Endovascular treatment of arteriovenous graft dysfunction as a result of graft delamination and fracture

Background Graft thrombosis due to fabric delamination is a rare cause of delayed failure of arteriovenous grafts. Graft delamination is primarily an imaging diagnosis and is confirmed with the help of ultrasound which shows the separation of graft fabric layers. Only two such cases have been described in the literature so far. Case presentation We present a case of upper extremity arteriovenous graft thrombosis in a 79 year old COVID-19 positive patient with end-stage renal disease. The diagnosis was established on ultrasonography which revealed separation of the graft fabric layers with thrombosis within the “false” and “true” lumen of the graft. The patient was managed with angioplasty and embolectomy of the clot material followed by stent-graft placement across the delaminated portion of the graft. Post-procedural angiography confirmed brisk flow across the graft and patient could successfully have subsequent hemodialysis sessions. Conclusions Identification of graft delamination as a cause of graft failure is important as its management differs from other conventional causes since it requires stent-grafts to cover the area of delamination to re-establish flow and salvage the AV graft. The recognition of this phenomenon is essential to provide quality care and successful reuse of the AV graft. Level of evidence Level 4, Case Report.

Abstract TP210: Histopathological Evaluation of Thrombus in Acute Stroke and Correlation with Stroke Etiology

Background: While more endovascular treatments for acute stroke are being performed, few studies evaluate clot composition with variable results. We sought to evaluate the feasibility of collecting and analyzing the RBC to platelet ratios in clots, and correlated our findings with stroke etiology. Methods: This is an ongoing prospective study analyzing clots retrieved by mechanical thrombectomy in acute stroke patients at our institution. Retrieved clot material was fixed and cut at 4-m thickness. All clots were stained with hematoxylin-eosin to identify red blood cells (RBC’s), and antibodies for platelet glycoprotein IIIa with CD61 (LifeSpan Biosciences, Seattle, Washington) for platelets. Stained slides were scanned at 200x magnification by using a Scanscope XT digital scanner (Apergio, Vista, California). Image-J software (National Institutes of Health, Bethesda, Maryland) was used for semiquantitative analysis of percentage RBC’s and platelets. Correlation of RBC to Platelet ratios with stroke etiology was performed. Results: A total of 18 clots from 18 patients were analyzed. Stroke etiology was cardioembolic in 8, Large vessel atherosclerosis (LVA) in 5, undetermined in 3 and carotid dissection in 2. The mean RBC to platelet ratio was 0.51:1 in cardioembolic and 0.64:1 in LVA strokes. Patients with undetermined etiology had similar clot composition (0.53:1) to cardioembolic stroke. The highest RBC content was found in carotid dissection thrombus with a ratio of 1.73:1 as compared to other etiologies (p=0.01 cardioembolic, p=0.04 undetermined, p=0.02 LVA). Conclusion: In our study’s first phase, clot processing and analysis was found to be feasible. Although a high mean RBC content was found in carotid dissections and strokes of undetermined etiology had similar clot composition to cardioembolic stroke, ongoing collection and analysis will help support these findings.

Analytical Comparison ofIn Vitro-Spiked Human Serum and Plasma for PCR-Based Detection of Aspergillus fumigatus DNA: a Study by the European Aspergillus PCR Initiative

The use of serum or plasma forAspergillusPCR testing facilitates automated and standardized technology. Recommendations for serum testing are available, and while serum and plasma are regularly considered interchangeable for use in fungal diagnostics, differences in galactomannan enzyme immunoassay (GM-EIA) performance have been reported and are attributed to clot formation. Therefore, it is important to assess plasma PCR testing to determine if previous recommendations for serum are applicable and also to compare analytical performance with that of serum PCR. Molecular methods testing serum and plasma were compared through multicenter distribution of quality control panels, with additional studies to investigate the effect of clot formation and blood fractionation on DNA availability. Analytical sensitivity and time to positivity (TTP) were compared, and a regression analysis was performed to identify variables that enhanced plasma PCR performance. When testing plasma, sample volume, preextraction-to-postextraction volume ratio, PCR volume, duplicate testing, and the use of an internal control for PCR were positively associated with performance. When whole-blood samples were spiked and then fractionated, the analytical sensitivity and TTP were superior when testing plasma. Centrifugation had no effect on DNA availability, whereas the presence of clot material significantly lowered the concentration (P= 0.028). Technically, there are no major differences in the molecular processing of serum and plasma, but the formation of clot material potentially reduces available DNA in serum. During disease,AspergillusDNA burdens in blood are often at the limits of PCR performance. Using plasma might improve performance while maintaining the methodological simplicity of serum testing.

Fibrinolysis-inhibitory capacity of clot-embedded surfactant is enhanced by SP-B and SP-C

Incorporation of pulmonary surfactant into fibrin inhibits its plasmic degradation. In the present study we investigated the influence of surfactant proteins (SP)-A, SP-B, and SP-C on the fibrinolysis-inhibitory capacity of surfactant phospholipids. Plasmin-induced fibrinolysis was quantified by means of a 125I-fibrin plate assay, and surfactant incorporation into polymerizing fibrin was analyzed by measuring the incorporation of3H-labeled L-α-dipalmitoylphosphatidylcholine into the insoluble clot material. Incorporation of a calf lung surfactant extract (Alveofact) and an organic extract of natural rabbit large surfactant aggregates (LSA) into a fibrin clot revealed a stronger inhibitory effect on plasmic cleavage of this clot than a synthetic phospholipid mixture (PLX) and unprocessed LSA. Reconstitution of PLX with SP-B and SP-C increased, whereas reconstitution with SP-A decreased, the fibrinolysis-inhibitory capacity of the phospholipids. The SP-B effect was paralleled by an increased incorporation of phospholipids into fibrin. We conclude that the inhibitory effect of surfactant incorporation into polymerizing fibrin on its susceptibility to plasmic cleavage is enhanced by SP-B and SP-C but reduced by SP-A. In the case of SP-B, increased phospholipid incorporation may underlie this finding.

Reperfusion after Thrombolytic Therapy of Embolic Stroke in the Rat: Magnetic Resonance and Biochemical Imaging

The effect of thrombolytic therapy was studied in rats submitted to thromboembolic stroke by intracarotid injection of autologous blood clots. Thrombolysis was initiated after 15 minutes with an intracarotid infusion of recombinant tissue-type activator (10 mg/kg body weight). Reperfusion was monitored for 3 hours using serial perfusion- and diffusion magnetic resonance imaging, and the outcome of treatment was quantified by pictorial measurements of ATP, tissue pH, and blood flow. In untreated animals, clot embolism resulted in an immediate decrease in blood flow and a sharp decrease in the apparent diffusion coefficient (ADC) that persisted throughout the observation period. Thrombolysis successfully recanalized the embolized middle cerebral artery origin and led to gradual improvement of blood flow and a slowly progressing reversal of ADC changes in the periphery of the ischemic territory, but only to transient and partial improvement in the center. Three hours after initiation of thrombolysis, the tissue volume with ADC values less than 80% of control was 39 ± 22% as compared to 61 ± 20% of ipsilateral hemisphere in untreated animals (means ± SD, P = .03) and the volume of ATP-depleted brain tissue was 25 ± 31% as compared to 46 ± 29% in untreated animals. Recovery of ischemic brain injury after thromboembolism is incomplete even when therapy is started as early as 15 minutes after clot embolism. Possible explanations for our findings include downstream displacement of clot material, microembolism of the vascular periphery, and events associated with reperfusion injury.

Clot-embedded natural surfactant: kinetics of fibrinolysis and surface activity

Polymerization of fibrin in the presence of pulmonary surfactant was recently noted to induce incorporation of phospholipids into the insoluble clot material, thereby effecting severe loss of surface activity (W. Seeger, A. Elssner, A. Gunther, H.-J. Kramer, and H. O. Kalinowski. Am. J. Respir. Cell Mol. Biol. 9: 213'220, 1993). In the present study, we investigated the influence of such incorporation of calf lung surfactant extract (CLSE) on the enzymatic cleavage of the fibrin network with the use of plasmin, trypsin, or elastase. Employing a fibrin-plate assay, the proteolytic release of radioactivity originating from 125I-labeled fibrinogen was assessed, and the pattern of split products was characterized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis technique. Surface activity of CLSE was measured in the pulsating bubble surfactometer. When incorporated into the fibrin clot, CLSE inhibited the cleavage of fibrin by all proteases in a dose-dependent manner without affecting the profile of scission products. Inhibition of plasmin-induced clot lysis was also noted on incorporation of CLSE into clotted plasma and on incorporation of dipalmitoylphosphatidylcholine into fibrin polymers. In contrast, corresponding concentrations of CLSE added to the incubation medium after preformation of the fibrin matrix did not substantially influence the kinetics of fibrinolysis. CLSE incorporation into the nascent fibrin clot resulted in complete loss of surface activity, but adsorption and surface tension-lowering properties were largely restored by subsequent plasmic clot lysis. Arising fibrin split products were shown to display similar inhibitory strength on CLSE surface activity compared with fibrinogen split products.(ABSTRACT TRUNCATED AT 250 WORDS