OBJECTIVETo report an initial experience with the endovascular repair of descending thoracic aortic aneurysm (DTAA).

METHODSEndoprostheses were placed into 41 patients with DTAA between January 2001 and July 2007 which were retrospectively analyzed. The preliminary right-left carotid and left carotid-subclavian bypass was performed in 4 cases in which the distances from the proximal aneurysm to the origin of the left common carotid artery were no longer than 15 mm. EVAR was conducted 1 week after the bypass or immediately.

RESULTSAll stent grafts were deployed in proper position. There were two deaths (4.9%) during perioperative period, resulting from multiorgan failure and acute cardiac infarction, respectively. Eighteen endoleaks occurred immediately after EVAR (43.9%), four disappeared after balloon dilatation. There were two acute renal insufficiencies (4.9%), one requiring hemodialysis for more than 30 days. Follow-up, which ranged from 1 to 60 months [median, (18.6 +/- 4.2) months] was carried out in 26 patients (63.4%). Type-I endoleak and type-III endoleak were detected in two patients in 4 years and 2 years after EVAR, might because of migration, and were corrected using another stent-graft each. Two patients died of other diseases during follow-up. Complete thrombosis of the thoracic aneurysm sac with no late migration or endoleaks was revealed on CT at 3 months postoperatively in the remaining patients. The decrease in maximal aneurysm diameter was 0-22 mm [median, (8.3 +/- 4.5) mm] and the prosthetic vascular grafts in four patients with preliminary carotid subclavian bypass surgery were patent during the follow-up period.

CONCLUSIONSThe treatment of descending thoracic aortic aneurysm with an endovascular approach is feasible with less trauma, quick recovery and less complications. It may offer the best means of therapy for high risk patients.

Adult ; Aged ; Aged, 80 and over ; Aortic Aneurysm, Thoracic ; surgery ; Blood Vessel Prosthesis Implantation ; adverse effects ; methods ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Postoperative Complications ; etiology ; prevention & control ; Retrospective Studies ; Treatment Outcome

OBJECTIVETo assess retrospectively the effects of different protective methods on brain in ascending aortic aneurysm surgery.

METHODSIn 65 patients, aneurysm was dissected to the aortic arch or right arch. To protect brain, deep hypothermic circulatory arrest (DHCA) combined with retrograde cerebral perfusion (RCP) through the superior vena cava (n = 50) and simple DHCA (n = 15) were used during the procedure. Blood samples for lactic acid level from the jugular vein were compared in both groups at different phase, and perfusion blood distribution and oxygen content difference between the perfused and returned blood were measured in some RCP patients.

RESULTSThe DHCA time was 35.9 +/- 18.8 min (10.0 - 63.0 min) and DHCA + RCP time was 45.5 +/- 17.2 min (16.0 - 81.0 min). The resuscitation time was 7.1 +/- 1.6 h (4.4 - 9.4 h) in DHCA patients and 5.4 +/- 2.2 h (2.0 - 9.0 h) in RCP patients. Operation death was 3/15 in the DHCA group and 1/50 in the RCP patients. Central nervous complication existed in 3/12 of DHCA patients and 1/49 of RCP patients (P < 0.01). The overall survival rate was 96% (RCP) vs 67% (DHCA), central nervous system dysfunction was 20% in DHCA vs 2% in RCP (P < 0.01). The blood lactic acid level increased significantly after reperfusion in DHCA than in RCP. The blood distribution measurement approximated to 20% of the perfused blood returned from arch vessels. Oxygen content between perfused and returned blood showed that oxygen uptake was adequate in the RCP group.

CONCLUSIONSThe application of RCP could prolong the safety duration of circulation arrest. Cerebral perfusion may reep the brain cool and flush out particulate and air embolism. Open anastomosis of the aortic arch to the prosthesis can be safely performed. RCP is acceptable for brain protection in clinical practice.

Adult ; Aortic Aneurysm, Thoracic ; surgery ; Cerebrovascular Circulation ; Extracorporeal Circulation ; Female ; Humans ; Hypothermia, Induced ; Hypoxia-Ischemia, Brain ; etiology ; prevention & control ; Male ; Middle Aged ; Perfusion ; methods ; Retrospective Studies ; Vena Cava, Superior

OBJECTIVE: To identify whether naringenin plays a protective role during thoracic aneurysm formation in Marfan syndrome. METHODS: To validate the effect of naringenin, Fbn1^C1039G/+ mice, the mouse model of Marfan syndrome, were fed with naringenin, and the disease progress was evaluated. The molecular mechanism of naringenin was further investigated via in vitro studies, such as bioluminescence resonance energy transfer (BRET), atomic force microscope and radioligand receptor binding assay. RESULTS: Six-week-old Fbn1^C1039G/+ mice were fed with naringenin for 20 weeks. Compared with the control group, naringenin significantly suppressed the aortic expansion [Fbn1^C1039G/+ vs. Fbn1^C1039G/++naringenin: (2.49±0.47) mm, n=18 vs. (1.87±0.19) mm, n=22, P < 0.05], the degradation of elastin, and the expression and activity of matrix metalloproteinase 2 (MMP2) and MMP9 in the ascending aorta of Fbn1^C1039G/+ mice. Besides, treatment with naringenin for 6 weeks also attenuated the disease progress among the 20-week-old Fbn1^C1039G/+ mice with established thoracic aortic aneurysms [Fbn1^C1039G/+ vs. Fbn1^C1039G/++naringenin: (2.24±0.23) mm, n=8 vs. (1.90±0.17) mm, n=8, P < 0.05]. To understand the underlying molecular mechanisms, we examined the effects of naringenin on angiotensin Ⅱ type 1 receptor (AT1) signaling and transforming growth factor-β (TGF-β) signaling respectively, which were the dominant signaling pathways contributing to aortopathy in Marfan syndrome as previously reported. The results showed that naringenin decreased angiotensin Ⅱ (Ang Ⅱ)-induced phosphorylation of protein kinase C (PKC) and extracellular regulating kinase 1/2 (ERK1/2) in HEK293A cell overexpressing AT1 receptor. Moreover, naringenin inhibited Ang Ⅱ-induced calcium mobilization and uclear factor of activated T-cells (NFAT) signaling. The internalization of AT1 receptor and its binding to β-arrestin-2 with Ang Ⅱ induction were also suppressed by naringenin. As evidenced by atomic force microscope and radioligand receptor binding assay, naringenin inhibited Ang Ⅱ binding to AT1 receptor. In terms of TGF-β signaling, we found that feeding the mice with naringenin decreased the phosphorylation of Smad2 and ERK1/2 as well as the expression of TGF-β downstream genes. Besides, the serum level of TGF-β was also decreased by naringenin in the Fbn1^C1039G/+ mice. Furthermore, we detected the effect of naringenin on platelet, a rich source of TGF-β, both in vivo and in vitro. And we found that naringenin markedly decreased the TGF-β level by inhibiting the activation of platelet. CONCLUSION Our study showed that naringenin has a protective effect on thoracic aortic aneurysm formation in Marfan syndrome by suppressing both AT1 and TGF-β signaling.
Angiotensin II/metabolism* ; Animals ; Aortic Aneurysm, Thoracic/prevention & control* ; Calcium/metabolism* ; Disease Models, Animal ; Elastin/metabolism* ; Fibrillin-1/metabolism* ; Flavanones ; Marfan Syndrome/metabolism* ; Matrix Metalloproteinase 2 ; Matrix Metalloproteinase 9 ; Mice ; Mice, Inbred C57BL ; Protein Kinase C/metabolism* ; Receptor, Angiotensin, Type 1/metabolism* ; Transforming Growth Factor beta/metabolism* ; Transforming Growth Factors/metabolism* ; beta-Arrestins/metabolism*