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Background and Aim of the Study Interrupted aortic arch (IAA) is a rare and fatal malformation. Most patients with IAA are diagnosed in early childhood because of the severity of their symptoms. IAA is classified into three morphologic types (A, B, or C), depending on the site of the interruption. In our case, this patient did not have a common brachiocephalic trunk, left carotid artery, or left subclavian artery, IAA classification of this case cannot be judged based on the existing interruption method. Methods We present a 6‐year‐old Chinese boy with a history of neck masses since birth, and an echocardiogram from a local county hospital revealing an IAA without any cardiac anomalies, was referred to our hospital. Results The patient was feeling good and was nearly asymptomatic. Computed tomography angiography was performed, which indicated an absent aortic arch, likely due to disruption during development, and aortic discontinuity. The ascending aorta gave rise to both carotid arteries, and the descending aorta was supplied by large subclavian arteries. The right vertebral artery was supplied by right large collateral vessels that connected the right carotid artery. The left side was similar in structure to the right side. The descending aorta was supplied by large subclavian arteries. The subclavian arteries and carotid arteries were connected by large collateral vessels. Due to the large collateral vessels, the child's lower body had sufficient blood supplied, so that the typical differential cyanosis did not occur, and the child without symptomatic can survive to now. Conclusions This patient did not have a common brachiocephalic trunk, left carotid artery, or left subclavian artery. Maybe, this patient belonged to a new type of IAA.

Purpose Excessive cardiac fibrosis and remodeling occur after myocardial infarction. Yes-associated protein (YAP) is a major transcriptional co-activator of the Hippo pathway and an important regulator of cardiac fibrosis. Verteporfin is a pharmacological inhibitor of YAP that effectively inhibits fibrosis and inflammatory responses. Therefore, this study aimed to explore the effects of verteporfin on cardiac fibrosis after myocardial infarction (MI) and its possible mechanisms. Methods Wild-type C57BL/6J mice were subjected to MI by ligating their left anterior descending coronary artery (LAD) and treating them with verteporfin (50 mg/kg/48 h) or phosphate-buffered saline for 2 weeks. Echocardiography was performed to evaluate cardiac function after 2 weeks, and hematoxylin and eosin and Masson staining were performed to evaluate the degree of myocardial fibrosis and inflammatory response. The protein expression levels of the YAP-Smad2/3 pathway, inflammatory factors, and fibrosis markers in the heart and in vitro were determined using western blotting and immunofluorescence staining. Results Compared to the MI group, verteporfin treatment improved cardiac function and fibrosis in mice post-MI. Moreover, myocardial YAP and SMAD2/3 expression were reduced in verteporfin-treated animals. Hematoxylin and eosin staining and molecular examination showed inflammatory factor and cardiac fibrosis marker expression in the heart sections. Conclusion Verteporfin can attenuate cardiac fibrosis and inflammatory responses and improve cardiac function by suppressing the YAP-Smad2/3 signaling pathway post-MI.

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