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B Steckmeier

Publications and source records attributed to B Steckmeier.

At least 19 recordsLinked to original sources

[Elective therapy of asymptomatic infrarenal aortic aneurysms. Comparison of mortality and morbidity between endovascular and open repair].

Summary. In recent years, endovascular operations on infrarenal aortic aneurysm (EVAR) have not only been acknowledged as an alternative, but have become an indispensable "tool of the trade" for the vascular surgeon. As documented in many studies, perioperative morbidity is definitely much lower than in open surgery. In the long term, open surgery is also subject to complications such as rupture or aorto-enteral fistulae which necessitate secondary operations with their associated risks. There are some valid studies documenting a significantly lower mortality for EVAR than for open surgery. These datas were recently confirmed with high evidence level by the published results of UK-EVAR trial 1. The other randomized trials are currently ongoing. If the lower morbidity and lethality rate for EVAR is confirmed in these studies, the establishment of the indication for aortic aneurysm must be reconsidered with regard to the risk profile and the maximum diameter. The fact that long-term results are not yet available for the endovascular operation introduces a factor of uncertainty. Intensive follow-up observation is therefore an absolute prerequisite in patients who have undergone endovascular treatment. If the establishment of the indication is appropriate, with the new vascular prosthesis endoleaks are no longer an insoluble problem. The two methods should not be regarded as mutually competitive, but as complementary components of the treatment spectrum at every vascular center.

Aortic Aneurysm, Abdominal↗

[Vascular injuries in extremities].

Vascular injuries of the extremities account for most instances of vascular trauma (ca. 70%), and they entail a risk of amputation about 10-20%. According to the kind of force that has acted, arterial trauma is classified as direct or indirect. The scale of hemorrhage and peripheral ischemia depend on the nature and severity of the arterial lesion. In patients with multiple injuries, routine use of Doppler sonography and duplex sonography can facilitate early diagnosis and treatment of vascular injuries. With great certainty, clinical examination and an AB or WB index of >1.0 can rule out the presence of vascular injury that requires treatment. After excluding further life-threatening injuries, surgery should be performed immediately when there is critical ischemia, squirting hemorrhage, or a rapidly expanding hematoma. Angiography or duplex sonography findings determine the further procedure in vascular injuries that do not require immediate treatment. Occlusion of a reconstructed artery, manifestation of a compartment syndrome, and insufficient anticoagulation are the main factors affecting the risk of amputation.

Amputation, Surgical↗

[Value of MR angiography in follow-up after cruro-pedal bypass surgery].

Patients after crural or pedal revascularization need a consequent surveillance to prevent graft failure. We compared the results of the clinical examination including duplexscanning with contrast-enhanced magnetic resonance angiography (MRA). 26 bypass grafts were evaluated for potential stenosis in five locations. Using both techniques, 93 of 109 locations were classified identically. 10 of 16 locations which were categorized differently were reviewed angiographically (DSA). In contrast to duplexscanning, MRA detected 3 high grade stenosis, which had to be dilatated percutaneously. MRA should be used regularly in surveillance programs of distal bypass grafting.

Adult↗

[Epidemiology of aortic disease: aneurysm, dissection, occlusion].

The physiological infrarenal aortic diameter varies between 12.4 mm in women an 27.6 mm in men. As defined, an aneurysmatic dilatation begins with 29 mm. According to that, 9% of all people above the age of 65 are affected by an abdominal aortic aneurysm (AAA). Compared with the female sex, the male sex predominates at a rate of about 5:1. The disease is predominant in men of the white race. In black men, black and white women the incidence of AAA is identical. 38 to 50 percent of the AAA patients (patients) suffer from hypertension, 33 to 60% from coronary, 28% from cerebrovascular and 25% from peripheral occlusive disease. The AAA expansion rate varies between 0.2 and 0.8 cm per year and is exponential from a diameter of 5 cm on. In autopsy studies, the rupture rates with AAA diameters of < 5 cm, between 5.1 and 6.9 cm, and of > 7 cm were below 5%, 39% and 65%, respectively. 70% of the AAA patients do not die of a rupture, but of a cardiac disease. Serum markers, such as metalloproteinases and procollagen peptides are significantly increased in AAA patients. Thoraco-abdominal aneurysms (TAA) make up only 2 to 5% of all degenerative aneurysms. 20 to 30% of the TAA patients are also affected by an AAA. 80% of the TAA are degenerative, 15 to 20% are a consequence of the chronic dissection--including 5% of Marfan patients--, 2% occur in case of infections and 1 to 2% in case of aortitis. The TAA incidence in 100,000 person-years is 5.9% during a monitoring period of 30 years. In case of TAA, an operation is indicated with a maximum diameter of 5.5 to 6 cm and more and, in case of a Marfan's syndrome (incidence of 1:10,000), with a maximum diameter of 5.5 cm and more. With regard to aorto-iliac occlusive diseases, there are defined 3 types of distribution. Type I refers to the region of the bifurcation itself. Type II defines the diffuse aorto-iliac spread of the disease. Type III designates multiple-level occlusions also beyond the inguinal ligament. Type I patients in most cases are female and more frequently suffer from hyperlipidaemia, while Type II patients are affected by hypertension and diabetes. Compared to Type II patients, Type I patients have a life expectancy that is 10 years higher. Type I and Type II patients often suffer from a pelvic claudication and, unlike Type III patients, are more frequently affected by arterio-arterial embolisms.

Aged↗

[Stage-adapted therapy concept in ascending thrombophlebitis].

Varicophlebitis is the most frequent and important acute complication of a varicosed long and/or short saphenous vein. In view of the controversial discussion about the either conservative or surgical treatment, a clinically relevant classification of this syndrome appears useful: Stage I includes varicophlebitis without involvement of the respective junctional valve--in the groin or at the knee--and deep veins. While in Stage II the proximal part of the thrombus has reached the respective junctional valves of the long or short sapheneous vein, in Stage III it has entered the deep veins by means of these valves. In Stage IV the thrombus migrates via insufficient perforating veins into the deep system. Stages I and IV should be treated conservatively first, removal of the varicous veins should be performed after regression of the acute symptoms. Stages II and III should be considered an indication for urgent surgery. The surgical strategy consists of crossectomy, resection of the saphenous vein without stripping, radical excision of all varicous veins and ligature of insufficient perforating veins. In stage III the thrombectomy of the deep veins using the Fogarty-procedure must be carried out before any other measures are taken. In 1996 a total number of 40 limbs with ascending varicophlebitis (stage I = 16, stage II = 19, stage III = 5) was observed. 10 extremities (stage I = 2, stage II = 5, stage III = 3) underwent surgical treatment. 1 patient developed a deep infection of the groin, the average stay in hospital was 9 days.

Aged↗

Expansion of CD60 helper lymphocytes detected in peripheral lymphocytes of HIV-1 infected individuals is not paralleled in lymph nodes.

BACKGROUND AND OBJECTIVE: A significant expansion of CD8 cells with capability of Th2 type helper function had been observed in hemophiliacs with HIV infection. These cells were characterised by the surface co-expression of CD8 and CD60 antigen. Our objective was to investigate this lymphocyte subset in relation to other subsets in homosexuals and drug users in two compartments: blood and lymph nodes. Blood and lymph nodes from not HIV-infected persons served as control. RESULTS: CD8+CD60+ cells were expanded in perpheral blood of HIV - infected patients as compared to age matched controls (10.0 versus 4.1%, p <0.05). This difference was not observed in lymph node cell suspensions (6.2 vs. 4.3% of all lymph node cells; p = n.s.). The CD 4/CD8 ratio was significantly less impaired in lymph nodes than in blood (2.27 vs. 0.83; p <0.05). Cytotoxic T cells were more abundant in the lymph nodes of patients with early stage HIV disease when compared two late stage patients (4.3 vs 2.1%; p <0.05). Immunohistochemistry on frozen lymph node cuts showed presence of CD60 cells mainly in the interfollicular and paracortical area. In 3 of 10 HIV infected patients these cells were also found in the germinal centers. In controls no CD60 cells were detected in the follicles. Numbers and percentages of CD60 cellls and CD8+CD60+ cells in blood and in lymph nodes did not correlate with HIV - stage, CD4 count or plasma viral load. No correlation with lymph node viral load was seen. CONCLUSIONS: Our data confirm that like in hemophiliacs expansion of CD8+CD60+ is also found in the blood of other HIV risk groups and seems not to be specific for hemophiliacs. However, the higher percentage in peripheral blood is not paralleled in lymph nodes. Redistribution phenomena seem to be the most plausible explanation. According to these data, a major impact of CD8+CD60+ cells in the immunopathogenesis of HIV infection does not seem likely.

Antigens, CD↗

Endoluminal repair of peripheral arterial aneurysms: 4-year experience with the cragg endopro system I.

PURPOSE: To assess the efficiency and long-term patency of the Cragg EndoPro System I in patients with peripheral arterial aneurysms. MATERIALS AND METHODS: In 10 patients, 13 stent-grafts were used to treat 15 arterial aneurysms. Aneurysms were located in the common iliac (n = 4), superficial femoral (n = 4), popliteal (n = 3), and subclavian arteries (n = 2), and in a femoropopliteal bypass-graft (n = 2). Follow-up ranged between 2 and 46 months (mean, 36 months). Examination included clinical status, color-coded duplex sonography, computed tomography angiography, and intra-arterial digital subtraction angiography (DSA). RESULTS: Technical success was achieved in all patients. Primary patency was four of four in iliac vessels and three of nine in non-iliac vessels; secondary patency in noniliac vessels was four of nine. Repairs included one local lysis, four percutaneous transluminal angioplasties, one surgical thrombectomy, and one bypass surgery. Stent wire disintegration was detected in one of four iliac stent-grafts and in seven of nine noniliac stent-grafts. In noniliac grafts, significant stenoses occurred in three of nine; occlusion occurred in five of nine. One complication at the iliac level was a vessel wall penetration at the proximal stent edge, with development of a new aneurysmal formation. No late endoleaks were found. CONCLUSION: Exclusion of peripheral arterial aneurysms with stent-grafts is feasible. Long-term results are excellent in iliac vessels. Mechanical weakness of the stent assembly and frequent re-stenoses or occlusions are significant drawbacks in noniliac vessels with low patency rates.

Adult↗

Collagen patch coated with fibrin glue components. Treatment of suture hole bleedings in vascular reconstruction.

BACKGROUND: Bleeding from suture holes during vascular reconstruction, particularly when polytetrafluoroethylene (PTFE) prostheses are used, is still a problem which can lead to intraoperative delay and increased blood loss. The aim of this prospective, randomised, open, controlled multicentre study was to evaluate whether the use of a new local haemostyptic would reduce intraoperative blood loss and the time to haemostasis. METHODS: Thirty patients received a new haemostyptic (TachoComb H, Nycomed Pharma AG), whereas another 30 patients were treated with compresses. The vascular reconstructions were either anastomoses or patch angioplasties and were performed using PTFE vascular prostheses. RESULTS: The mean time to haemostasis of suture hole bleeding in the haemostyptic group (326.0 sec) was significantly shorter compared to the control group (514.3 sec) (p=0.006). The median intraoperative blood loss was 24.5 g in the treatment group and 57.3 g in the control group (p=0.045). CONCLUSIONS: It was shown that collagen patches coated with components of fibrin glue significantly reduce the time to haemostasis as well as blood loss at the operation site in patients undergoing vascular reconstruction with PTFE grafts.

Aged↗

[Preoperative changes in fluid filtration capacity in patients undergoing vascular surgery].

UNLABELLED: Patients undergoing major vascular surgery frequently require a substantial intraoperative fluid replacement to assure hemodynamic stability, which is in excess of the expected fluid requirements due to starving, blood and insensible losses. This leads to a positive fluid balance which can not be readily explained. METHOD: We have used venous congestion plethysmography (VCP) a non-invasive method for measurement of microvascular parameters in limbs to investigate the changes in microvascular permeability (FFK) and the balance of Starling forces of patients undergoing surgery for unilateral femoral artery reconstruction (FEM) under epidural anaesthesia or abdominal aortic aneurysm repair (AAA) under general anaesthesia. The control group consisted of patients scheduled for inguinal hernia repair or hand surgery under general anaesthesia. All patients were measured 24 hours pre-operatively, immediately after the induction of anaesthesia or completion of epidural anaesthesia and on the 1st, 5th and 10th postoperative day. The perioperative patient management followed a standard protocol and all patients with vascular disease were invasively monitored using indwelling arterial lines and central venous catheters. Continuous infusion of Ringers lactate and 6% Dextran 60 was sustained during the induction period. Each patient gave informed consent. RESULTS: Preoperatively we found no significant difference in the mean FFK-values of controls (4.1 +/- 0.4, ml.min-1 100 ml tissue-1 mmHg-1 x 10(-3) = FFKU), the AAA (3.6 +/- 0.3 FFKU) and FEM (4.2 +/- 0.3 FFKU). After induction of anaesthesia the mean FFK value in the controls fell to 3.5 +/- 0.5 FFKU (p = 0.07), whereas in the AAA patients we observed a significant increase to 4.7 +/- 0.2 FFKU (p < 0.005) and after epidural anaesthesia in FEM to 5.5 +/- 0.4 FFKU (p < 0.001) respectively. Those post anaesthetic FFK values where significantly higher in FEM and AAA than in the controls (p < 0.02). In AAA we found a significant positive correlation between the increase in FFK and the intraoperative fluid balance (r2 = 0.69, p < 0.01). No such correlation was found in controls and FEM. The postoperative values of FFK where unchanged in the control group, whereas a further increase was seen in both patient groups with vascular disease, with a maximum in AAA on the 1st postoperative day (to 5.4 +/- 0.4 FFKU mean both legs) and the 5th postoperative day in FEM (to 7.3 +/- 1.7 non-ischemic leg, 7.1 +/- 1.2 ischemic leg FFKU). In both groups normal FFK values where found on the 10th day after the operation. CONCLUSION: The data presented suggests an increase in extravascular fluid loss in patients undergoing vascular surgery, which becomes evident after the induction of general anaesthesia or completion of epidural anaesthesia. The positive correlation with the intraoperative fluid requirements may partially explain the often reported large intraoperative fluid requirements of patients undergoing AAA repair. The fact that the maximum change in fluid filtration capacity is found postoperatively may be explained by the additional effect of an ischemia/reperfusion injury in response to both the clamping an declamping of the artery and the increase in arterial blood flow to the limb due to the successful reconstruction of the blood vessel.

Adult↗

Mechanisms underlying increased platelet reactivity in patients with peripheral arterial disease. Preliminary results.

BACKGROUND: In peripheral arterial disease (PAD) atherosclerosis is disseminated and thrombosis risk is high. We have not only shown the platelets of PAD patients to by hyperreactive and aspirin resistant, but have recently verified them to be hypersensitive to heparin as well. In the present study we have begun to clarify the mechanisms underlying these regularly observed clinical findings. METHODS: Platelet function was tested with conventional, ADP-primed aggregation and with stagnation point flow adhesio-aggregometry (SPAA). SPAA permits real time, quantitative assessment of platelet adhesion and aggregation under biologically relevant flow conditions. The platelets from a female patient with congenital afibrinogenemia, were analyzed before and after intravenous fibrinogen substitution. In 14 PAD patients and 14 controls, platelet reactivity was assessed before and after incubation with the two platelet membrane glycoprotein (GP)-IIb/IIIa inhibitors Ro 43-8857 and 7E3. Lastly, experiments were performed before and after addition of plasma aliquots stemming from 4 PAD patients to platelet rich plasma and to solutions of gel-filtered platelets (GFP) stemming from 4 healthy volunteers. Before fibrinogen substitution, the platelets of the afibrinogenemic patient were unable to adhere in the SPAA-system and maximal ADP-primed aggregability was below 10%. After substitution, normal platelet adhesion was measured and primed aggregation increased three-fold. Mean baseline adhesion in the patient collective was twice that compared to controls (p<0.001). SPAA-measured, spontaneous aggregation was observed in ten patients and in none of the controls (p<0.001). RESULTS: Both SPAA-measured and primed aggregation were abolished at the lowest substrate concentrations (0.1 microM Ro 43-8857, 1 microg/ml 7E3). At these concentrations adhesion was reduced by 65% and 40% (respectively) in patients, and by 55% and 25% in controls. Total abolition of adhesion in both groups was seen with 0.5 microM Ro 43-8857 and 10 microg/ml 7E3. Platelet response to inhibitory agent was similar in patients and controls, as were the differences in dose-response between aggregation and adhesion. Upon addition of patient plasma to volunteer PRP, the platelets of all 4 healthy individuals aggregated spontaneously and the mean adhesivity in the group rose three-fold. The overall ability of the GFP to adhere when re-added to their own plasma was decreased, whereas, in the presence of patient plasma, adhesion increased significantly. CONCLUSIONS: On the basis of these findings we conclude that: 1) SPAA measures and quantifies platelet interactions with both fluid-phase (aggregation) and immobilized (adhesion) fibrinogen, 2) these reactions are mediated by the GP, IIb/IIIa receptor complex 3) the binding affinity, metabolic pathways and signal transduction underlying platelet adhesion differ from those involved in aggregation (possibly reflecting their varying roles in hemostasis), 4) the functionally normal platelets of patients with PAD are primed in vivo by a circulating plasma constituent, which leads to enhanced recruitment of activated GP, IIb/IIIa onto the platelet surface and, thereby, to an overall increase in reactivity.

Acetates↗

[Simultaneous vascular and endovascular surgery of complex vascular diseases].

Complex vascular disease requires combined, intraoperative endovascular and reconstructive therapy. Hereby, transprosthetic, transluminal angioplasty is particularly well suited for this purpose. The 5-year patency rate after combined inguinal patch plasty and femoral balloon dilation (n = 58) was 70%. The 5-year patency rates following transgraft angioplasty, with subsequent stent implantation and cross-over bypass (n = 46) and after transprosthetic, popliteal-crural dilation was 83% and 63%, respectively. Three patients with a type IIb (after Allenberg) aneurysm were treated with an aortoiliac stent prosthesis, combined with a cross-over bypass. The follow-up examinations at 2, 16 and 36 months were uneventful.

Aneurysm↗

[Ascending varicose vein phlebitis--classification and therapy].

Ascending varicophlebitis can cause pulmonary embolism by entering the deep venous system. Classification into four stages permits a differentiated therapeutic strategy: if the thrombus reaches or enters the deep venous system, immediate surgery consisting of crossectomy, resection of the saphenous vein, radical excision of all varicosed veins and ligature of insufficient perforating veins are indicated.

Aged↗

[Instrumental diagnosis for therapeutic decision: intra-arterial DSA versus 3D CT-angiography in abdominal aortic aneurysms].

Compared to intraarterial DSA, 3D spiral CT-angiography could be an reliable alternative method for preoperative evaluation and planning of abdominal aortic aneurysms. 3D data reconstruction with new rendering techniques (especially "volume rendering") provides unique information about mural thrombus, calcified plaques, vessel kinking and renal/visceral arteries. However, the more invasive intraarterial DSA should be performed in patients with complex occlusive disease of the iliac arteries, renal or visceral artery stenoses, or pathological findings in peripheral duplex sonography or if intraluminal exclusion with endostent placement is planned.

Angiography, Digital Subtraction↗

[Combined interventions in transfemoral stent implantation in infra-renal abdominal aortic aneurysm].

The transluminally placed endovascular graft (TPEG) is a novel method for the treatment of abdominal aortic aneurysms (AAA). Aortobiiliacal application requires three anchor sites and can often not be performed in cases of aneurysm, occlusion, or elongation of the iliac arteries. Here the aorto-uniiliacal stent implantation combined with crossover bypass provides an alternative procedure, and thus broadens the therapeutic endovascular spectrum.

Aortic Aneurysm, Abdominal↗

Increased platelet and coagulatory activity indicate ongoing thrombogenesis in peripheral arterial disease.

In peripheral arterial disease (PAD) risk of thrombosis is high and systemic haemostatic derangement thought contributory. We investigated platelet and coagulatory activity in patients with PAD and sought to find the best disease indicator. Stagnation point flow adhesion-aggregometry (SPAA) enables real-time quantitative assessment of platelet adhesion and aggregation under well-defined flow conditions. SPAA and agonist-induced aggregometry (Born method) were performed and concentrations of fibrinogen, fibrin monomer (FM), D-dimer, and thrombin-antithrombin complex (TAT) measured in 92 PAD patients and 70 healthy volunteers. Agonist-induced aggregometry detected no differences between patients and controls. SPAA-measured platelet adhesion and spontaneous aggregation (p < 0.001), and concentrations of fibrinogen (p < 0.001), FM (p < 0.001), TAT (p < 0.02) and D-dimer (p < 0.001) were all significantly increased in patients. Neither platelet function nor coagulatory activity was altered in patients receiving aspirin. Sensitivity and specificity in detecting PAD were as follows: SPAA (95%, 93%), fibrinogen (36%, 91%), FM (48%, 84%), TAT (36%, 78%), D-dimer (73%, 80%). Our findings support the concept of ongoing thrombogenesis as being contributory to the progression and possibly to the initiation of PAD. Aspirin alone did not prevent haemostatic hyperreactivity in these patients and flow-mediated platelet function was the most sensitive and specific indicator of advanced disease. This technique thus appears to be valuable, not only for evaluating therapeutic strategies to prevent platelet activation, but also in elaborating platelet-related mechanisms involved in thrombogenesis and atheroma formation.

Adult↗

Platelets of patients with peripheral arterial disease are hypersensitive to heparin.

We sought to verify earlier reports of increased platelet reactivity in patients with peripheral arterial disease (PAD) during perioperative heparin administration, and to test the hypothesis of platelet hypersensitivity to heparin in these patients. Before and after incubation of platelet rich plasma with unfractionated (UH), low molecular weight heparin (LMWH), and a low molecular weight heparinoid, real-time quantitative assessment of platelet function was performed by stagnation point flow adhesio-aggregometry (SPAA) in 21 patients with PAD and 14 healthy volunteers. With SPAA the occurrence of spontaneous aggregation is pathological. In the 15 patients requiring operation, platelet function and count were measured at regular intervals. To detect heparin dependent antibodies, the heparin induced platelet activation assay (HIPA) was performed preoperatively and after 10 days of heparin therapy. Mean baseline platelet adhesion in patients was double that observed in controls (p < 0.001). Spontaneous aggregation was seen in 9 (43%) patients and no controls (p < 0.001). In controls heparinoid reduced, whereas UH and LMWH slightly increased adhesion. Spontaneous aggregation was observed once with UH. Platelets from patients showed significantly enhanced adhesiveness and aggregability (p < 0.05) with UH and LMWH when compared to controls. Effects with the heparinoid were less pronounced and non-significant. In patients requiring operation, postoperative increases in platelet function and reductions in count were significant (p < 0.001). Ten (67%) experienced a fall in platelet count of > 50%. Preoperatively the HIPA assay showed no evidence of antibodies, whereas after heparin administration antibodies were verified in 4 (32%) patients and could not be ruled out in 6 (40%). Three developed postoperative thrombosis, in one case fatal. A hypersensitive in vitro and in vivo platelet response to heparin was verified in patients with PAD and a large number developed the immunological type of heparin-associated thrombocytopenia. Our findings suggest that a thrombin antagonist which does not interact with platelets may give the best perioperative protection in these patients.

Adult↗

Platelets of patients with peripheral arterial disease demonstrate a hypersensitive response to heparin.

We sought to verify earlier reports of increased platelet reactivity in patients with peripheral arterial disease (PAD) during perioperative heparin administration, and to test the hypothesis of platelet hypersensitivity to heparin in these patients. Before and after incubation of platelet rich plasma with unfractionated (UH), low molecular weight heparin (LMWH), and a low molecular weight heparinoid, real-time quantitative assessment of platelet function was performed by stagnation point flow adhesio-aggregometry (SPAA) in 21 patients with PAD and 14 healthy volunteers. With SPAA the occurrence of spontaneous aggregation is pathological. In the 15 patients requiring operation, platelet function and count were measured at regular intervals. To detect heparin dependent antibodies, the heparin induced platelet activation assay (HIPA) was performed preoperatively and after 10 days of heparin therapy. Mean baseline platelet adhesion in patients was double that observed in controls (p < 0.001). Spontaneous aggregation was seen in 9 (43%) patients and no controls (p < 0.001). In controls heparinoid reduced, whereas UH and LMWH slightly increased adhesion. Spontaneous aggregation was observed once with UH. Platelets from patients showed significantly enhanced adhesiveness and aggregability (p < 0.05) with UH and LMWH when compared to controls. Effects with the heparinoid were less pronounced and nonsignificant. In patients requiring operation, postoperative increases in platelet function and reductions in count were significant (p < 0.001). Ten (67%) experienced a fall in platelet count of > 50%. Preoperatively the HIPA assay showed no evidence of antibodies, whereas after heparin administration antibodies were verified in 4 (32%) patients and could not be ruled out in 6 (40%). Three developed postoperative thrombosis, in one case fatal. A hypersensitive in vitro and in vivo platelet response to heparin was verified in patients with PAD and a large number developed the immunological type of heparin-associated thrombocytopenia. Our findings suggest that a thrombin antagonist which does not interact with platelets may give the best perioperative protection in these patients.

Adult↗

Increased platelet and coagulatory activity in peripheral atherosclerosis flow mediated platelet function is a sensitive and specific disease indicator.

The importance of flow in both athero- and thrombogenesis is well established. In peripheral arterial disease (PAD) atherosclerosis is disseminated, thrombosis risk high and systemic hemostatic derangement believed contributory. We studied platelet and coagulatory activity in PAD patients, thereby evaluating the clinical efficacy of Stagnation Point Flow Adhesio-Aggregometry (SPAA). SPAA provides real-time quantitative assessment of platelet adhesion and aggregation under convective, low-shear flow conditions. 62 nondiabetic PAD patients and 66 healthy volunteers were examined, whereby SPAA and conventional aggregometry were performed and circulating fibrinogen, fibrin monomer (FM), the fibrin degradation product D-Dimer and thrombin-antithrombin-complex (TAT) assessed. Conventional aggregometry detected no differences between patients and controls. SPAA-measured platelet function (p < 0.001), fibrinogen (p < 0.001), FM (p < 0.001), TAT (p < 0.02) and D-Dimer (p < 0.001) were significantly increased in patients and not effected by aspirin therapy. Respective sensitivity and specificity in detecting PAD was as follows: SPAA (96%/95%), fibrinogen (36%/92%), FM (46%/88%), TAT (40%/73%), D-Dimer (75%/80%). Increased platelet and coagulatory activity was verified in PAD, whereby flow-mediated platelet adhesion and aggregation proved the most sensitive and specific parameter. These findings indicate the usefulness of SPAA for delineating platelet-related disease mechanisms and evaluating therapeutic strategies to prevent platelet activation.

Antithrombin III↗