EDITORIAL

Pathogenesis of pulmonary arteriovenous malformations: role of hepatopulmonary interactions

J J Vettukattil

Correspondence to:
Correspondence to:
Dr Joseph J Vettukattil, Wessex Cardiac Unit, E Level East Wing, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK;
joseph.vettukattil@suht.swest.nhs.uk

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Pulmonary arteriovenous malformations—abnormal communications between pulmonary arteries and veins—can lead to serious haemodynamic consequences, predisposing to varying degrees of intrapulmonary shunting, resulting in cyanosis, clubbing, polycythemia, and impaired exercise tolerance

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Keywords: pulmonary ateriovenous malformations; hepatopulmonary syndrome

Abbreviations: CHPS, cardiogenic hepatopulmonary syndrome; HF, hepatic factor(s); HPS, hepatopulmonary sydrome; PAVMs; pulmonary arteriovenous malformations; PVF, portal venous factor(s)

The first 150 words of the full text of this article appear below.

The significance of organ interaction in the pathophysiology of tissue dysfunction is increasingly being recognised as a key determinant influencing resolution of tissue injury. The modulatory effects of such interactions, that incorporate the expanding number of markers of molecular and receptor level cell-to-cell communications, is complex. The liver is a unique organ as it is connected in series with the lung and portal system. It receives all the venous effluent from the portal system and directs its metabolites to the lungs before perfusing any other organ in the body.

Pulmonary arteriovenous malformations (PAVMs) are abnormal communications between pulmonary arteries and veins. They may be hereditary as in Osler-Weber-Rendu disease or acquired as in liver disorders, systemic diseases, venous anomalies, and after palliation of complex cyanotic congenital heart disease. They tend to be progressive and lead to serious haemodynamic consequences, predisposing to varying degrees of intrapulmonary shunting. This results in cyanosis, . . . [Full text of this article]

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