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Rheumatic fever can cause a variety of cardiac conduction disturbances. A case of rheumatic fever with rare complication of narrow QRS - complex complete heart block in a 12 year old girl is presented. The complete heart block has persisted even after 12 months of followup.
Lidocaine-induced atrioventricular (AV) conduction disturbances are an ill-defined phenomenon. Electrophysiological studies in both animal and human subjects have shown that therapeutic doses of lidocaine have no significant effect on AV nodal and His-Purkinje conduction time in the presence of intact AV conduction. Sporadic reports of accelerated AV conduction or complete heart block following lidocaine administration have been published. One case of Mobitz type II heart block has been reported in a patient with a prolonged QTc interval (0.61 sec) who was also receiving prenylamine. Electrophysiological studies designed to evaluate lidocaine's effects on AV conduction present conflicting observations. We report a case of Mobitz type II heart block following therapeutic doses of lidocaine in the absence of acute myocardial infarction or concomitant cardioactive drug administration. This case, in conjunction with other reported data, suggests the occurrence of lidocaine-induced AV block to be unpredictable. Although its occurrence may be infrequent, the severity of these reactions warrants careful selection and monitoring of patients who are to receive lidocaine.
We describe a 63-year-old female patient with rheumatoid arthritis who developed complete heart block and features of polymyositis within a few weeks of starting treatment with D-penicillamine. We believe she is one of only three published patients in whom complete heart block accompanies penicillamine-induced polymyositis. The literature on penicillamine myositis is reviewed with special emphasis on cardiac problems. Patients taking D-penicillamine who develop features suggestive of polymyositis may develop insidious, but potentially life-threatening cardiac involvement and must be carefully monitored.
Complete congenital heart block (CCHB) is a rare disease of the newborn that carries significant morbidity and mortality. It generally occurs as a result of the presence of maternal autoantibodies that are transferred to the fetus and affect the fetal heart, or it may be associated with a congenital structural abnormality of the heart. Infants with CCHB are at risk for diminished cardiac output and the subsequent development of congestive heart failure. Many infants require the placement of a cardiac pacemaker. It is essential that the nurse caring for these infants have a good understanding of the disease process and be familiar with the unique problems that these infants and their families may encounter.
Severe cardiac manifestations are rare complications of Reiter's syndrome. The literature describes 11 cases of complete heart block. We report a case of complete atrioventricular heart block in a 38-year-old man with HLA-B27 positive Reiter's syndrome. Conduction returned to normal after institution of steroid treatment.
Fetal heart movement and fetal heart rate are easily observed with real-time ultrasonography. Certain aspects of fetal cardiac disorders can thus be further evaluated by M-mode echocardiography. Congenital heart block and associated connective tissue disorders are discussed.
Although a strong clinical association exists between congenital heart block (CHB) and an immune response to SSA/Ro and SSB/La proteins, a causative role of these antibodies in the pathogenesis is just emerging. In a preliminary report, we have demonstrated that IgG fractions isolated from the sera of mothers whose children have CHB are arrhythmogenic in the human fetal heart. To more precisely define the arrhythmogenic effect of anti-SSA/Ro-SSB/La antibodies, we used the readily available rat heart model to record: 1) ECGs from Langendorff beating hearts; 2) action potentials from atrioventricular (AV) nodal preparations; 3) L-type Ca currents, I(Ca) at the whole-cell and single channel levels; and 4) other currents such as the transient outward K+ current, I(to), the inward rectifier K+ current, I(K1), and the Na+ current, I(Na). Perfusion of hearts with purified IgG (800 microg/mL), isolated from the serum of a mother with SSA/Ro and SSB/La antibodies whose child had CHB, resulted in bradycardia associated with 2:1 AV block. Simultaneous action potentials were recorded from dissected atrial and AV nodal areas of the rat heart. Superfusion of these preparations with the same mother's IgG fraction resulted in 2:1 AV block followed by complete inhibition of AV nodal action potential. Because AV nodal electrogenesis is largely dependent on I(Ca), the effect of these antibodies on I(Ca) was subsequently determined. Superfusion of myocytes with whole serum or purified IgG (80 microg/mL) from the same mother consistently inhibited whole cell I(Ca), ensemble average Ba2+ currents (I(Ba)) and open state probability, p(o), without affecting the channel conductance. IgG had no significant effect on I(to), I(K1), or I(Na). Whole sera and IgG fractions from a healthy mother with no detectable anti-SSA/Ro or SSB/La antibodies did not inhibit I(Ca) or I(Ba). These results demonstrate that IgG containing anti-SSA/Ro and -SSB/La antibodies induces complete AV block in beating hearts and in multicellular preparations, thus implicating a preferential interaction of these autoantibodies with Ca channels and/or associated regulatory proteins. This is consistent with the observed inhibition of Ca channels that may be a critical factor contributing to the pathogenesis of CHB.
An apparently fit young man with sarcoidosis developed complete heart block during an emergency mastoidectomy. A temporary transvenous pacemaker was inserted, but permanent pacing was required in the postoperative period. The clinical and pathological features of cardiac sarcoidosis are described; complete heart block is the commonest presentation of cardiac involvement. The role of anaesthesia as the precipitating factor in this case is discussed.
A 32-year-old woman with systemic lupus erythematosus was found to have a fetus with heart block and fetal ascites at 23 weeks gestation. Treatment with high-dose corticosteroids ameliorated the early signs of heart failure, although the fetal heart rate gradually fell from 48 beats/min to 42 beats/min by 34 weeks. Sudden deterioration of the fetal state occurred at 35 weeks, and this only partially responded to digitalisation. Neonatal death occurred on Day 18 from the consequences of severe birth asphyxia. The relationship and pathogenesis of anti-Ro antibodies, congenital heart block and hydrops fetals are discussed, together with the in utero management of this condition.
One hundred and twelve patients with heart block and chronic tendency to syncope were ECG-monitored during syncope. Ventricular tachycardia and/or fibrillation (VT-VF) was observed as the cause of syncope in 11 patients: in 6 of 20 patients with chronic third degree A-V block, in 3 of 65 with paroxysmal A-V block and in 2 of 27 with S-A block. The R-R interval preceding the escape beat which initiated VT-VF varied between 1.2 and 2.2 seconds. The cerebral attacks were amenable to long-term pacemaker treatment. However, relapses of VT-VF were observed during pacing with a low rate of 55 per minute and during short interruptions in pacing, as produced by intermittent pacemaker failure or threshold determination. In one patient, supplementary treatment with a beta-blocking agent had to be given to suppress exercise-induced attacks of VT-VF after pacemaker implantation.
BACKGROUND: The perinatal management of congenital complete heart block (CCHB) remains controversial. The purpose of this study was to present a therapeutic modality for CCHB. METHODS: We collected retrospective cases of all pregnant women admitted to our hospital between January 1992 and June 1999 whose babies developed CCHB antenatally. After a series of examinations, maternal, fetal and neonatal data were analyzed. RESULTS: Nine fetuses from six mothers (cases 1-6) in nine different pregnancies were studied. In case 1, both consecutive fetuses had CCHB and in case 2, all three consecutive fetuses had CCHB. The other mothers (cases 3-6) had only one fetus each with CCHB. Of the seven fetuses with isolated CCHB, four underwent observation only due to late-onset, or nonimmunologic CCHB, two received dexamethasone and/or intravenous immunoglobulin therapy because of the presence of hydropic signs, and one received dexamethasone at 23 weeks' gestation due to early-onset CCHB. Shortening fractions of the right ventricle had good compensation in four fetuses, without any treatment, and improving compensation in two of three fetuses receiving dexamethasone therapy. All seven fetuses were delivered smoothly and pacemakers were implanted shortly after birth. Two other fetuses had a poor outcome due to associated ventricular septal defect or hemoglobin Bart's disease. Furthermore, we gave dexamethasone (2 mg/day) instead of prednisolone (10 mg/day) for the next pregnancies of patients 3 to 5, beginning at 12 weeks of gestation. No fetal CCHB developed again. CONCLUSIONS: For pregnant women with previous fetal immunologic CCHB, early initiation of dexamethasone instead of prednisolone might be effective to cross the placenta and avoid recurrences. Dexamethasone is also effective for fetal CCHB of early onset, fetal hydrops or heart failure. Observation only is suggested for nonimmunologic CCHB and remote or late-onset immunologic CCHB. Other modalities were tried for very sick fetuses, but their effectiveness was not predictable.
We present the case of a nine-year-old boy afflicted with Ondine's curse, who developed complete atrioventricular heart block after a single bolus of propofol for induction of anaesthesia for strabismus surgery. Ondine's curse, the other name for congenital central hypoventilation syndrome, is characterized by a generalized disorder of autonomic function. Propofol has no effect on the normal atrioventricular conduction system in humans but it reduces sympathetic activity and can highly potentiate other vagal stimulation factors. Heart block has been documented after propofol bolus use in adults but, to our knowledge, not in children. It would appear that propofol is not a good choice for anaesthesia in congenital central hypoventilation syndrome.
Out of 100 patients with chronic heart block 16 had one or more autoimmune disorders-namely, vitiligo (5,) hypothyroidism (4), Graves's disease (1), pernicious anaemia (2), and diabetes mellitus (9). All these disorders occurred with greater frequency than normal and were more prevalent than in a group of hospital inpatients of comparable age. Autoantibodies were not increased. We suggest that among patients with idiopathic heart block there is a subgroup with multiple autoimmune disorders.
Epicardial fetal pacing via thoracotomy has the potential of being a safer and more reliable procedure to treat congenital complete heart block (CHB) associated with fetal hydrops refractory to medical therapy. To assess the acute electrophysiological characteristics of two ventricular epicardial leads, a new experimental model of fetal heart block induced by cryosurgical ablation of the AV node without the need for fetal cardiac bypass was performed in 12 pregnant ewes at 110-115 days gestation. A modified screw-in lead (1 1/2 turns) was used in six fetal lambs and a stitch-on lead in the other six lambs. CHB was achieved in 100% of the fetal lambs, with no ventricular escape rate noticed in any of the lambs. The acute stimulation thresholds were consistently low for both leads, with lower values for the screw-in lead at pulse duration below 0.9 msec (P < 0.03). Current measured at voltage threshold with pulse width below 0.5 msec was lower for the screw-in lead (P < 0.048). Stimulation resistance, measured during constant-voltage pacing, was not statistically different between the two leads (441.8 +/- 13.7 omega for the screw-in lead vs 480.2 +/- 59.2 omega for the stitch-on lead). No significant differences (P > 0.20) were found in R wave amplitude between the two electrodes. Slew rates were significantly higher in the screw-in group than in the stitch-on group (1.40 +/- 0.2 vs 0.62 +/- 0.2 V/sec, P = 0.04). This model of CHB is a simple and reproducible method to assess fetal pacing. We find the screw-in electrode to be a better option when fetal pacing is indicated.
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Gelatin-resorcin-formaldehyde-glutaraldehyde (GRF) biologic glue is an available adjunct to repair acute ascending aortic dissections. Permanent complete heart block complicated the operative repair of 2 of 6 patients. The pathophysiology of heart block resulting from either the acute dissecting process or the technique of applying GRF glue is discussed.
In 5 children and adolescents with congenital complete heart block functional studies were performed at rest and during submaximal and maximal work load. With reference to height standards the mean values of aerobic capacity and maximal cardiac output were reduced to 86% and 81%, respectively, whereas stroke volume during maximal oxygen uptake was elevated to 150%. Ventricular rate increased from a mean value of 50 min-1 at rest to a mean maximal value of 112 min-1 by the factor 2.2, atrial rate from 84 min-1 at rest by the factor 2.3 to 192 min-1 at maximum. The mean value of maximal arteriovenous oxygen difference was 14.5 ml/100 ml, the mixed venous oxygen content at maximal oxygen uptake was 4.3 ml/100 ml. The results show that compensation of the reduced ventricular rate not only at rest but also during work was mainly achieved by the increase of stroke volume. The compensatory elevation of stroke volume was, within certain limits, the greater, the more maximal ventricular rate was reduced. As an additional but considerably less effective compensatory mechanism the arteriovenous difference could be evaluated, whose maximal value was about 10% higher than normal.
Congenital heart block (CHB) that is a manifestation of neonatal lupus syndrome (NLS) carries a poor prognosis. The treatment response of established heart block in NLS is usually unsatisfactory. Preventive treatment during pregnancy, however, before the critical period of cardiac development, can prevent the development of CHB. A Taiwanese woman with systemic lupus erythematosus (SLE) was positive for anti-Sjögren's syndrome A (SSA)/Ro antibody. Her first pregnancy resulted in intra-uterine fetal death. Her second pregnancy resulted in CHB, despite dexamethasone treatment, and neonatal death at age 1 day despite pacemaker implantation. During her third pregnancy, dexamethasone was given starting at week 10, azathioprine at week 18, and plasmapheresis was performed every other day for 5 times starting at week 20 of gestation. Cesarean section was performed due to oligohydramnion at week 31 of gestation and a healthy girl was delivered. This case suggests that judicious use of fluorinated glucocorticoids, immunosuppressants, and plasmapheresis may prevent development of CHB in pregnant women with SLE who are anti-SSA/Ro antibody positive and have previous children with CHB.