Although there are multiple rodent models of the metabolic syndrome, very few develop vascular complications. In contrast, the JCR:LA-cp rat develops both metabolic syndrome and early atherosclerosis in predisposed areas. However, the pathology of the normal vessel wall has not been described. We examined JCR:LA control (+/+) or cp/cp rats fed normal chow diet for 6 or 18 mo. JCR:LA-cp rats developed multiple features of advanced cystic medial necrosis including "cysts," increased collagen formation and proteoglycan deposition around cysts, apoptosis of vascular smooth muscle cells, and spotty medial calcification. These appearances began within 6 mo and were extensive by 18 mo. JCR:LA-cp rats had reduced medial cellularity, increased medial thickness, and vessel hypoxia that was most marked in the adventitia. In conclusion, the normal chow-fed JCR:LA-cp rat represents a novel rodent model of cystic medial necrosis, associated with multiple metabolic abnormalities, vascular smooth muscle cell apoptosis, and vessel hypoxia.NEW & NOTEWORTHY Triggers for cystic medial necrosis (CMN) have been difficult to study due to lack of animal models to recapitulate the pathologies seen in humans. Our study is the first description of CMN in the rat. Thus the JCR:LA-cp rat represents a useful model to investigate the underlying molecular changes leading to the development of CMN.
We describe a rare case of aorto-oesophageal fistula and aortic pseudoaneurysm in a middle-aged man, who presented with chest pain and haematemesis 1 week after swallowing a fish bone. Oesophagogastroduodenoscopy and computed tomographic angiography findings were consistent with oesophageal perforation, proximal descending aortic pseudoaneurysm, and aorto-oesophageal fistula. Thoracic endovascular aortic repair was performed. The patient died from severe mediastinal sepsis. Early surgical intervention and broad-spectrum antibiotic therapy are crucial in preventing life-threatening mediastinal infection.