in patients with heart block, as compared to the controls. The incidences of various complications, including dizziness and syncope, transient hypotension, cardiogenic shock, and congestive heart failure, were also higher in the group with heart block, while sinus nodal distrubances and atrial arrhythmias occurred with equal frequency. The mortality in those with heart block was 28 percent compared to 13 percent for the control. It is concluded that patients with heart block complicating acute inferior myocardial infarction have a greater amount of myocardial necrosis, a higher incidence of complications, and a higher mortality. Insertion of a temporary pacemaker should be considered when specific indications are present and not routinely.

Acute Disease↗
PubMed1994

Clinical significance of maternal anti-Ro/SS-A antibodies in children with isolated heart block.

OBJECTIVES: We studied 30 consecutive children with isolated heart block to assess the clinical impact of the presence of maternal anti-Ro/SS-A antibodies for isolated heart block. BACKGROUND: Isolated heart block in children, often associated with maternal autoimmune disease leading to anti-Ro/SS-A auto-antibody production, is an infrequent but potentially lethal disorder. METHODS: Thirty children with isolated heart block were studied with respect to medical history and electrocardiographic (ECG) analysis. The presence of anti-Ro/SS-A antibodies was determined in the maternal serum. We also examined the ECGs of all brothers and sisters of the patients for conduction abnormalities. RESULTS: Twenty-one of the 30 children had an anti-Ro/SS-A-positive mother (group A); the other 9 children had an anti-Ro/SS-A-negative mother (group B). Comparison of the clinical data from both mothers and children revealed that these two groups differed significantly with respect to the following: Prenatal diagnosis and obstetric complications occurred more often in group A, whereas progression to complete block, QRS width > 0.08 s, premature ventricular contractions and ventricular standstills > 4.5 s occurred more often in group B. In addition, mothers of children in group A reported more spontaneous abortions. All siblings of children in groups A and B had normal ECGs, excluding a subclinical form of heart block. CONCLUSIONS: Two types of heart block can be recognized: Congenital heart block is associated with maternal anti-Ro/SS-A antibodies and numerous obstetric and neonatal complications. It is diagnosed prenatally or at birth and is usually complete at onset and probably has a substantial recurrence risk. Heart block that is acquired later in life is not associated with maternal autoimmunity and has no risk for recurrence. It often presents as a partial block but progresses to complete block in time.

Adolescent↗
PubMedDate not supplied

Experimental models of complete heart block.

Methods of creating experimental complete heart block developed since 1883 are reviewed in detail. The three most commonly used techniques at present are: (I) Thoracotomy, atriotomy and ligation of the A-V bundle. (II) Thoracotomy and injection of a chemical into the A-V node or bundle. (III) Injection of a chemical through a transvenous catheter into the node or bundle. The results in different species, complications, and variations in procedure are discussed. The bibliography provides a comprehensive index of work performed in animals with experimental complete heart block. We produced complete heart block in sixteen pigs but subsequently eleven died during Stokes-Adams attacks. Pigs have not been used previously as models of heart block for experimental purposes and prophylactic pacing appears mandatory in this species.

Adams-Stokes Syndrome↗
PubMed2003

Use of a subcutaneous beta-sympathomimetic pump for the treatment of fetal congenital complete heart block. A case report.

BACKGROUND: Complete heart block is the most common congenital heart block diagnosed in the fetalneonatal period. Maternal administration of beta-sympathomimetic agents has been used to treat this condition in the fetus. We know of no previous reports of the delivery of beta-sympathomimetics via a continuous subcutaneous pump for management of this condition. CASE: An intrauterine gestation at 28 5/7 weeks complicated by fetal congenital complete heart block was successfully managed to term with maternal administration of a beta-sympathomimetic agent via a continuous subcutaneous pump. CONCLUSION: Maternal administration of beta-sympathomimetic agents by a continuous subcutaneous pump in cases of fetal congenital complete heart block may help prolong pregnancy by preventing hydrops fetalis and avoiding confounding problems of prematurity. However, it should be used with caution due to the potential for dilated cardiomyopathy in the infant.

Adult↗
PubMed1989

Fetal complete heart block: antenatal diagnosis, significance and management.

Complete heart block was diagnosed prenatally in 21 fetuses. Associated structural cardiac defects were present in 18 fetuses, in particular complete atrioventricular canal with atrial isomerism (5 cases), and 'corrected' transposition of the great arteries (4 cases). Maternal systemic lupus erythematosus was proved in only one case. In 11 fetuses, intra-uterine congestive heart failure with the signs of non-immune hydrops fetalis occurred. In all 11 fetuses, the hydrops was associated with a cardiac defect, in particular complete atrioventricular canal with atrial isomerism in 5 cases. A review of the literature confirms that only the association of complete heart block and cardiac malformation can cause intra-uterine congestive heart failure, whereas in the case of fetal complete heart block without cardiac malformation or with prenatally hemodynamically insignificant cardiac malformation, congestive heart failure is rare. Only 30% of newborns with complete heart block have associated cardiac malformations. In our series, however, 86% of the fetuses with complete heart block had cardiac malformations. The most important reason for this percentage discrepancy is that almost all fetuses with associated severe cardiac defects, in particular atrioventricular canal defects, develop heart failure which frequently results in prenatal death. Thus, fetal deaths are not included in pediatric statistics. Nevertheless, fetuses with isolated complete heart block generally do not develop heart failure and in almost all of the cases are born alive.

Adult↗
PubMed1975

Fascicular conduction blocks and their relationship to complete heart block in Nigerians.

Following electrocardiographic analysis, isolated or combined blocks in the intraventricular trifascicular system including predivisional left bundle branch block with left posterior hemiblock in Nigerians are presented and the underlying causes reviewed. The rarity of complete heart block, despite the not uncommon fascicular blocks, is of interest and may be related to the population age structure considering the invariably slow rate of degeneration of conduction fibres in the system.

Adolescent↗