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We present a patient with congenital complete heart block who underwent multiple anaesthetic exposures for eye examination and bilateral cataract surgery. The diagnosis was made during the first general anaesthetic. Various complications encountered during the multiple exposures are discussed.
The case is described of an 18 months old boy with sudden onset complete heart block, heralded by Stokes-Adams attacks. General signs of viral illness preceded and accompanied the syndrome; this, along with angiographic evidence of poorly contracting left ventricle, led to the diagnosis of non bacterial myocarditis. Serologic tests disclosed a significant rise in antibodies against mycoplasma pneumoniae (1/16 to 1/128). The His-bundle electrogram showed a block above the His-bundle, but fairly widespread damage to the conduction system is suspected. The complete heart block proved to be permanent and a fixed rate pacemaker had to be implanted.
A case with complete A-V heart block in whom retrograde P- waves following some of the ventricular complexes were due to an ectopic junctional activity with the characteristics of parasystole is reported. His bundle electrogram showed an infrahisian block. After administration of 1 mg atropine intravenously the retrograde P- waves were detached from the ventricular automatic complexes and an H' deflection preceded each inverted P- wave with an H'-A' interval of 40 msec.
Progressive familial heart block (type I) has been identified in the RSA. Since 1977 many families have been referred for pedigree tracing. The present probands of some 9 pedigrees are the descendants of specific children of an immigrant; other genetic diseases appear in these pedigrees. The necessity of identifying, diagnosing and possibly treating the descendants of carriers is emphasized.
A case of polysplenia with congenital heart block, infarction of a splenic mass, and a short pancreas was reported. The infant died of severe heart failure at the age of 28 days. Deformity of the SA node was suspected to be the cause of congenital heart block but could not be demonstrated because of some limitations of autopsy procedure. Redundant splenic pedicle might cause infarction of a splenic mass after birth. The author suggests that, in addition to the semi-annular pancreas, the pancreatic anomalies of this syndrome should include the short pancreas.
We analyzed the high-fidelity left atrial and left ventricular pressures and the echocardiograms of the mitral valve, left atrium, and left ventricle in patients with complete heart block. During left ventricular diastole, the mitral valve opened, and no pressure gradient was observed between the left atrium and the left ventricle before the left atrial contraction. After the left atrial contraction, the mitral valve closed with persistent higher left ventricular than left atrial pressure. These findings indicated that during the left ventricular diastole in patients with complete heart block, the mitral valve closed after the left atrial contraction, which appeared to be maintained by the pressure gradient between the left ventricle and the left atrium.
An association between complete congenital heart block (CCHB) and anti-Ro/SSA antibody is well recognized but has never been reported in Thailand. We report here a 37-year-old female who was admitted because of massive epistaxis secondary to immune thrombocytopenia. She had given birth to a child with CCHB 2 years previously, when she was healthy. Antinuclear antibody and anti-Ro/SSA were positive in her sera, but were negative in her son. The relationship between anti-Ro/SSA antibody and outcome of mothers with infants with CCHB is reviewed.
OBJECTIVE: To investigate the association between complete congenital heart block (CCHB) in the fetus and adult disease. METHODS: We prospectively studied 111 consecutive patients with systemic lupus erythematosus (SLE) or a positive extractable nuclear antigen (Ro, La, or RNP) attending a connective tissue disease (CTD) clinic and 19 patients who had had children with CCHB. Electrocardiographs were recorded on all patients and subsequently analyzed blindly. RESULTS: There was a significantly shorter PR interval in the mothers of children with CCHB compared to patients attending the CTD clinic (p < 0.02). There was no significant difference in PR interval between Ro positive and Ro negative patients in the CTD clinic. There were no significant differences in QRS or QTc duration between mothers with CCHB children and Ro positive or Ro negative patients attending the CTD clinic. The shorter PR interval in the mothers with CCHB children may be explained by their significantly younger age compared to patients in the CTD clinic (p < 0.02, 95% CI) and the lower incidence of CTD. CONCLUSION: We were unable to confirm the association between anti-Ro antibodies and cardiac conduction defects in adults. This supports theories that CCHB is due to vulnerability peculiar to the fetal heart during a particular stage of development between 16 and 30 weeks of gestation.
An instrument and technique have been devised for the production of complete atrioventricular heart block in anesthetized, closed-chest animals. The instrument is inserted into the right atrium via the right external jugular vein. Localization of the atrioventricular node region by the visualization of intracardiac landmarks with fluoroscopy makes electrical recording unnecessary. Discrete injections of a radiopaque necrosing solution produces the heart block. Procedure time is under 30 min a success rate of 90%.
Congenital heart block (CHB) affects offspring of mothers with autoantibodies (positive IgG) to intracellular SSA/Ro and SSB/La ribonucleoproteins and is associated with high morbidity and mortality. Here, we show that maternal anti-Ro/La antibodies immunoreact with human fetal cardiomyocyte sarcolemma, recognize human L-type Ca channel alpha(1C)-protein and functionally inhibit expressed current in oocytes injected with alpha(1C) cRNA and Purkinje L-type Ca current. Furthermore, cardiac myocytes from pups born to SSA/Ro-immunized mice exhibited reduced L-type Ca current density. All together, the data establish that L-type calcium channel is a target for maternal antibodies and may provide a functional basis for the electrocardiographic abnormalities seen in infants with CHB.
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The effects of amiodarone, perhexiline and bepridil, which decrease effort cardioacceleration although they have no adrenergic beta blocking properties, were studied in the unanesthetized dog in chronic heart block. All three products decreased atrial rate in a durable way after an initial phase of tachycardia. Amiodarone had no depressant effect on idioventricular rate; however, this was significantly slowed by the other two compounds.
Congenital heart block (CHB) can result in intrauterine cardiac failure leading to fetal or neonatal loss. To establish perinatal hemodynamic factors which might predict adverse outcome, six fetuses with CHB diagnosed between 20 and 30 gestational weeks were examined by echocardiography at 2-week intervals. Neonatal morbidity and outcome in infancy are detailed. The fetuses showed a significant decrease in ventricular rate (VR) with advancing gestation (60 +/- 7 vs 51 +/- 4 beats/min, p = 0.03). Cardiac decompensation defined as hydrops or pericardial effusion was associated with VR of lower than 55 beats/min in two fetuses. Three mothers had a therapeutic trial with a sympathomimetic and digoxin. Salbutamol increased VR 10% in one of three fetuses treated. Digoxin decreased pericardial effusion in one hydropic fetus with autoimmune myocarditis. In this fetus, poor left ventricular fractional shortening (LVFS) was accompanied with high umbilical artery resistance index (RI). High amniotic fluid erythropoietin indicated severe hypoxia preceding death. Pacemaker was indicated in all the newborns. At the age of 2 weeks all the surviving infants had tricuspid regurgitation and a shunt through foramen ovale due to asynchronized atrioventricular contraction. During the 12-month follow-up two of five surviving infants had no symptoms. One had symptomatic neonatal lupus. Two infants had patent ductus arteriosus, one with dilated cardiomyopathy. In conclusion, poor fetal outcome was associated with low VR, low LVFS, and high RI. Despite early pacing, morbidity was high in infancy due to cardiomyopathy and associated heart defects. Regular echocardiographic monitoring during pregnancy and after delivery is required in order to optimize care and timing of any interventions.
A young girl born to a mother with systemic lupus erythematosus (SLE) had congenital heart block and developed symptoms of a connective tissue disorder at the age of 13 y. When first seen at the age of 15 y she was found to have an unclassified connective tissue disorder and to be seropositive for anti Ro/SSA and U1 RNP. This constellation of clinical/serological features has not been described among the reported handful of patients with congenital heart block and subsequent development of a connective tissue disorder.
A healthy pregnant was referred at 34 weeks gestation because an obstetrical ultrasound examination had shown fetal bradycardia and nonimmune hydrops. The heart was anatomically normal but complete heart block was present with a ventricular rate of 22bpm and atrial of 101bpm. We injected isoproterenol by cordocentesis direct in the umbilical vein of the fetus and a significant increase into the ventricular and atrial rates were obtained. The direct therapy with sympathomimetic drugs is a simple technique and may save fetuses with complete heart block and hidrops.
A 62-year-old man who was under observation following an episode of severe chest pain developed complete heart block and hypotension after receiving sublingual nitroglycerin. The reaction occurred while the patient was receiving an intravenous maintenance infusion of lidocaine but did not occur in response to either nitroglycerin alone or lidocaine alone. There was no evidence of acute cardiac ischemia nor of clinically significant underlying heart disease. Complete heart block after sublingual nitroglycerin in the absence of significant cardiac disease is an exceedingly rare phenomenon.
Alcohol septal ablation is a novel catheter-based technique for the treatment of obstructive hypertrophic cardiomyopathy. Complete heart block complicates the procedure in 7%-30% of cases and necessitates the prophylactic insertion of a temporary pacing wire in all patients who do not have a permanent pacemaker. We describe a case of alcohol septal ablation complicated by complete heart block and failure to capture by both a permanent pacemaker and an implantable cardioverter defibrillator (ICFD) with pacing capabilities.
To investigate whether the concentration of potassium ion in cardioplegic solution was related to the incidence of complete heart block in patients undergoing myocardial revascularisation 163 consecutive cases were studied. Cardiac arrest was with St. Thomas' hospital cardioplegic solution in all patients. Ongoing myocardial protection was provided with St. Thomas' hospital solution (potassium concentration 20 mmol/l) in 56 patients (group A) and with Ringer's injection (potassium concentration 4 mmol/l) in 107 patients (group B). These two groups were studied sequentially. The incidence of complete heart block was higher in group A than in group B. Following aortic unclamping, 27 per cent of patients in group A compared to 14 per cent in group B exhibited the phenomenon (p less than 0.05). At the time of weaning from cardiopulmonary bypass the incidence was 20 per cent in group A compared to 10 per cent in group B (p less than 0.1). No differences were demonstrated between the two groups in terms of myocardial recovery, morbidity or mortality.