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D Plissonnier

Publications and source records attributed to D Plissonnier.

At least 19 recordsLinked to original sources
PubMed2006

[Interest of D-lactate as a colic hypoperfusion marker during aortic abdominal aneurysm surgery].

OBJECTIVE: D-lactate is the dextrogyre form of the lactate usually measured in intensive care. Its bacterial origin should make it a marker of translocation during gut ischemia. The aim was to test D-lactate as a postoperative marker of colic hypoperfusion measured during aortic surgery. STUDY DESIGN: Prospective observational cohort study. PATIENTS AND MEASUREMENTS: Patients operated for abdominal aortic aneurysm. Two groups were stratified on inferior mesenteric arterial residual pressure (IMArP) measured during the surgery: Colic hypoperfusion during surgery (CHs) group: patients with an IMArP < 40 mmHg. CONTROL GROUP: patients with an IMArP > or = 40 mmHg. Baseline data such as age, duration of aortic clamping and severity score (IGS II) were collected. The D-lactate was measured in postoperative at admission time in ICU and then daily. D-lactate(max) defined the maximum value of D-lactate for one patient. MAIN RESULTS: Twenty-nine patients were included, 23 in the control group and 6 in the CHs group. Groups were comparable at baseline. D-lactate(max) was significantly higher in the CHs group (median: 0.13 mmol/l; min-max: 0.03-0.9 mmol/l) than in the control group (0.03; 0-0.26 mmol/l, p=0.007). CONCLUSION: D-lactate could be postoperative marker of colic hypoperfusion measured during surgery for abdominal aortic aneurysm.

Adult↗
PubMed2006

[Infectious or inflammatory aortitis? One case report].

INTRODUCTION: The infectious or inflammatory nature of an aortitis is difficult to assert because the microbiological results are often negative. The development of an aneurysm under treatment is rare, but requires a change in the therapeutic strategy and the etiologic diagnosis needs to be discussed again. EXEGESIS: We report the case of a 69-year-old woman treated by corticotherapy for an aortitis thought to be inflammatory, who required emergency surgery when a dissected aneurysm appeared. The peroperative samples were positive to Streptococcus pneumoniae using polymerase chain reaction and allowed a change of the diagnosis. The patient evolved favorably under antibiotic therapy. CONCLUSION: The decision to treat an aortitis by corticotherapy must be made with caution even if the microbiological tests are negative.

Adrenal Cortex Hormones↗
PubMed2006

Percutaneous repair of aortic aneurysms: a prospective study of suture-mediated closure devices.

PURPOSE: To evaluate prospectively the safety and efficacy of totally percutaneous placement of abdominal and thoracic aortic endografts using the Prostar XL suture-mediated closure system. METHODS: From January 2002 to January 2005, we attempted to insert percutaneously all bifurcated abdominal aortic and thoracic endografts. Consecutive patients (25 men, four women), with mean age 74.9 years (range 44-84), underwent endovascular repair for 20 abdominal aortic aneurysms (AAA) and nine thoracic aortic aneurysms (repeat operation in one case). Endografts used included 21 Zenith (Cook), eight Talent (Medtronic), one AneuRx (Medtronic). For the < > technique, two Prostar XL 8F were used to close 22-24F access sites and one Prostar XL 10F to close 16F access sites. RESULTS: Procedural success was achieved in 21/29 (72.4%) patients and in 39/47 access sites (83%). Closure of 22-24F access sites with tandem 8F Prostar devices was successful in 23/29 (79.3%) cases. Closure of 16F access sites with 10F Prostar device was successful in 16/18 (88.8%) cases. There were seven peri-procedural failures requiring surgery to repair the femoral artery in three cases. Four access complications healed without intervention. Overall 25/29 (86.2%) patients had complete percutaneous repair. No late complications were detected during follow-up (median 17.5 months). CONCLUSIONS: Percutaneous treatment of patients with AAA and thoracic aneurysms is feasible in most cases, with a very low risk of access-related complication, providing that the operator has sufficient practical experience of this technique.

Adult↗
PubMed2002

Closure of carotid bifurcation endarterectomy using a polyurethane patch. A multicentre prospective study with 252 patients.

BACKGROUND: In order to evaluate the results of carotid endarterectomy with closure using a polyurethane patch, a multicentre prospective study of 252 patients (263 interventions) undergoing this operation was performed between November 1996 and August 2001. METHODS: One hundred and seventy-one men and 81 women with a mean age of 70 years were studied. Fifty-five percent of the patients had neurological symptoms. The degree of carotid stenosis evaluated using the European carotid surgery trialist's collaborative group (ECST) criteria was greater than or equal to 70% in 95% of cases. RESULTS: The combined mortality-morbidity operation rate (CMMR) was 2% (1 death from cerebrovascular haemorrhage on Day 3, 1 non-regressive cerebrovascular accident (CVA), 3 regressive CVAs). The patients had follow-up clinical examinations and Doppler ultrasound scans for 2 years. Fifteen patients died during follow-up, 8 of these patients died from heart-related causes and 2 patients died from CVA. Four patients presented with CVAs ipsilateral or contralateral to the endarterectomy. Two false aseptic aneurysms and 1 false septic aneurysm required further surgery. Three asymptomatic carotid occlusions occurred during follow-up. The rate of restenosis greater than 50% was 1.2% at 6 months, 2.3% at 1 year and 5.3% at 2 years. CONCLUSIONS: These results confirm the value of po-lyurethane patch closure of carotid endarterectomy.

Aged↗
PubMed2001

Prosthetic graft infection after descending thoracic/ thoracoabdominal aortic aneurysmectomy: management with in situ arterial allografts.

PURPOSE: Prosthetic graft infection is an uncommon but life-threatening complication of descending thoracic/thoracoabdominal aortic aneurysmectomy. The purpose of this study was to assess the value of in situ arterial allografts in the management of this complication. METHODS: From 1992 to 2000 we treated 11 consecutive patients with prosthetic graft infection after descending thoracic/thoracoabdominal aortic aneurysmectomy by replacing the prosthetic graft with an in situ arterial allograft. There were 10 men and one woman with a mean age of 50.8 years (range, 32-73 years). The primary aortic disease was degenerative aneurysm in 6 patients, chronic type B dissection in 2 patients, inflammatory aneurysm in 1 patient, Marfan's disease in 1 patient, and Behçet's disease in 1 patient. Replacement involved only the descending thoracic aorta in three patients and more or less extensive segments of the thoracoabdominal aorta in eight patients. Signs of severe infection were present in all patients, and false anastomotic aneurysms were noted in six patients. Aortoenteric fistula occurred in three patients and aortobronchial fistula in two patients. The causative organisms were identified in nine patients. The mean interval between the primary surgery and reoperation was 33.4 +/- 27.5 months. Reoperation was performed under emergency conditions because of hemorrhage in three patients. Cardiopulmonary bypass with deep hypothermic circulatory arrest was used in seven patients. Allograft replacement of the aorta was associated with reimplantation of intercostal and/or visceral arteries in all patients. RESULTS: One patient died intraoperatively of heart failure during emergency surgery. Two patients died of persistent infection during the postoperative period at 19 and 58 days. Mean follow-up was 34 +/- 19 months. One patient died during the late follow-up period after surgery of the infrarenal aorta. Another patient underwent surgery for stenoses of one branch of a bifurcated allograft and a renal bypass graft to a solitary kidney. CONCLUSIONS: The use of in situ arterial allografts is a significant advance in the management of prosthetic graft infection after descending thoracic/thoracoabdominal aortic aneurysmectomy provided that reoperation is performed early.

Adult↗
PubMed2001

Endoluminal smooth muscle cell seeding limits intimal hyperplasia.

PURPOSE: Intimal hyperplasia is one of the main responses of the vascular wall to injury. In the current study, we tested the hypothesis that endoluminal seeding of host syngeneic vascular cells could limit intimal hyperplasia induced by either mechanical deendothelialization or chronic allograft rejection in rat aorta. METHODS: An experimental model of in situ seeding of syngeneic endothelial cells, smooth muscle cells (SMCs), and fibroblasts (FIBs) was used in mechanically deendothelialized and allografted aortas. In a preliminary study, the ability of the three cell types (n = 5 per group) to seed on the deendothelialized luminal surface of the aortic wall was evaluated after 2 days, with the use of fluorescent PKH as marker. In the first model, the abdominal aorta of Lewis rats was deendothelialized (n = 6) or deendothelialized and seeded with either SMCs (n = 6) or FIBs (n = 6) before flow was restored. In the allograft model, aortas were harvested from dark agouti rats and orthotopically grafted in Lewis receivers, directly (n = 6) or after deendothelialization. Deendothelialization was performed alone (n = 6) or associated with the seeding of similar host (Lewis) syngeneic SMCs (n = 6) or FIBs (n = 6). Results were evaluated at 2 months with histologic and morphometric methods. RESULTS: SMCs and FIBs were able to adhere in situ to the deendothelialized aortic wall, whereas endothelial cells were not. In mechanically deendothelialized aortas, the seeding of syngeneic SMCs led to a significant reduction in intimal thickness compared with deendothelialized aortas or FIB-seeded aortas (26.9 +/- 1.7 microm vs 55.5 +/- 1.7 and 56.7 +/- 1.7 microm, respectively), and a lower nuclear content (382.2 +/- 35.7 microm(2) vs 779.6 +/- 65.9 and 529.6 +/- 24.3 microm(2), respectively) of neointima. After SMC seeding, intimal hyperplasia was richer in elastin, whereas after FIB seeding it was richer in collagen. In allografts, the seeding of syngeneic SMC led to a significant reduction in intimal thickness compared with control aortas, deendothelialized aortas, or FIB-seeded aortas (31.6 +/- 1.1 microm vs 88.55 +/- 2.8, 74.6 +/- 2.9, and 85.7 +/- 2.6 microm, respectively), and a reduced nuclear content of the neointima (444.9 +/- 23.4 microm(2) vs 1529.1 +/- 116, 972.3 +/- 50, and 645.2 +/- 32.4 microm(2), respectively). Differences observed in the extracellular matrix composition were equivalent to those observed in the mechanically deendothelialized model. CONCLUSIONS: Our results suggest that endoluminal seeding of syngeneic SMCs can be effective in reducing intimal hyperplasia both in a deendothelialization model and in arterial allografts. SMC and FIB endoluminal seeding led to a significatively different accumulation of extracellular matrix in the intima.

Analysis of Variance↗
PubMed2001

[Humoral effectors and cellular targets of chronic arterial wall allorejection].

Contrasting with acute rejection, chronic rejection of arterial allograft don't involve leukocyte passengers from the graft to the host. Chronic rejection involves the proteins of the major histocompatibility complexes. Experimental studies in rats showed that the process evolved in three stages: a first stage of histo-incompatibility recognition mediated by the graft endothelium, a second stage of immune antibody-dependent injury of allogenic smooth muscle cells of the media associated with inflammatory infiltration of the adventitia, lastly a third stage of scarring process including intimal proliferation and adventitial fibrosis.

Animals↗
PubMed2000

Involvement of antibody-dependent apoptosis in graft rejection.

BACKGROUND: Both humoral factors and apoptosis have been recently suggested to play a role in chronic allograft rejection. However, a link between alloantibodies and grafted cell apoptosis has never been proposed. Using the aortic allograft model in the rat, we have previously demonstrated the presence of IgG associated with the disappearance of donor endothelial and medial smooth muscle cells. In the present study, we tested the interaction between recipient allosera, enriched with antibodies by presensitization, and primary culture of cardiovascular cells of donor origin. METHODS: For this purpose endothelial cells, smooth muscle cells, adventitial fibroblasts, and cardiac myocytes of donor origin were cultured. Binding of alloantisera to these cells was analyzed by flow cytometry. Apoptosis of donor cells was evaluated by Tdt-mediated d' UTP-FITC nick end labeling, 4',6-diamidino-2-phenylindole and DNA ladder techniques. The alloantisera were compared with anti-MHC class I monoclonal antibodies. Finally the colocalization of antibodies and apoptosis was investigated in vivo. RESULTS: In vitro, alloantisera bind to cardiovascular cells of donor origin. These cells expressed MHC class I but not MHC class II. There was a partial competition between anti-MHC I mouse monoclonal antibody and alloantisera mainly of the IgG isotype. Alloantisera bound to, but did not induce lysis of, donor RBC. Alloantisera induced apoptosis of donor cardiovascular cells as assessed by the typical morphological aspect of the donor cells after 24 hr of incubation. These data were confirmed by the Tdt-mediated d' UTP-FITC nick end labeling positivity of the cells and the fragmentation of the nucleus visualized by 4',6-diamidino-2-phenylindole and DNA ladder techniques. Similar apoptosis was induced by specific monoclonal antibodies directed against the MHC class I of donor cells. Primary culture of similar vascular cells of recipient origin was insensitive to alloantisera directed against donor alloantigens. Finally, in vivo, using allopresentization and aortic allografts, an association of alloantibody binding and endothelial cell apoptosis was observed at day 5, and a similar association with smooth muscle cell apoptosis on day 12 after grafting. CONCLUSION: These data demonstrate the role of humoral injury in chronic allograft rejection and suggest new therapeutical approaches focused on the induction of resistance to antibody-dependent apoptosis.

Animals↗
PubMed2000

[Inflammatory abdominal aortic aneurysm. Role of corticosteroid therapy].

For more than 20 years it has been generally acknowledged that operation for inflammatory abdominal aortic aneurysm (IAAA) using the common in-lay-graft procedure will induce the regression of peri-aortic fibrosis. However in prospective studies, after a 2 years follow-up, no regression appeared in approximated 8% of the cases (table I). Moreover in some IAAA a corticosteroid treatment (CS) was prescribed and it produced a regression of fibrosis and therefore facilitated the operation. Nevertheless the usefulness of the CS remains debated. We report 4 new cases of IAAA with CS. Based on our cases and an analysis of the literature we conclude that when there is no urgency to operate (diameter inferior to 50 mm) CS is the best option in IAAA with either severe inflammation or ureter involvement. Due to the regression of the fibrosis it can facilitate the surgical procedure. However it needs to be conducted with an adequate dose and duration. Finally the CS is the only possibility when the inflammation persist following the treatment of the IAAA.

Adrenal Cortex Hormones↗
PubMed1999

Prosthetic reinforcement of varicose saphenous vein grafts for infrainguinal bypass.

Use of varicose saphenous veins for infrainguinal bypass is often contraindicated because of the risk of immediate rupture or long-term aneurysm. In this report we describe four cases in which prosthetic reinforcement allowed successful femoropopliteal bypass grafting using highly varicose saphenous veins while preserving normal endothelium. No thrombosis or any other complication was observed after a mean follow-up of 41 months.

Aged↗
PubMed1999

Bacterial resistance of refrigerated and cryopreserved aortic allografts in an experimental virulent infection model.

PURPOSE: The bacterial resistance of refrigerated and cryopreserved aortic allografts in a highly virulent infection in a dog model was studied. METHODS: The infrarenal aorta of 12 dogs was replaced with either a cryopreserved aortic allograft (group I, n = 6) or a refrigerated aortic allograft (group II, n = 6) in infected sites. Allografts were harvested from dogs and stored for 1 week, either by cryopreservation (-140 degrees C) or refrigerated method (4 degrees C), in a preservation medium. At the time of implantation, induction of infection was achieved with an infected piece of knitted Dacron placed just beneath the allograft. The Dacron was contaminated in vitro by soaking it in a solution with Staphylococcus aureus PR209. All 12 dogs received no adjunct antibiotic or antithrombotic therapy. Four weeks after implantation, the animals were killed to recover the grafts for bacteriological and histological analyses. Bacterial results were expressed as colony-forming units (CFU)/cm2 of graft material. RESULTS: In group I, only one allograft grew bacteria at 2. 16 x 10(6 )CFU/cm2, with a blood culture positive for S aureus. In group II, one dog died at 3 weeks from a false septic aneurysm rupture, all the allografts were infected (P <.05) with a mean bacterial count of 9.41 +/- 6.8 x 10(4) CFU/cm2, and three blood cultures were positive for S aureus. The patency of the grafts was analyzed at the time of recovery. Three laminar thrombi without occlusion were present in group I; none were present in group II. A better preserved endothelium in group I was revealed by means of histologic analysis staining with factor VIII antibody before implantation. After 4 weeks of implantation in the infected site, infected allografts presented polynuclear infiltrates in the media with a high degree of inflammatory reaction, and endothelial recovery was more significant in group I, with numerous young plump cells. CONCLUSION: This study demonstrates that cryopreserved allografts implanted in infected sites in a dog model can produce greater bacterial resistance.

Animals↗
PubMed1997

Femoropopliteal bypass: in situ or reversed vein grafts? Ten-year results of a randomized prospective study.

One hundred femoropopliteal bypass procedures performed in 91 patients between October 1980 and January 1985 were randomly divided into two statistically comparable groups including 50 in situ vein grafts and 50 reversed vein grafts. The indication for bypass was chronic critical ischemia in 97% of cases. The lower anastomosis was made on the distal popliteal artery in 75% of cases. Follow-up ranged from 10 years (for the last patient included) to 14 years. Three patients have been lost to follow-up. Median survival was 54 months in the in situ graft group and 76.5 months in the reversed graft group. Actuarial survival at 10 years was 30.8% in the in situ graft group and 29.5% in the reversed graft group. Actuarial limb salvage at 10 years was 73.5% in the in situ graft group and 74.4% in the reversed graft group. Graft occlusion was observed in 10 cases during the perioperative period (six in the in situ graft group and four in the reversed graft group) and in 19 cases during the late postoperative period (12 in the in situ graft group and seven in the reversed graft group). Reoperation during follow-up was required in 13 cases in the in situ graft group (11 patients) and in nine cases in the reversed graft group (five patients). Discounting residual arteriovenous fistulas (FAV) (five ligations in four patients), the incidence of lesions involving the bypass and anastomoses threatening graft patency was 6% in the in situ graft group and 8% in the reversed graft group. Actuarial primary patency at 10 years was 41.7% in the in situ graft group and 64.5% in the reversed graft group (p < 0.05). Actuarial secondary patency at 10 years was 64.8% in the in situ graft group and 70.2% in the reversed graft group (NS). As a function of vein diameter, actuarial secondary patency at 10 years in the in situ graft group was 37.5% for bypasses using veins with a diameter of 4 mm or less and 80.6% for bypasses using veins larger than 4 mm (p < 0.05). In the reversed graft group the patency rate was 71.2% for bypasses using veins with a diameter of 4 mm or less and 65.5% for bypasses using veins larger than 4 mm. In addition to requiring a training period the in situ technique raises the problem of valve removal especially for small diameter veins. The absence of these disadvantages makes the reversed technique the procedure of choice for femoropopliteal bypass.

Aged↗
PubMed1997

[Surgery of carotid lesions after irradiation. Apropos of 15 cases].

Out of 15 patients operated on for a carotid stenosis 3 to 19 years after a cervical irradiation, 2 were treated by a subclavian-carotid by-pass, 3 by a common carotid-internal carotid by-pass, 10 by an endarterectomy (6 closed with a patch), 3 of these endarterectomy extended largely down on the common carotid. Although the surgical approach was often difficult through the sclerotic tissues and 8 times the scar of a lymphadenectomy, the removal of the atherosclerotic core was as easy as usual. We observed neither mishap in arterial and cutaneous healings nor post operative stenotic myointimal hyperplasia.

Adult↗
PubMed1997

[Lumbar sympathectomy by retroperitoneal endoscopy: feasibility study].

Endoscopic surgery has been used as a new procedure to simplify different surgical processes. The goal of this study was to evaluate the benefits of endoscopic retroperitoneal surgery for lumbar sympathectomies. Between February 93 and November 95 we performed 35 lumbar sympathectomies using this technique. All patients were arteritic. The results were as follows: for 25% of the patients, conversion classical open technique was required; 6% complications (septic); 3% of the patients died. In comparing the various techniques of sympathectomy and sympatholysis, it would appear that the endoscopic technique produces fewer complications. However we believe that a learning period is necessary before this technique can be fully mastered.

Adult↗
PubMed1996

Presensitization accelerates allograft arteriosclerosis.

Transplant arteriosclerosis is the major factor influencing allograft survival after the first year posttransplantation. The host's immunologic response is one of the principal effectors responsible for the constitution of this vascular wall lesion, but the effector pathway and the factors influencing the immune injury are not clear. In a rat abdominal aortic allograft model, we used a skin priming method to study the influence of sensitization on the occurrence of vascular wall lesions. Primed rats developed transplant arteriosclerosis lesions involving medial decellularization and intimal proliferation before the 21st day, whereas naive animals had the same lesions at 2 months posttransplantation. A significant difference between primed and naive rats was found for medial thickness (48.00 +/- 2.85 microm versus 79.34 +/- 2.55 microm, P<0.001) and smooth muscle cell content (160 +/- 28 cell/mm versus 466 +/- 19 cell/mm, P<0.001) at 21 days posttransplantation, and intimal hyperplasia was seen in primed animals at that time, whereas it was not observed in naive rats until the 60th day. The immune profile in naive and primed animals was different. The immune cells infiltrating the arterial wall in naive rats, were principally macrophages and CD8+ T-lymphocytes. No Ig or complement deposition was detected. IgG and complement activated fraction were present in the media of primed animals as early as the fifth day posttransplantation and CD4+ T lymphocytes were the dominant immune cell population. In conclusion, sensitization influences the immune mechanisms responsible for the development of transplant arteriosclerosis and alters the rate of its evolution.

Animals↗