Anatomy, physiology and natural history of simple ventricular septal defects∗

Dammann, J. Francis; Thompson, Webb M.; Sosa, Omar; Christlieb, Ignacio Y.

doi:10.1016/0002-9149(60)90194-6

Cited by 31 publications

(10 citation statements)

References 11 publications

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“…Such defects are presumably reduced or obliterated by systolic contraction (Dammann et al, 1960;Edwards, 1960;Imperial et al, 1960;Saab et al, 1966;Schrire et al, 1965;Vogelpoel et al, 1961). Our angiographic studies suggest that the defects are near the outflow tract, and the observations are consistent with a postero-inferior muscular defect.…”

Section: Discussion Levin and His Groupsupporting

confidence: 62%

“…The latter has been reported as indicative of large shunts (Bleifer, Donoso, and Grishman, 1960). The angiographic studies belie the auscultatory findings in that no systolic shunt is visualized despite the murmur generally attributed to left-to-right flow (Bleifer et al, 1960;Dammann et al, 1960;Van der Hauwaert and Nadas, 1961).…”

Section: Discussion Levin and His Groupsupporting

confidence: 55%

“…Saab et al (1966) showed that 11 out of 23 muscular defects were located in this area. In our cases there was no evidence of multiple defects or for an apical location (Dammann et al, 1960;Edwards, 1960).…”

Section: Discussion Levin and His Groupsupporting

confidence: 44%

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Hydrogen-detected ventricular septal defects.

Herbert¹

1969

Heart

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Section: Discussion Levin and His Groupsupporting

confidence: 62%

Section: Discussion Levin and His Groupsupporting

confidence: 55%

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Hydrogen-detected ventricular septal defects.

Herbert¹

1969

Heart

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“…According to Kroop and Grishman (1950) and Dammann, Thompson, Sosa, and Christlieb (1960), there is also dilatation of arteries. Wagenvoort, Neufeld, DuShane, and Edwards (1961) showed that the amount of muscle in small vessels per unit area of lung was increased, and Naeye (1966), using planimetry, that this was due to an increase in the size of muscle cells, not in their number.…”

Section: The Present Casementioning

confidence: 99%

New pathological findings in emphysema of childhood: 3. Unilateral congenital emphysema with hypoplasia--and compensatory emphysema of contralateral lung

Henderson

Hislop

Reid

1971

Thorax

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A quantitative study is here reported on the lungs of a child of 9 months with unilateral emphysema associated with hypoplasia, and with compensatory emphysema in the contralateral lung. The left lung was judged to show congenital hypoplasia because of the reduced number of bronchi and arteries, its small volume, and a total alveolar number less than that normally found at birth. This last was due mainly to reduction in the number of acini, the intra-acinar number seeming little affected. As the alveoli were eight times the normal volume, the case was considered to be one of congenital hypoplastic emphysema.The right lung was evidently normal at birth, since it had a normal number of bronchi, arteries, and alveoli. The lung was increased in volume due to an increase in alveolar volume-an example of compensatory emphysema.This case is discussed with relation to two previously reported cases of lobar emphysema and other cases in the literature. It is emphasized that a quantitative analysis of the state of bronchi, alveoli, and blood vessels is important to establish the nature of the pathological change. A preliminary classification based on the anatomical features is offered.The degree of growth of airways, alveoli, and arteries in cases of childhood lobar emphysema has recently been assessed quantitatively. In one case the condition was due to a 'polyalveolar' lobe (Hislop and Reid, 1970) and in another to overinflation of a normally developed lobe . In the first paper (Hislop and Reid, 1970) This baby was born on 17 March, 1965. She had a cleft lip and anterior palate. She was seen at 6 months for repair of the lip but only a limited repair was considered possible because of her poor physical condition. At this time she was thought to have an enlarged left ventricle with a loud systolic murmur at the left sternal edge together with a murmur at the apex interpreted as being due to increased blood flow.The radiograph on 3 September, 1965 ( Fig. 1) was in partial expiration, the left dome being low compared with the right, suggesting air trapping in the left lung, although the heart was not displaced: the left lung was hypertransradiant and avascular, these changes being least marked in the medial part of the left upper lobe where the blood flow seemed better but still not normal. The right lung was plethoric, the heart and pulmonary trunk enlarged, and the aortic knuckle small. The apical lower lobe was partially collapsed. Angiography confirmed that the vessels to the right lung were enlarged with dilatation and tortuosity mainly of the proximal intrapulmonary vessels. No medium entered the left lung; an infracristal septal defect was seen.

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“…Another characteristic feature of patients with VSD is the progressive increase in pulmonary vascular resistance with medial hypertrophy and intimal proliferation (16). The basic mechanisms giving rise to such manifestations remain to be clarified (3).…”

Section: Discussionmentioning

confidence: 99%