刘鹏红
中国医学科学院阜外医院 病房
OBJECTIVES:The purpose of this study was to assess the efficacy of the hybrid total arch procedure for the treatment of DeBakey type I dissection by analyzing mid-term results.METHODS:From November 2009 to September 2014, 56 patients with DeBakey type I dissection underwent hybrid total arch repair without deep hypothermic circulatory arrest. During the follow-up, computed tomographic imaging was performed to evaluate the aortic diameter, true lumen diameter, false lumen diameter and false patency at the following three levels: pulmonary bifurcation, diaphragm and superior mesenteric artery.RESULTS:The hospital mortality rate was 3.6% (2/56 patients). Three patients exhibited type Ia endoleak during the operation and 1 patient demonstrated type II endoleak 5 days after surgery. During the follow-up, false lumen complete thrombosis was observed at the level of the pulmonary bifurcation in 94% of patients (P < 0.001). At the level of the diaphragm and superior mesenteric artery, false lumen thrombosis was observed in 68% (P < 0.001) and 36% (P < 0.001) of patients, respectively. No patient had type I or III endoleak and no reoperation was related to residual dissected aorta. The actuarial 1-, 3- and 5-year survival rates were 96.4% [95% confidence interval (95% CI), 91.5-100], 92.3% (95% CI, 85-99.6) and 89.6% (95% CI, 80.8-98.4), respectively.CONCLUSIONS:For patients with DeBakey type I dissection, the hybrid total arch procedure can be safely adopted with good mid-term results and with low morbidity and mortality. Longer-term follow-up is required to confirm the viability of this technique.
Interactive cardiovascular and thoracic surgery 2016
In this study, we hypothesized that angiotensin II (Ang II) induces matrix metalloproteinase 2 (MMP-2) upregulation in aneurysmal smooth muscle cells (ASMCs) derived from ascending thoracic aortic aneurysms (ATAAs). We compared MMP-2 protein levels in ascending aortic specimens using Western blot and plasma concentrations by enzyme-linked immunosorbent assay between ATAA (n = 40) and coronary heart disease patients (n = 40). Additionally, the protein level of angiotensinogen (AGT) in the ascending aorta and the plasma concentration of Ang II were detected by Western blot and radioimmunoassay, respectively, in ATAA and coronary heart disease patients. In ATAA patients, Ang II and MMP-2 plasma levels were significantly increased (P < 0.05). Additionally, AGT and MMP-2 protein levels in the aorta of ATAA patients were higher (P < 0.01). Enhanced AGT suggested that the amount of Ang II in aneurysmal aorta specimens may be also increased, which was confirmed by immunofluorescent staining for Ang II. Moreover, we investigated the effect of Ang II on MMP-2 upregulation by ASMCs and determined the Ang II receptors and intracellular signaling pathways that are involved. Our results showed that treatment with Ang II significantly increased the expression of MMP-2 through the Ang II type 1 receptor (AT1R) and activated the 3 major mitogen-activated protein kinases (MAPKs), JNK, ERK1/2, and p38 MAPK. In conclusion, these results indicate that Ang II can induce MMP-2 expression elevation through AT1R and MAPK pathways in ASMCs and suggest that there is therapeutic potential for angiotensin receptor blocker drugs and MAPK inhibitors in the prevention and treatment of ATAAs.
Journal of cardiovascular pharmacology 2015
