Value of the deep femoral artery as alternative inflow source in infrainguinal bypass surgery.

BACKGROUND: The purpose of this study was to analyze the long-term results of infrainguinal bypass surgery using the deep femoral artery (DFA) as the inflow source. METHODS: Between 1998 and 2011, 88 bypasses of the lower limb were placed in 86 patients (mean age 71 years) using the deep femoral artery as inflow. Patients' records were retrieved from a computerized database and analyzed retrospectively. RESULTS: Critical limb ischemia (rest pain/tissue loss) was the indication in the majority (87.5%) of cases. The distal anastomosis of the bypass grafts was located at the popliteal level in 32 cases and the tibial (pedal) level in 52 cases, respectively, with the autologous vein as conduit in 94% of cases. Perioperative mortality was 2.3% and 77 patients (79 limbs) were followed over a mean period of 48 months. Overall primary, primary assisted, and secondary patency rates of 64.2%, 74.9%, and 92.3% were noted at 60 months, respectively. The limb salvage rate was 97%, with an overall survival of 48.7% at 60 months. CONCLUSIONS: The deep femoral artery can serve as reliable inflow source for infrainguinal bypass surgery in difficult situations like redo groin surgery, limited conduit length, and circumferential nonobstructive calcification of the common femoral artery.

Use and durability of femoral vein for autologous reconstruction with infection of the aortoiliofemoral axis.

OBJECTIVE: To analyze early and late mortality, venous morbidity, reinfection, and freedom from reintervention after using the femoral vein (FV) for vascular reconstruction with infection of the aortoiliofemoral axis. METHODS: By reviewing our database, 86 patients could be identified with implantation of FV grafts in infected fields between November 1995 and July 2012. The patient records were retrospectively analyzed and follow-up information obtained from patients or their general physician. Seventy-one patients presented with prosthetic graft infection and 15 with an infected aneurysm. For data analysis, patients were divided into an aortoiliac (n = 67) and a femoral group (n = 19). Study end points assessed were early and late mortality, incidence of deep vein thrombosis of the FV donor limb, graft patency, limb salvage, reinfection, and freedom from reintervention. RESULTS: Sixty-seven aortoiliac reconstructions were performed using 84 FV grafts with an operative mortality of 9%. After a mean follow-up of 45 months, survival, patency, limb salvage, and freedom from reintervention were 45%, 97%, 94%, and 91%, respectively, at 5 years. Twenty FV grafts were employed for 19 femoral reconstructions with an operative mortality of 10.5%. Here, mean follow-up was 35 months and survival, patency, limb salvage, and freedom from reintervention were 29%, 87%, 93%, and 81%, respectively, at 5 years. Specimen culture confirmed Staphylococcus (epidermidis and aureus) as the predominant microorganism. Venous morbidity after FV harvest showed an incidence of deep venous thrombosis of 13.7% for popliteal and 10.6% for tibial level at a follow-up of 24 months with only mild clinical symptoms (21% limb swelling). CONCLUSIONS: Vascular reconstruction using autologous FV in arterial and graft infection of the aortoiliofemoral axis provides durable long-term results with acceptable mortality and morbidity.

Strategies for endovascular aortic repair in aortobronchial and aortoesophageal fistulas.

OBJECTIVE: To report our experience of thoracic endovascular aortic repair (TEVAR) for acute bleeding originating from the thoracic aorta in patients with aortobronchial fistula (ABF) or aortoesophageal fistula (AEF). PATIENTS AND METHODS: A total of nine patients (three woman) were treated from September 1995 to March 2012 by TEVAR for ABF (n = 5) and AEF (n = 4). The implants (N = 14) were introduced with fluoroscopic guidance via the aorta (n = 1), the iliac (n = 2), or femoral (n = 11) artery, respectively. RESULTS: All aortic lesions could be sealed successfully. Perioperative morbidity was 0% in the ABF group and 50% (2 of 4) in the AEF group and no procedure-related morbidity was noted except one patient who received aortofemoral reconstruction because of iliac occlusive disease. After an overall mean follow-up of 56 months, three patients of the ABF group are alive and well and two patients died of nonrelated cause. Of the AEF group, one patient is alive after 22 months, and one died from metastasized esophageal cancer after 7 months. CONCLUSION: TEVAR is a safe and reliable procedure in the management of ABF. For AEF, TEVAR provides a successful first-line treatment to seal the fistula and control bleeding. However, prognosis is limited by the esophageal lesion and by ongoing mediastinitis/sepsis.

Co-expression of receptor tyrosine kinases in esophageal adenocarcinoma and squamous cell cancer.

This study aimed to define the co-expression pattern of target receptor tyrosine kinases (RTKs) in human esophageal adenocarcinoma and squamous cell cancer. The co-expression pattern of vascular endothelial growth factor receptor (VEGFR)1-3, platelet-derived growth factor receptor (PDGFR)alpha/beta and epidermal growth factor receptor 1 (EGFR1) was analyzed by RT-PCR in 50 human esophageal cancers (35 adenocarcinomas and 15 squamous cell cancers). In addition, IHC staining was applied for the confirmation of the expression and analysis of RTK localisation. The adenocarcinoma samples revealed VEGFR1 (97%), VEGFR2 (94%), VEGFR3 (77%), PDGFRalpha (91%), PDGFRbeta (85%) and EGFR1 (97%) expression at different intensities. Ninety-four percent of the esophageal adenocarcinomas expressed at least four out of six RTKs. Similarly, squamous cell cancers revealed VEGFR1 (100%), VEGFR2 (100%), VEGFR3 (53%), PDGFRalpha (100%), PDGFRbeta (87%) and EGFR1 (100%) expression at different intensities. All esophageal squamous cell carcinomas expressed at least four out of six RTKs. While VEGFR1-3 and PDGFRalpha and EGFR1 was expressed by tumor cells, PDGFRbeta was restricted to stromal cells, which also depicted a PDGFRalpha expression. Our results revealed a high rate of RTK co-expression in esophageal adenocarcinoma and squamous cell cancer and may encourage application of multi-target RTK inhibitors within a multimodal concept as a promising novel approach for innovative treatment strategies.

Protective effects of ischemic preconditioning and application of lipoic acid prior to 90 min of hepatic ischemia in a rat model.

AIM: To compare different preconditioning strategies to protect the liver from ischemia/reperfusion injury focusing on the expression of pro- and anti-apoptotic proteins. Interventions comprised different modes of ischemic preconditioning (IP) as well as pharmacologic pretreatment by alpha-lipoic acid (LA). METHODS: Several groups of rats were compared: sham operated animals, non-pretreated animals (nt), animals receiving IP (10 min of ischemia by clamping of the portal triad and 10 min of reperfusion) prior to sustained ischemia, animals receiving selective ischemic preconditioning (IPsel, 10 min of ischemia by selective clamping of the ischemic lobe and 10 min of reperfusion) prior to sustained ischemia, and animals receiving 500 micromol alpha-LA injected i.v. 15 min prior to the induction of 90 min of selective ischemia. RESULTS: Cellular damage was decreased only in the LA group. TUNEL-positive hepatocytes as well as necrotic hepatocyte injury were also decreased only by LA (19 +/- 2 vs 10 +/- 1, P < 0.05 and 29 +/- 5 vs 12 +/- 1, P < 0.05). Whereas caspase 3- activities in liver tissue were unchanged, caspase 9- activity in liver tissue was decreased only by LA pretreatment (3.1 +/- 0.3 vs 1.8 +/- 0.2, P < 0.05). Survival rate as the endpoint of liver function was increased after IP and LA pretreatment but not after IPsel. Levels of lipid peroxidation (LPO) in liver tissue were decreased in the IP as well as in the LA group compared to the nt group. Determination of pro- and anti-apoptotic proteins showed a shift towards anti-apoptotic proteins by LA. In contrast, both our IP strategies failed to influence apoptotic cell death. CONCLUSION: IP, consisting of 10 min of ischemia and 10 min of reperfusion, protects only partly against ischemia/reperfusion injury of the liver prior to 90 min of selective ischemia. IPsel did not influence ischemic tolerance of the liver. LA improved tolerance to ischemia, possibly by downregulation of pro-apoptotic Bax.

Protection from hepatic ischemia/reperfusion injury and improvement of liver regeneration by alpha-lipoic acid.

The aim of this study was to characterize the in vivo action of lipoic acid (LA) in hepatic ischemia/reperfusion injury (IRI) and its effects on liver regeneration involving the investigation of mechanisms of action and effects on animal survival. Two groups of rats were compared: one group received 500 micromol alpha-LA injected via the inferior vena cava 15 min before the induction of 90 min of selective ischemia. The untreated group received vehicle. Influence of LA on IRI of the liver was determined in short- and long-term experiments. Cellular damage was decreased under preconditioning conditions with LA. Caspase 3, 8, and 9 activities were significantly lower in the LA group accompanied by a decrease in terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive hepatocytes. Electron micrographs in the untreated group showed massive mitochondrial damage. The survival rate as end point of liver function was markedly increased after pretreatment with LA. Increased levels of tumor necrosis factor alpha was shown by enzyme-linked immunosorbent assay as well as real-time reverse transcription-polymerase chain reaction in the LA group accompanied by increased mitotic index and Ki-67 staining in liver tissue. Attenuation of IRI of the rat liver in vivo by LA is accompanied by reduction of necrosis and apoptosis-related cell death, whereas liver regeneration is increased.

Different protection mechanisms after pretreatment with glycine or alpha-lipoic acid in a rat model of warm hepatic ischemia.

BACKGROUND/AIM: Alpha-lipoic (LA) acid pretreatment has previously been described to reduce ischemia/reperfusion injury (IRI) after warm liver ischemia, whereas glycine pretreatment has been shown to be protective mostly in models of cold hepatic ischemia. The aim of this study was to determine whether glycine decreases IRI after warm hepatic ischemia. Furthermore we investigated whether doses of LA other than those used previously are also protective against IRI after warm hepatic ischemia. METHODS: Selective liver ischemia was maintained over a period of 90 min. In long-term as well as short-term experiments we studied IRI in several groups comparing animal survival as the pivotal endpoint. RESULTS: Animal survival was improved by glycine and 5,000 micromol LA, whereas all animals died within 3 days after pretreatment with 50 micromol LA. In the glycine group we observed a tendency towards decreased apoptosis-related cell death measured by the activity of caspase-3 in liver tissue and the percentage of TUNEL-positive hepatocytes in comparison to the untreated group. Serum alpha-glutathione S-transferase, lipid peroxidation, and caspase-3 activity as well as the percentage of TUNEL-positive hepatocytes and the percentage of liver necrosis were only significantly decreased by 5,000 micromol LA pretreatment. Liver tissue levels of tumor necrosis factor (TNF)alpha were reduced only in the glycine group whereas TNFalpha was increased in the untreated as well as the LA group. Levels of TNFalpha mRNA were upregulated in both the glycine- and LA-pretreated groups. CONCLUSION: Our data show that increased animal survival by glycine was accompanied by a reduced TNFalpha content in liver tissue. Protection by glycine is likely to result from a reduction in adverse TNFalpha effects. Administration of high-dose LA on the other hand led to a significant reduction in necrosis- and apoptosis-related cell death in IRI of the liver without a reduction in liver TNFalpha.