Literature DB >> 15680049

The biological "scrabble" of pulmonary arteriovenous malformations: considerations in the setting of cavopulmonary surgery.

Robert M Freedom1, Shi-Joon Yoo, Donald Perrin.   

Abstract

Pulmonary arteriovenous fistulas are vascular malformations, which, by virtue of producing abnormal vascular connections proximal to the units of gas exchange, result in intrapulmonary right-to-left shunting. These malformations or fistulas reflect at least in part disordered angiogenesis, and less commonly recruitment and dilation of pre-existing vascular channels. Pulmonary arteriovenous fistulas occur in a number of diverse clinical settings. Such fistulas are a well-established feature of the Weber-Osler-Rendu complex, or hereditary haemorrhagic telangiectasia, an autosomal dominant vascular dysplasia characterized by mucocutaneous telangiectasis, epistaxis, gastrointestinal haemorrhage, and arteriovenous malformations in the lung, brain, liver and elsewhere. They are also seen in the patient with acute or chronic liver disease, disease that is usually but not invariably severe, or those with non-cirrhotic portal hypertension. They may occur as congenital malformations, single or diffuse, large or small in isolation, and when large or extensive enough may result in hypoxaemia, clinical cyanosis, and heart failure. Cerebral vascular accidents are also a well-known complication of this disorder. An extensive literature has accumulated with regard to the pulmonary arteriovenous fistulas seen in the setting of the Weber-Osler-Rendu complex, and there is considerable information on the genetics, basic biology, clinical findings, complications and therapeutic interventions of these malformations in the setting of this syndrome. These issues, however, are not the primary considerations of this review, although some aspects of this fascinating disorder will be discussed later. Rather the focus will be on pulmonary arteriovenous malformations that develop in the setting of cavopulmonary surgery, and their relationship to the pulmonary arteriovenous fistulas occurring in the hepatopulmonary syndrome. The complex tapestry of these overlapping and intersecting clinical observations will be unfolded in the light of their chronology.

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Year:  2004        PMID: 15680049     DOI: 10.1017/S1047951104004111

Source DB:  PubMed          Journal:  Cardiol Young        ISSN: 1047-9511            Impact factor:   1.093


  6 in total

1.  Constitutively active endothelial Notch4 causes lung arteriovenous shunts in mice.

Authors:  Doug Miniati; Eric B Jelin; Jennifer Ng; Jianfeng Wu; Timothy R Carlson; Xiaoqing Wu; Mark R Looney; Rong A Wang
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2009-11-20       Impact factor: 5.464

2.  Arterial desaturation due to pulmonary arteriovenous malformations after the Kawashima Operation.

Authors:  Rohit S Loomba
Journal:  Ann Pediatr Cardiol       Date:  2016 Jan-Apr

3.  Hepatic factor may not originate from hepatocytes.

Authors:  Monica Merbach; Ramani Ramchandran; Andrew D Spearman
Journal:  Front Cardiovasc Med       Date:  2022-09-06

Review 4.  Pulmonary Vascular Sequelae of Palliated Single Ventricle Circulation: Arteriovenous Malformations and Aortopulmonary Collaterals.

Authors:  Andrew D Spearman; Salil Ginde
Journal:  J Cardiovasc Dev Dis       Date:  2022-09-17

5.  Endostatin, an inhibitor of angiogenesis, decreases after bidirectional superior cavopulmonary anastamosis.

Authors:  Aida Field-Ridley; Ritva Heljasvaara; Taina Pihlajaniemi; Ian Adatia; Christine Sun; Roberta L Keller; Wen Hui Gong; Sanjeev Datar; Peter Oishi; Jeffrey R Fineman
Journal:  Pediatr Cardiol       Date:  2012-09-08       Impact factor: 1.655

6.  Histologic evidence of intrapulmonary anastomoses by three-dimensional reconstruction in severe bronchopulmonary dysplasia.

Authors:  Csaba Galambos; Sunder Sims-Lucas; Steven H Abman
Journal:  Ann Am Thorac Soc       Date:  2013-10
  6 in total

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