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Atypical aortic coarctation is a rare condition associated with Takayasu arteritis, and is characterized by symptoms caused either by hypotension in the lower half of the body or secondary hypertension in the upper half of the body, and heart failure. We report a rare case of axillofemoral bypass to improve congestive heart failure for atypical aortic coarctation complicating Takayasu arteritis. Augmented vascular bed and retrograde renal blood flow after axillofemoral bypass surgery could achieve effective blood pressure control and improve renal function and cardiac function (LVEF: 30% → 55%, BNP: 2943 pg/mL → 128 pg/mL). There were two contributing factors for improvement of heart failure such as the increased vascular bed and the increase in retrograde renal blood flow. We believe that axillofemoral bypass is effective for Takayasu arteritis patients with refractory heart failure. In daily practice, careful attention should be paid to an impact of cardiorenal‐aorta interaction in atypical aortic coarctation complicating Takayasu arteritis.

An 81-year-old woman presented with massive melena. She required urgent hospitalization because of hyperprothrombinemia (international normalized ratio >9.9), induced by warfarin treatment following double valve replacement surgery she underwent 35 years prior, and had cirrhosis caused by chronic liver congestion. The next day, she became comatose (serum ammonia level, 417 μg/dL) and was diagnosed with hepatic encephalopathy with acute hyperammonemia. Despite the decrease in serum levels (53 μg/dL) following 3-day lactulose and rifaximin treatment, her consciousness level remained low (Glasgow Coma Scale, 6). Electroencephalogram on day 8 showed triphasic waves, but no obvious epileptic discharges. Brain magnetic resonance imaging (MRI) on day 1 was unremarkable (Fig. 1A–C) and showed bilateral and symmetrical cortical swelling in the insular, cingulate, frontal, and occipital cortices on day 10 (Fig. 1D–F), and showed reduction in the extent of the lesion at 3 weeks post-hospitalization (Fig. 1G–I). Her consciousness level recovered slightly later than the MRI findings. Ammonia detoxification in the brain occurs through glutamine formation through the glutamine synthesis pathway in astrocytes, leading to glutamine-induced astrocyte swelling and subsequent cerebral edema and even encephalopathy.1 Brain MRIs – which are essential in differential diagnoses – show symmetrical signal abnormalities in the insular and cingulate cortices.2-4 Close attention should be paid to secondary encephalopathy in patients with hyperammonemia.

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome and its etiology and pathogenesis have not been well understood. Intracoronary imaging modalities with intravascular ultrasound and optical coherence tomography would enable a precise diagnosis in this entity. Coronary angioscopy is also a unique tool for allowing direct visualization of the luminal surface of a vessel. We described an interesting case of SCAD documented with multimodality intracoronary imaging showing the presence of superficial lipid plaque nearby the coronary dissection entry point, which might have been associated with fragility of the arterial wall and the subsequent development of SCAD.