Abstract
Pulmonary arteriovenous malformations (PAVMs) carry significant risks [1, 2]. Pulmonary arterial blood passing through these right-to-left shunts cannot be oxygenated, leading to hypoxaemia, with arterial oxygen tension and arterial oxygen saturation ( S a,O2) inversely related to the size of the shunt fraction. The fragile wall of the PAVM sac may rupture, leading to haemoptysis or haemothorax [3]. In addition, the absence of a filtering capillary bed allows particulate matter to reach the systemic circulation where it impacts in other capillary beds, including those of the cerebral circulation, resulting in embolic cerebrovascular accidents and cerebral abscesses. In a recent series of 219 patients that corrected for ascertainment bias, the rates for ischaemic stroke and cerebral abscess were 11.3% and 9%, respectively, with risks unrelated to PAVM severity or symptoms [4]. Treatment of PAVMs by embolisation is an effective means of reducing lifetime risks of paradoxical embolic stroke and cerebral abscess [4], improving oxygenation [1, 5, 6], and treating PAVM-induced haemoptysis [3, 7]. Embolisation usually carries minimal risk in expert hands and, as a result, is generally offered to patients with PAVMs of a size amenable to embolisation, irrespective of the presence of respiratory symptoms. PAVMs themselves have a lower vascular resistance than that of the surrounding normal lung, due to the absence of a microvascular network of capillary vessels. However, most individuals with PAVMs have underlying hereditary …
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