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Biomedical subjects

B Dorweiler

Publications and source records attributed to B Dorweiler.

13 recordsLinked to original sources

Sequential femorodistal composite bypass with second generation glutaraldehyde stabilized human umbilical vein (HUV).

OBJECTIVE: To evaluate the performance of sequential composite bypasses with second generation glutaraldehyde stabilized human umbilical vein (HUV) and autologous vein. DESIGN: Retrospective study of consecutive patients, in a single centre. PATIENTS: From January 1998 to December 2003, 54 femoro-distal HUV-autologous vein sequential composite bypasses were constructed in 52 patients with critical leg ischemia and absence of sufficient length of autologous vein. METHODS: All infra-inguinal bypass operations were registered in a computerized database and prospectively followed. Bypasses using sequential HUV-composite technique were reviewed for graft patency, limb salvage and patient survival. RESULTS: Primary patency and secondary patency rates at 1, 2, 3 and 4 years were 71, 61, 53 and 53% and 89, 80, 73 and 67%, respectively. Corresponding limb salvage rates were 96, 92, 88 and 88%. Patient survival was 56% at 4 years. After 30 days additional procedures to maintain graft patency were necessary in six bypasses. Asymptomatic occlusion of one sequential anastomosis was found in five patients. CONCLUSION: Graft patency and limb salvage rate support the use of the sequential composite technique with second generation HUV in femorodistal bypass surgery, when autologous vein of sufficient length is not available.

Aged↗

External reinforcement of varicose veins with PTFE prosthesis in infrainguinal bypass surgery -- clinical results.

OBJECTIVE: Segmental varicose degeneration of the autogenous greater saphenous vein may limit its use in infrainguinal bypass surgery. Wrapping a PTFE prosthesis around dilated veins has emerged as an option to create externally reinforced vein bypasses. Results regarding graft patency and limb salvage were analyzed. METHODS: Between September 1995 and January 2001, 35 infrainguinal bypass operations in 33 patients were performed with greater saphenous veins exhibiting segmental varicose dilatation. Grafts were followed by duplex scan and retrospective analysis of graft patency and limb salvage was performed. RESULTS: One bypass prompted successful revision for early occlusion. Four bypasses required additional reintervention during follow-up. 48 months primary, primary assisted and secondary patency rates were 66%, 82% and 82%, respectively, with a limb salvage rate of 97%. Duplex scan failed to demonstrate stenosis of the reinforced vein segments or aneurysmal degeneration of the residual vein. CONCLUSION: External reinforcement with a PTFE prosthesis allows the use of autogenous greater saphenous veins with varicose dilatation and enables the construction of all autogenous bypasses with promising graft patency and limb salvage.

Aged↗

Limb trauma with arterial injury: long-term performance of venous interposition grafts.

BACKGROUND: In contrast to arterial occlusive disease, data on long-term outcomes after vein grafts in limb trauma with arterial injury are sparse. PATIENTS: From 1991 through 2001, 22 trauma victims received 23 interposition vein grafts performed by an interdisciplinary team of trauma and vascular surgeons. Indications included both blunt and penetrating injuries with critical limb ischemia in the majority of cases. RESULTS: Operative treatment of the injured vessels (brachial n = 5, radial/ulnar n = 7, popliteal n = 6, tibial n = 3, pedal n = 2) encompassed venous interposition graft of either saphenous (n = 15) or cephalic vein (n = 8). All patients survived the operative procedure. 4 graft occlusions were noted and 3 major amputations had to be performed (one despite patent graft). 13 patients (76%) were available for duplex ultrasound examination after a mean follow-up of 59 months where patent grafts could be detected in all cases. CONCLUSION: A multidisciplinary approach ensures optimal treatment strategy of arterial injury in extremity trauma. Interposition vein grafts provide durable long-term results and should be attempted even in single-vessel injuries of forearm and lower leg.

Adolescent↗

[Limb salvage in diabetic foot syndrome with pedal bypass using the in-situ technique].

INTRODUCTION: Treatment of the ischemic diabetic foot syndrome still represents a medical and economic challenge. Contrary to the aims of the Saint Vincent declaration a dramatic reduction of major amputations in Germany was not noted, although in the diabetic patients the predominant type of tibial artery occlusion allows construction of pedal bypasses for limb salvage. METHOD: In patients with ischemic diabetic foot syndrome following angiographic evaluation of the ischemic limb, the indication for surgical revascularisation of patent pedal arteries was established. The in-situ technique was preferred in the presence of a suitable ipsilateral greater saphenous vein whenever possible. Revascularisation was followed by treatment of foot ulcerations or, if necessary, minor amputations. Patients were followed by clinical examination and duplex scan investigation of the bypass in regular intervals. RESULTS: From 01/89 to 12/01 in 79 patients (59 men and 20 women) with non healing ulcerations or established gangrene from a total of 175 pedal bypasses 84 pedal bypass operations in 84 limbs were performed using the in-situ technique. All patients were diabetic and in addition 13.9% were dependent on hemodialysis for end stage renal disease. 59.5% of the bypasses originated from the popliteal artery (distal origin bypass). The dorsalis pedis artery was chosen for the distal anastomosis in 83% and the posterior tibial artery in 17%. Two patients (2.4%) died postoperatively from cardiac events. Early bypass occlusion occurred in 8.4% resulting in a major amputation rate of 6%. After 60 months primary, primary assisted and secondary patency was 67.7%, 71.5% and 75.3% respectively with a limb salvage rate of 78%. CONCLUSION: Pedal bypass using the in-situ technique provides excellent long term limb salvage rates in a disease with a generally unjustified bad prognosis with respect to limb salvage.

Adult↗

[Short distal origin vein graft in diabetic foot syndrome].

PURPOSE: World wide increase of diabetes compound with diabetic foot syndrome becomes a challenge in vascular surgery to avoid limb loss. In diabetics a special pattern of atherosclerosis is prevalent with disease limited to the infrageniculate arteries but sparing inflow vessels and distal tibial and pedal arteries. This provides short bypass grafting from popliteal to tibial and pedal arteries, a concept first described by F. Veith in 1981. METHODS: Diabetics with severe atherosclerotic disease and limb-threatening ischemia got general evaluation and vascular imaging. Falling in this special category the patients underwent short vein bypass grafting originating at the first or third popliteal segment extending to the tibial or pedal arteries. Follow up of patency and limb salvage was nearly complete. RESULTS: From 1988 to 2001 124 diabetics received 140 vein bypass grafts for limb salvage, 95.7% already preoperatively with foot necrosis. Operative mortality rate was 1.4%, major morbidity rate was 9.3%, early graft failure rate 8.5% and early amputation rate was 3.8%. 2 year primary patency, primary assisted patency, secondary patency rates and limb salvage were 73.3%, 75.7%, 76.4% and 87.2%. 5 years results were 63.6%, 69.2%, 70.0% and 81.9% respectively. DISCUSSION: This series revealed exceptionally good results in patients with diabetes mellitus after short vein bypass grafting in concert with earlier studies since 1981. Compared to long femorodistal grafts there was no difference in longterm patency. Bypass grafting in diabetic foot syndrome is still regarded to have a poor prognosis. Just the contrary is the case. This study in concert with former studies revealed distal origin bypass grafting a durable and effective procedure to fight limb loss in diabetic foot syndrome. CONCLUSION: Distal origin vein bypass grafting is an excellent method just for patients with diabetes. Looking at limb salvage rates over 80 % in 5 years, this procedure should be offered more often suitable patients with diabetic foot syndrome.

Adult↗

Arterial embolism to the upper extremity in a patient with factor V Leiden mutation (APC resistance)--a case report and review of the literature.

Factor V Leiden mutation has emerged as one of the leading abnormalities in inherited blood coagulation disorders, resulting in a markedly increased risk for deep leg vein thrombosis. A 24-year-old woman presented with acute onset of critical ischemia of her left thumb and index finger. Intraarterial angiography revealed an embolus in the distal radial artery and a thrombotic occlusion of the digital artery of the thumb and index finger. Immediate therapy encompassed a selective surgical embolectomy of the distal radial artery followed by a local intraarterial lysis that was continued for 3 days. Additionally, therapeutic anticoagulation and vasodilating drugs (prostaglandin E) were administered. Within 2 days, capillary refill reappeared and the initial loss of sensory function at the tip of the thumb and index finger diminished. A screening test for thrombophilic disorders led to the diagnosis of a heterozygous mutation of factor V (Leiden mutation). Arterial thromboembolic events of factor V Leiden mutation are rare and have to date been described only in the supraaortic and coronary circulation. Therefore, the arterial embolism to the left hand presented in this report constitutes a rarity that could be successfully salvaged by the combined use of a vascular surgical procedure and intensified medical management.

Activated Protein C Resistance↗

Pedal arterial bypass for limb salvage in patients with diabetes mellitus.

OBJECTIVE: to evaluate pedal bypass grafting in patients with diabetes mellitus with critical limb ischaemia. PATIENTS AND METHOD: from 1994 to 1999, 49 consecutive pedal bypass grafts were performed in 46 patients with a median age of 69 years (range 37-85 years). The incidence of insulin-dependent diabetes mellitus was 87%. The distal anastomosis was located at the dorsalis pedis artery in 36, at the inframalleolar posterior tibial artery in 9 and at the plantar artery in 4 cases, respectively. RESULTS: one patient died perioperatively. Two bypass occlusions and one major amputation accounted for a primary patency rate of 96% and a limb salvage rate of 98% at 30 days, respectively. During a median follow-up of 28 months (range 1-70 months), 21 patients died of nonrelated causes. Three additional graft occlusions and 4 major amputations were noted resulting in a primary patency rate of 89% and a limb salvage rate of 87% at 48 months, respectively. CONCLUSION: Pedal bypass grafting utilising the greater saphenous vein with in-situ technique is a reliable and effective procedure to achieve durable limb salvage in patients with diabetes mellitus.

Adult↗

Endovascular treatment of acute bleeding complications in traumatic aortic rupture and aortobronchial fistula.

OBJECTIVE: Herein we report our experience in placement of endovascular stentgrafts in the descending aorta in patients with acute bleeding complications due to traumatic rupture or aortobronchial fistula. METHODS: Six patients (one woman, five men, mean age 47+/-19 years) were treated from September 1995 to February 2000 by implantation of endovascular stentgrafts in the descending aorta. Indications included traumatic ruptures of the aortic isthmus (n=3) and aortobronchial fistulas (n=3). All procedures were performed under general anaesthesia. The implants were introduced under fluoroscopic guidance via the aorta (n=1), the iliac (n=4) or femoral (n=2) artery, respectively. RESULTS: All aortobronchial fistulas and ruptures were sealed up successfully. There was no perioperative morbidity and no procedure-related morbidity except one patient who received aortofemoral reconstruction because of iliac occlusive disease. All patients are alive and well after a mean follow-up of 31 months (range 6-60). Two patients had recurrent hemoptysis, in one case, the patient received a second implant (distal extension), the other patient was managed conservatively. CONCLUSION: Endovascular treatment by a stentgraft is a safe and reliable procedure in the management of acute bleeding complications in patients with aortic rupture or aortobronchial fistulas.

Acute Disease↗

Autogenous reconstruction of infected arterial prosthetic grafts utilizing the superficial femoral vein.

BACKGROUND: Prosthetic infection after reconstructive vascular surgery is a most serious complication, associated with high mortality and amputation rates. Following excision of the infected graft, several methods of reconstruction are available. We present here our experience with autogenous reconstruction of infected prosthetic arterial grafts using the superficial femoral vein (SFV). METHODS: From November 1995 to December 1999, we used the SFV in seven patients (mean age 70 years) for reconstruction of an infected aortobifemoral (n = 2), aortoiliac (n = 1), femorofemoral bypass (n = 1), femorotibial (n = 2) and carotid crossover bypass (n = 1). Treatment encompassed complete prosthetic excision and autogenous reconstruction with the SFV alone or as a spliced graft with the greater saphenous vein (GSV) or basilic vein. RESULTS: There were no perioperative deaths or amputations. Two patients exhibited transient moderate swelling of the donor limb. In the follow-up, six patients are alive and well without any signs of recurrent infection. One patient died with an unrelated cause 24 months postoperatively. All donor limbs were asymptomatic for venous congestion in the long-term follow-up. CONCLUSION: The SFV provides a reliable tool for autogenous reconstruction after resection of infected prosthetic arterial grafts. Harvesting the SFV is well tolerated as long as the deep femoral and the popliteal vein are preserved.

Aged↗

Complement activation by oxidatively modified low-density lipoproteins.

BACKGROUND: Oxidatively modified low-density lipoproteins (LDLs) have been implicated in the pathogenesis of atherosclerosis and are found in human vascular lesions. There is increasing evidence that complement activation may also play a role in atherogenesis. Activated complement proteins have been demonstrated to be present in early atherosclerotic lesions, and lipids isolated from lesions have been shown to activate complement, hence their designation as lesion complement activator (LCA). The question now arose whether oxidized LDLs would also activate complement. MATERIAL AND METHODS: The complement-activating capacity of a lesion complement activator preparation and of minimally as well as heavily oxidized LDL was investigated by measuring SC5b-9 formation in normal human serum. In addition, C3 conversion was followed using two-dimensional immunoelectrophoresis. RESULTS: Minimally and heavily oxidized LDL generated small but significant amounts of SC5b-9 (7.9 microgram mL-1, SD 3.5, and 10.8 microgram mL-1, SD 1.2, respectively; n = 6) compared with native LDL (3.3 microgram mL-1, SD 1.4; P < 0.05), whereas LCA generated substantially larger amounts of the terminal complex (32.0 microgram mL-1, SD 3.2). Both oxidized LDL preparations caused only minor C3 conversion. CONCLUSIONS: These findings show that oxidation does not confer relevant complement-activating properties on LDL, suggesting that the lesion complement activator is not directly related to oxidized LDL. Oxidized LDL is probably of minor importance for complement activation in atherosclerotic lesions.

Arteriosclerosis↗

Immunohistochemical demonstration of enzymatically modified human LDL and its colocalization with the terminal complement complex in the early atherosclerotic lesion.

Treatment of low density lipoprotein (LDL) with degrading enzymes transforms the molecule to a moiety that is micromorphologically indistinguishable from lipoproteinaceous particles that are present in atherosclerotic plaques, and enzymatically modified LDL (E-LDL), but not oxidized LDL (ox-LDL), spontaneously activates the alternative complement pathway, as do lesion lipoprotein derivatives. Furthermore, because E-LDL is a potent inducer of macrophage foam cell formation, we propose that enzymatic degradation may be the key process that renders LDL atherogenic. In this article, we report the production of two murine monoclonal antibodies recognizing cryptic epitopes in human apolipoprotein B that become exposed after enzymatic attack on LDL. One antibody reacted with LDL after single treatment with trypsin, whereas recognition by the second antibody required combined treatment of LDL with trypsin and cholesterol esterase. In ELISAs, both antibodies reacted with E-LDL produced in vitro and with lesion complement activator derived from human atherosclerotic plaques, but they were unreactive with native LDL or ox-LDL. The antibodies stained E-LDL, but not native LDL or ox-LDL, that had been artificially injected into arterial vessel walls. With the use of these antibodies, we have demonstrated that early human atherosclerotic coronary lesions obtained at autopsy as well as lesions examined in freshly explanted hearts always contain extensive extracellular deposits of E-LDL. Terminal complement complexes, detected with a monoclonal antibody specific for a C5b-9 neoepitope, colocalized with E-LDL within the intima, which is compatible with the proposal that subendothelially deposited LDL is enzymatically transformed to a complement activator at the earliest stages in lesion development.

Antibodies, Monoclonal↗

Atherogenic properties of enzymatically degraded LDL: selective induction of MCP-1 and cytotoxic effects on human macrophages.

The mechanisms underlying the selective accumulation of macrophages in early atherosclerotic lesions are poorly understood but are likely to be related to specific properties of altered low density lipoprotein (LDL) deposited in the subendothelium. Enzymatic, nonoxidative degradation of LDL converts the lipoprotein to a potentially atherogenic moiety, enzymatically altered LDL (E-LDL), which activates complement and is rapidly taken up by human macrophages via a scavenger receptor-dependent pathway. Immunohistological evidence indicates that E-LDL is present in an extracellular location in the early lesion. We report that E-LDL causes massive release of monocyte chemotactic protein 1 (MCP-1) from macrophages and that expression of interleukin 8 or RANTES remains unchanged. Release of MCP-1 was preceded by a rapid expression of MCP-1 mRNA, which was detectable after 15 minutes, reached maximum levels after 1 hour, and remained detectable for 12 hours after exposure to concentrations as low as 10 microg/mL E-LDL. MCP-1 mRNA induction and protein release by E-LDL exceeded that evoked by oxidized LDL. Release of MCP-1 was dependent on de novo protein synthesis and on the activity of tyrosine kinases. At higher concentrations, E-LDL, but not oxidized LDL, exerted toxic effects on macrophages that in part appeared to be due to apoptosis. The results show that E-LDL possesses major properties of an atherogenic lipoprotein.

Arteriosclerosis↗

On the pathogenesis of atherosclerosis: enzymatic transformation of human low density lipoprotein to an atherogenic moiety.

Combined treatment with trypsin, cholesterol esterase, and neuraminidase transforms LDL, but not HDL or VLDL, to particles with properties akin to those of lipid extracted from atherosclerotic lesions. Single or double enzyme modifications, or treatment with phospholipase C, or simple vortexing are ineffective. Triple enzyme treatment disrupts the ordered and uniform structure of LDL particles, and gives rise to the formation of inhomogeneous lipid droplets 10-200 nm in diameter with a pronounced net negative charge, but lacking significant amounts of oxidized lipid. Enzymatically modified LDL (E-LDL), but not oxidatively modified LDL (ox-LDL), is endowed with potent complement-activating capacity. As previously found for lipid isolated from atherosclerotic lesions, complement activation occurs to completion via the alternative pathway and is independent of antibody. E-LDL is rapidly taken up by human macrophages to an extent exceeding the uptake of acetylated LDL (ac-LDL) or oxidatively modified LDL. After 16 h, cholesteryl oleate ester formation induced by E-LDL (50 micrograms/ml cholesterol) was in the range of 6-10 nmol/mg protein compared with 3-6 nmol/mg induced by an equivalent amount of acetylated LDL. At this concentration, E-LDL was essentially devoid of direct cytotoxic effects. Competition experiments indicated that uptake of E-LDL was mediated in part by ox-LDL receptor(s). Thus, approximately 90% of 125I-ox-LDL degradation was inhibited by a 2-fold excess of unlabeled E-LDL. Uptake of 125I-LDL was not inhibited by E-LDL. We hypothesize that extracellular enzymatic modification may represent an important step linking subendothelial deposition of LDL to the initiation of atherosclerosis.

Arteriosclerosis↗