Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previous decision analysis examined a patient with severe CAD, diminished ventricular function, and an abdominal aortic aneurysm and also concluded that CABG followed by aneurysm repair was optimal. This patient, who had well-preserved cardiac function but severely compromised pulmonary status, stood to gain less from CABG than would a patient with more severe coronary disease, thus accounting for the "close-call" between the CABG-AAA and AAA only strategies. Nevertheless, the analysis did emphasize the benefit of aneurysm repair, whether done alone or after CABG. The analysis also highlighted the significant risk of aneurysm rupture the patient is exposed to while recovering from CABG surgery. The operative mortality risks of the two procedures are similar; thus, the patient's total operative risk is approximately doubled if he undergoes both procedures rather than aneurysm repair alone. The key question raised by the analysis is whether this double jeopardy is more than compensated by the degree to which prior CABG reduces both short-term cardiac risk at subsequent aneurysm repair and long-term cardiac mortality. For this patient, who had good cardiac function, the gains appeared sufficient to offset the interval risk of aneurysm rupture and the additional risk associated with a surgical procedures. THE REAL WORLD The patient indeed underwent and tolerated CABG, although he had a stormy prolonged postoperative course due to pulmonary failure. After discharge from the hospital, he declined readmission for repair of the aneurysm. We did not model that possibility, clearly an inadequacy in our tree. Some six months later, the patient was still alive and was, reluctantly, readmitted for aneurysmorrhaphy. At that time, however, his pulmonary function had deteriorated and both the anesthesiologist and the pulmonary consultant stated unequivocally that further surgery was now impossible. In retrospect, the expected utility of CABG without aneurysm repair (thus providing only a decrease in the long-term mortality risk from his CAD) would have been 1.95 (DEALE) or 2.06 (Markov) years. Sensitivity analysis revealed that, even if long-term cardiac risk were completely eliminated by CABG, immediate aneurysm repair would have been a better approach had the patient's physicians known he would be likely to refuse or not be a candidate for the second operation. In summary, although the patient's comorbidities did indeed place him at significant operative risk for either aneurysmorrhaphy alone or two sequential procedures, the benefits to be gained were shown to far outweigh the risks when compared with expectant observation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Aortic aneurysm in a 74-year-old man with coronary disease and obstructive lung disease: is double jeopardy enough? 279 36

Abdominal aortic aneurysm (AAA) is fatal meanwhile unpredictable asymptomatic cardiovascular disease. Available data suggests the potential participation of circular RNAs (circRNAs) in AAA pathogenesis. But direct evidence is limited. The present study is to functionally and mechanically characterize circRNA CCDC66 (circCCDC66) in AAA. Previous work indicated the differentially expressed circCCDC66 in AAA. At molecular level, circCCDC66, miR-342-3p and CCDC66 transcript were measured through real-time quantitative polymerase chain reaction assay. Functionally, we examined the cellular behaviours of circCCDC66-depleted or CCDC66-depleted vascular smooth muscle cells (VSMCs) including proliferation and apoptosis. It elucidated that depletion of circCCDC66 induced proliferation facilitation and apoptosis reduction. Mechanically, we addressed the interplay among circCCDC66, miR-342-3p and CCDC66 transcript using RNA immunoprecipitation, RNA pull-down and luciferase reporter experiments. Through mechanical validation, we discovered the positive regulation of circCCDC66 on its host gene CCDC66. Loss of CCDC66 mimicked the effects of circCCDC66 silencing on VSMC growth. Moreover, it uncovered that circCCDC66 regulated CCDC66-dependent VSMC growth through sponging miR-342-3p. Rescue experiments aimed to address the functional role of regulatory network formed by circCCDC66, miR-342-3p and CCDC66 in VSMC growth and apoptosis. Suppressing miR-342-3p or overexpressing CCDC66 could reverse VSMC growth caused by circCCDC66 deficiency. Our study further emphasized and first unveiled the function of circCCDC66 in VSMC proliferation. CircCCDC66 upregulated its host gene through its role of miR-342-3p sponge, and hinted a novel molecular mechanism in AAA. SIGNIFICANCE OF THE STUDY: It was firstly displayed in our study that depletion of circCCDC66 induced proliferation augmentation and apoptosis reduction of vascular smooth muscle cells (VSMCs). Meanwhile, circCCDC66/miR-342-3p/CCDC66 axis was proved can play the function of modulating the cell proliferation and apoptosis of VSMCs, which provided us a novel molecular mechanism in AAA.
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PMID:Circular RNA CCDC66 facilitates abdominal aortic aneurysm through the overexpression of CCDC66. 3199 4