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Complete heart block is a rare complication of systemic lupus erythematosus, as well as other rheumatic diseases. We describe a patient with systemic lupus erythematosus who presented with complete heart block as the initial manifestation of the disease. Anti-Sjögren's syndrome antibodies as well as antiribonucleoprotein antibodies were present in the patient's serum.
Complete heart block (CHB) in infants and children is usually congenital. Nonsurgical acquired CHB is rare. Occasionally, transient acquired CHB is seen in association with viral myocarditis. We describe here an unusual case of transient CHB in a 12-year-old boy with endomyocardial biopsy-proven myocarditis and evidence of Mycoplasma pneumoniae infection.
Intraventricular together with atrial-axis and nodoventricular discontinuity, in which various parts of the conduction system are replaced by fibrous or fatty tissue, constitute the three major pathological categories of isolated congenitally complete heart block. Intraventricular discontinuity is distinctly rare, with only two previous cases reported in the literature, one of which was associated with a familial history of heart block. The cardiac conduction systems of two cases of isolated congenitally complete heart block were serially sectioned and analyzed histopathologically. The findings were correlated with the clinical features, in particular, the family histories and maternal serum anti-Ro antibodies. Both cases, a 9-day-old neonate and an 8-year-old schoolgirl, showed a combination of nodoventricular and intraventricular discontinuity, with absence of the atrioventricular penetrating bundle, the entire right, and the proximal portion of the left bundle branch. The branching bundle was absent in the first case and replaced by fatty tissue in the second. In contrast to the commoner atrial-axis discontinuity in which the atrioventricular node itself is usually replaced by fibrous or fatty tissue with variable involvement distally, the sinus node, and in particular, the atrioventricular node were normal in both of our cases. There was no family history in either case, whereas tests for the maternal serum anti-Ro antibody were positive in the first but negative in the second case. Intraventricular discontinuity as a cause of isolated congenitally complete heart block is very rare. In our cases, it co-existed with nodoventricular discontinuity. It can be sporadic, familial, or associated with positive maternal serum anti-Ro antibodies.
Stokes-Adams attacks are fairly common in children with congenital complete heart block, but the occurrence of cerebral infarction is quite unusual. We present the case of a 13-year-old boy with congenital heart block and an embolic stroke involving the cerebral artery. Echocardiography revealed no valvular regurgitation, hypokinetic segments, mural thrombus, or myxoma. Electrocardiographic monitoring demonstrated good response of ventricular rate to exercise and no episodes of atrial or ventricular dysrhythmia. It is assumed that embolism occurred due to bradycardia.
A patient with acute inferior myocardial infarction developed on the second day complete heart block with normal QRS duration, and the block was found to be distal to the His bundle. To our knowledge, this is the first such documented case in the English literature. Failure of the preceding Wenckebach periods and of complete heart block to respond to intravenous atropine may be a clinical clue to the nature of this type of heart block. The implications and possible explanations are discussed in the light of recent knowledge concerning the nature of heart block in inferior wall myocardial infarction.
A child aged 3 years who developed a respiratory syncytial virus infection is described. His admission was complicated by the development of an irregular pulse. He initially had a variable first or second degree heart block with transient electrocardiographic evidence suggestive of pericarditis and/or myocarditis and later developed complete heart block. He has remained asymptomatic for the past four years. A search for other causes of the heart block proved negative. It is tempting to suggest an association between the acute RSV infection and the development of the heart block but such an association at this stage remains speculative.
A patient is presented in whom the heart reverted spontaneously to sinus rhythm 11 years after surgical closure of a ventricular septal defect complicated by complete heart block. It seems unlikely that regeneration of fibres in the bundle of His, if these had indeed been destroyed, could account for the restoration of sinus rhythm after so long an interval.
Clinically normal adult dogs and pups 8 to 24 weeks of age were monitored for 2nd-degree atrioventricular (AV) heart block. Radiotelemetry was used to obtain the electrocardiogram (ECG) of resting, unanesthetized, unrestrained dogs. Second-degree AV heart block was detected in 64% of 11 adult dogs and 100% of 12 pups between 8 and 11 weeks of age. The dropped beats, prolonged P-R intervals, and prolonged P-P intervals appeared to be associated with the respiratory cycle. Atropine quickly reduced the frequence of dropped beats. It was concluded that occasional dropped ventricular beats due to 2nd-degree AV heart block may be normal in dogs, especially young dogs.
After spontaneously acquiring complete heart block, two children presented with torsade de pointes as a result of inappropriate prolongation of the QT interval. Although both remain well following pacemaker insertion, their cases illustrate the importance of QT interval assessment in patients with atrioventricular block, and demonstrate that syncopal episodes, and possibly sudden death, in children with acquired heart block can be due to bradycardia-induced ventricular tachyarrhythmias, rather than extreme bradycardia per se.
Persistent bradycardia is an uncommon cardiac problem in fetuses but carries a high mortality in those with a ventricular rate <55 bpm. Fetal heart block is one of the most common causes of persistent fetal bradycardia (PFB). An optimal method for assessing and monitoring cardiovascular compensation in the setting of PFB due to heart block has not been fully established. We report the application of two-dimensional and Doppler echocardiography in close monitoring of cardiac function and hemodynamics in a third-trimester fetus with a ventricular rate <55 bpm due to heart block, which assisted in successful management of the pregnancy to term. Hemodynamic and cardiac adaptive changes in compromised fetuses, particularly due to heart block, are discussed.
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A large group of patients with chronic heart block was studied for evidence of neurological disorder. Six out of 892 patients were found who had neuromuscular disease related to the conduction disturbance. In four patients, cardiac involvement appeared selectively to affect the conducting tissues. Three of these patients had a scapuloperoneal syndrome, the fourth, the oculocraniosomatic syndrome. In the remaining two patients, one with limb girdle dystrophy and the other with dystrophia myotonica, cardiomyopathy was present in addition to the conduction disturbance.
Thyrotoxicosis developed in a patient while receiving thyroid hormone therapy for clinical hypothyroidism. The development of second-degree heart block of Mobitz type 1 variety was followed by third- and then first-degree heart block. We conclude that the varying degrees of heart block were secondary to hyperthyroxinemia caused by Graves' disease and exogenous thyroid hormone.
The return of A-V conduction is described in a patient after two decades of high-grade or complete congenital heart block. Similar cases have been reported by others, with remission or even recovery commencing up to the fourth decade or later. A similar phenomenon is also described in four patients with acquired heart block of four to ten years' duration; in them, remission was usuallly brief but persisted for seven years in one patient. No full report of this seems to have been published previously. Possible explanations are discussed, but no conclusion is reached. Apart from its interest, the phenomenon is of importance with respect to the selection of demand-type electronic pacemakers in the management of patients with heart block.
A prospective study was carried out to determine the prognostic factors in patients with second-degree and complete heart block following acute myocardial infarction and to re-examine the indications for artificial transvenous pacing. Of the 117 consecutive patients with proved acute myocardial infarction, 15 developed advanced heart block (second degree and complete). The presence of the following factors, either alone or in combinations, were attended with poor prognosis: preceding Stokes-Adams syndrome, cardiogenic shock, congestive heart failure, complications secondary to cardiac arrest, anterior infarction and wide QRS complex. In the nine cases requiring artificial transvenous pacemaker because of Stokes-Adams attacks, congestive heart failure or frequent multifocal ventricular ectopic beats, there were five deaths. The remaining six patients, who were without complications and were not paced, all survived; these patients had normal QRS duration with heart rates above 60 per minute. This study indicates that prophylactic transvenous catheter insertion in acute heart block does not appear justified unless specific indication(s) arise. Postmortem studies revealed significant narrowing of all the major coronary vessels in all five fatalities. The overall mortality in this series of cases of acute heart block was 33%.