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Hereditary haemorrhagic telangiectasia (HHT) is a rare autosomal dominant disorder resulting in uncontrolled multisystem angiogenesis. The pathogenesis of this disease is thought to relate to elevated levels of transforming growth factor beta and vascular endothelial growth factor (VEGF). The frail arteriovenous malformations (AVMs) give rise to complications including haemorrhage and shunting. These have classically included recurrent epistaxis and gastrointestinal bleeding and associated iron-deficiency anaemia. More recently, high-output heart failure has been recognized in patients with significant hepatic involvement. This is thought to occur as a result of low systemic resistance due to shunting of blood through liver AVMs with an associated compensatory increase in cardiac output. Bevacizumab is a humanized monoclonal that acts to cause VEGF inhibition. Previously, this drug has been shown to benefit patients with HHT by reducing transfusion requirements and frequency of epistaxis. In addition, there is a growing body of evidence that bevacizumab may be associated with amelioration of high-output cardiac failure associated with HHT-induced hepatic shunting. We believe this case supports the use of bevacizumab in this context.

A case report of successful treatment of high-output heart failure secondary to hereditary haemorrhagic telangiectasia with bevacizumab