Congenital Heart Block

Smithells, R. W.; Outon, E. B.

doi:10.1136/adc.34.175.223

Cited by 11 publications

(3 citation statements)

References 10 publications

(4 reference statements)

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“…It is extremely difficult to assess, on clinical grounds, the incidence of congenital heart block in a group of patients presenting for the first time in their 6th decade of life, but Campbell and Suzman (1934) stated that congenital heart block was probably more common than was thought. Congenital heart block is compatible with a normal development and survival (Yater, 1929;Campbell and Thorne, 1956;Nakamara and Nadas, 1964), but there is no doubt that Adams-Stokes attacks, though rare, can occur and probably reflect a poor prognosis (Smithells and Outon, 1959;Molthan et al, 1962;Nakamura and Nadas, 1964). It is of interest that the patient with congenital heart block in this series was quite well until she was 41 years old and then had recurrent syncopal attacks for 13 years.…”

Section: Av Anmentioning

confidence: 99%

Aetiology of chronic heart block. A clinico-pathological correlation in 65 cases.

Harris¹,

Davies²,

Redwood³

et al. 1969

Heart

101

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Section: Av Anmentioning

confidence: 99%

Aetiology of chronic heart block. A clinico-pathological correlation in 65 cases.

Harris¹,

Davies²,

Redwood³

et al. 1969

Heart

101

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“…As other authors have found, congenital A-V block is almost always due to a complete or incomplete developmental defect of the common A-V bundle (Langendorf and Pick, 1954;Campbell and Thorne, 1956;Donoso et al, 1956;Paul, Rudolf, and Nadas, 1958;Smithells and Outon, 1959;Nakamura and Nadas, 1964). Patients with congenital A-V block do not have serious Adams-Stokes attacks.…”

mentioning

confidence: 89%

Electrocardiographic findings in patients with complete atrioventricular block.

Lopez¹

1968

Heart

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The introduction of the artificial electrical pacemaker for the treatment of patients with complete A-V block has been accompanied by renewed interest in the pathogenesis of this disorder. It has been considered that most cases of complete block are due to organic or functional lesions either in the A-V node or in the common A-V bundle. Barker conduction through both bundle-branches was unequally impaired. In both of these situations, one would observe a complete right or left bundlebranch block with prolongation of the P-R interval.Complete block would be the manifestation of failure of conduction through the more depressed branch, while prolongation of the P-R interval would be the manifestation of depressed conduction through the less impaired branch. They stressed that true bilateral bundle-branch block must show a prolonged A-V conduction time. Mahaim (1931), and more recently Lenegre and Moreau (1962), and Lenegre (1964), have conducted pathological studies in the hearts of patients who had complete A-V block. They confirmed the electrocardiographic impression that in the great majority of patients this type of block was due to an anatomical bilateral bundle-branch block.To elucidate further the relation between bilateral bundle-branch block and A-V block, we have analysed the records of all patients with complete A-V block admitted to the University Hospital, Saskatoon, in the five-year period between 1960 and 1965. Patients with surgical A-V block and those in whom the history and clinical diagnosis suggested digitalis toxicity were excluded. The results of our study form the basis of this communication.SUBJECTS AND RESULTS Between 1960 and 1965, 57 patients with an electrocardiographic diagnosis of complete A-V block were studied at the University Hospital. In many instances previous electrocardiograms were available. The age of the patient, the clinical history, and electrical axis in the frontal plane were carefully recorded.The 57 patients were divided into two main groups, according to the contour of the ventricular complexes during the periods of complete A-V

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“…Congenital complete heart block is compatible with normal development and survival (Yater, 1929;Campbell and Thorne, 1956;Donoso, Braunwald, Jick, and Grushman, 1956;Ikkos and Hanson, 1960;Hill, 1963;Nakamura and Nadas, 1964), but there is no doubt that Stokes-Adams attacks, though rare, can occur, and probably reflect a poor prognosis (Smithells and Outon, 1959;Molthan, Miller, Hastreiter, and Paul, 1962;Nakamura and Nadas, 1964).…”

mentioning

confidence: 99%