A 46-year-old man with no known past medical history presented with syncope followed by slurred speech and facial droop. Magnetic resonance imaging of the brain revealed an acute infarction of the left superior cerebellar artery territory (Figure 1A) and evidence of prior infarctions. Transthoracic and transesophageal echocardiography with agitated saline contrast demonstrated bubbles in the left atrium within 3–5 cardiac cycles without evidence of intracardiac shunting (Figure 1B). Computed tomography (CT) angiography identified a large tubular structure in the right lung communicating with the right lower pulmonary vein, consistent with a pulmonary arteriovenous malformation (PAVM) with a feeding vessel diameter of 1.3 cm (Figures 1C and 1D). Lower extremity Doppler ultrasound showed no evidence of deep vein thrombosis. Systemic anticoagulation was initiated. After completing a neurorehabilitation course, the patient underwent successful PAVM embolization. PAVMs are often asymptomatic (9–66%) (1), even when associated with hypoxemia (1, 2), and are commonly first identified incidentally by chest CT, which is the most common mode of detection (3). Large PAVMs are more often symptomatic owing to dyspnea (15–51%) (3), hypoxemia, polycythemia, or paradoxical embolization (1, 4–7), as in this case. In half the cases, ischemic stroke after paradoxical embolization is the initial presentation of PAVM (7, 8). Unfortunately, with neurologic presentations, the diagnosis of PAVM is often delayed by an average of 2 years (3). Consensus recommendations suggest intravascular embolization for all PAVMs once detected, or surgical resection if embolotherapy is not possible (9, 10). As this case of a patient with evidence of multiple prior strokes illustrates, a high clinical suspicion is critical for timely diagnosis and definitive management of PAVMs to prevent further neurologic injury.

Figure 1. (A) Magnetic resonance image of the brain demonstrating acute infarction of the left superior cerebellar artery territory with evidence of prior infarctions in the posterior circulation territory. (B) Transthoracic echocardiogram with agitated saline demonstrating bubbles in the left atrium within 3–5 cardiac cycles. (C) Computed tomography angiography of the chest demonstrating a large tubular structure in the right lung communicating with the right lower pulmonary vein, consistent with pulmonary arteriovenous malformation (PAVM) with a feeding vessel diameter of 1.3 cm. (D) Reconstructed three-dimensional image showing a large vascular tubulosaccular lesion in the posterolateral segment of the right lower lobe, consistent with PAVM.

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