Abstract T MP20: A Rapid Clot Lysis Assay to Predict Response to IV rt-PA in Stroke

Background: The cornerstone of acute stroke therapy is intravenous rt-PA, with the goal of rapid thrombolysis and restoration of blood flow. Unfortunately, less than half of patients treated have a favorable outcome. Since recanalization is closely correlated with the clinical response, endogenous resistance to rt-PA may inhibit thrombolysis and neurologic improvement. The primary objective of this research study was to evaluate whether an in vitro clot lysis assay and thrombolytic biomarkers could predict response to IV rt-PA in acute ischemic stroke patients Methods: Ischemic stroke patients who received IV rt-PA were recruited from two sites (Augusta, GA and Udine, Italy). Blood samples were collected prior to rt-PA administration and a favorable clinical response to rt-PA was specified as an NIHSS score of two or less at 24 hours. The time required for 50% platelet-poor clot lysis (C50%) was measured by an in vitro turbidimetric assay. The endogenous major fibrinolytic inhibitors (tissue plasminogen inhibitor, PAI-1; and α2-antiplasmin, α2-AP), D-dimer, fibrinogen and pro-thrombin time (PT), were assessed and correlated with clinical outcome. Results: We enrolled 54 rt-PA recipients (63±15 years; 72% male, and 85% white). The mean NIHSS was 11.2±5.1 at admission and 8.2±8.1 at 24 hours; 36% of patients had a favorable clinical response. There was a moderate reduction in C50% among patients with a favorable clinical outcome compared to those with an unfavorable outcome (669.5±46.3 vs. 704.7±91.6; p=0.075). There was no significant difference in PT (13.6±0.8 sec vs. 13.8±1.2 sec; p=0.444), PAI-1(28.2±34.1 pg/mL vs. 19.8±25.9 pg/mL; p=0.321), α2-AP (85.1±7.2 % vs. 88.8±10.1 %; p=0.153), D-dimer (269.5±232.2 ng/mL vs. 368.2±444.6 ng/mL; p=0.303) or fibrinogen (318.1±71.4 mg/dL vs. 343.0±173.1 mg/dL; p=0.465) levels between subjects with favorable and unfavorable response to rt-PA. Summary: Lack of response to IV rt-PA in stroke patients may reflect endogenous resistance to fibrinolysis reflected by prolonged clot lysis in vitro. The utility of clot lysis to predict rt-PA unresponsiveness should be tested in a larger clinical study.

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Incorporation of α2-Plasmin Inhibitor into Fibrin Clots and Its Association with the Clinical Outcome of Acute Ischemic Stroke Patients

Biomolecules ◽

10.3390/biom11030347 ◽

2021 ◽

Vol 11 (3) ◽

pp. 347

Author(s):

Zsuzsa Bagoly ◽

Barbara Baráth ◽

Rita Orbán-Kálmándi ◽

István Szegedi ◽

Réka Bogáti ◽

...

Keyword(s):

Ischemic Stroke ◽

Acute Ischemic Stroke ◽

Intracranial Hemorrhage ◽

Intravenous Thrombolysis ◽

Fibrin Clot ◽

Clot Lysis ◽

Stroke Patients ◽

Plasmin Inhibitor ◽

Fibrin Clots

Cross-linking of α2-plasmin inhibitor (α2-PI) to fibrin by activated factor XIII (FXIIIa) is essential for the inhibition of fibrinolysis. Little is known about the factors modifying α2-PI incorporation into the fibrin clot and whether the extent of incorporation has clinical consequences. Herein we calculated the extent of α2-PI incorporation by measuring α2-PI antigen levels from plasma and serum obtained after clotting the plasma by thrombin and Ca2+. The modifying effect of FXIII was studied by spiking of FXIII-A-deficient plasma with purified plasma FXIII. Fibrinogen, FXIII, α2-PI incorporation, in vitro clot-lysis, soluble fibroblast activation protein and α2-PI p.Arg6Trp polymorphism were measured from samples of 57 acute ischemic stroke patients obtained before thrombolysis and of 26 healthy controls. Increasing FXIII levels even at levels above the upper limit of normal increased α2-PI incorporation into the fibrin clot. α2-PI incorporation of controls and patients with good outcomes did not differ significantly (49.4 ± 4.6% vs. 47.4 ± 6.7%, p = 1.000), however it was significantly lower in patients suffering post-lysis intracranial hemorrhage (37.3 ± 14.0%, p = 0.004). In conclusion, increased FXIII levels resulted in elevated incorporation of α2-PI into fibrin clots. In stroke patients undergoing intravenous thrombolysis treatment, α2-PI incorporation shows an association with the outcome of therapy, particularly with thrombolysis-associated intracranial hemorrhage.

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Abstract P683: Thrombin Generation in Plasma of Stroke Patients With Atrial Fibrillation

Stroke ◽

10.1161/str.52.suppl_1.p683 ◽

2021 ◽

Vol 52 (Suppl_1) ◽

Author(s):

Sarina Falcione ◽

Gina Sykes ◽

Joseph Kamtchum Tatuene ◽

Danielle Munsterman ◽

Twinkle Joy ◽

...

Keyword(s):

Atrial Fibrillation ◽

Ischemic Stroke ◽

Thrombin Generation ◽

Thrombus Formation ◽

Lag Time ◽

Thrombin Time ◽

Stroke Patients ◽

Time To Peak ◽

Generation Capacity

Background and Purpose: Thrombus formation is central to pathophysiology of stroke in patients with atrial fibrillation. Whether factors in plasma contribute to thrombus generation in patients with atrial fibrillation remains unclear. In this study we sought to determine whether plasma contributes to thrombin generation in patients with atrial fibrillation. Methods: There were 78 acute ischemic strokes with atrial fibrillation and 37 non-stroke controls. Plasma thrombin generation was measured by thrombin generation assay, resulting lag time, peak thrombin, time to peak and area under the curve was assessed. Thrombin generation capacity was compared in stroke patients with atrial fibrillation to non-stroke controls. The relationship to anticoagulation was assessed. In vitro, the effect of anticoagulation on plasma thrombin generation was determined. Results: Thrombin generation capacity was increased (shorter lag time and time to peak) in ischemic stroke patients with atrial fibrillation compared to non-stroke atrial-fibrillation controls (p<0.05 and p<0.01, respectively). Anticoagulation decreased plasma induced thrombin generation. Ischemic stroke patients with atrial fibrillation treated with anticoagulation (DOAC or warfarin) had lower plasma induced thrombin generation compared to atrial-fibrillation patients not on anticoagulation (p<0.05). Thrombin generation by plasma could be further reduced by DOAC in an in-vitro assay. Conclusions: Stroke patients with atrial fibrillation have a higher plasma induced thrombin generation compared to atrial fibrillation controls. Factors in plasma such as leukocyte derived tissue factor likely contribute to thrombus formation in patients with atrial fibrillation. As such, components in plasma may represent new targets to reduce thrombus formation and stroke risk in patients with atrial fibrillation.

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Increased von Willebrand factor, P-selectin and fibrin content in occlusive thrombus resistant to lytic therapy

Thrombosis and Haemostasis ◽

10.1160/th15-12-0985 ◽

2016 ◽

Vol 115 (06) ◽

pp. 1129-1137 ◽

Cited By ~ 15

Author(s):

Bruno Del Blanco ◽

Marisol Ruiz-Meana ◽

Jaume Francisco ◽

José Barrabés ◽

Jaume Figueras ◽

...

Keyword(s):

Coronary Intervention ◽

Clot Lysis ◽

St Segment Elevation ◽

Coronary Thrombus ◽

Healthy Donors ◽

St Segment ◽

Blood Lysis ◽

Pai 1 ◽

D Dimer

SummaryTherapeutic fibrinolysis is ineffective in 40 % of ST-segment elevation acute myocardial infarction (STEMI) patients, but understanding of the mechanisms is incomplete. It was our aim to compare the composition of coronary thrombus in lysis-resistant STEMI patients with that of lysis-sensitive patients. Intracoronary thrombi (n=64) were obtained by aspiration in consecutive STEMI patients. Of them, 20 had received fibrinolysis and underwent rescue percutaneous coronary intervention (r-PCI, lysis-resistant patients) and 44 underwent primary PCI (p-PCI). Lysis-sensitivity was determined in vitro by clot permeability measurements and turbidimetric lysis in plasma of 44 patients undergoing p-PCI and 20 healthy donors. Clot-lysis sensitivity was defined as a clot-lysis time not greater than 1 SD over the mean of healthy donors. Coronary thrombus composition in 20 lysis-resistant and in 20 lysissensitive patients was analysed by immunofluorescence with confocal microscopy. Plasma biomarkers (P-selectin, VWF, PAI-1, t-PA, D-dimer, TF pathway markers, plasmin and CD34+) were measured simultaneously on peripheral blood. Lysis-resistant clots had higher levels of fibrin (p=0.02), P-selectin (p=0.03) and VWF (p=0.01) than lysis-sensitive clots. Among thrombi obtained ≤ 6 hours after onset of symptoms, those from lysis-resistant patients showed a higher content in fibrin than those from p-PCI patients (p=0.01). Plasma PAI-1 (p=0.02) and D-dimer levels were significantly higher (p=0.003) in lysis-resistant patients, whereas plasmin levels were lower (p=0.03). Multivariate analysis showed the content of fibrin and VWF within thrombus as predictors of thrombolysis resistance. In conclusion, coronary thrombi in STEMI patients resistant to fibrinolysis are characterised by higher fibrin, P-selectin and VWF content than lysis-sensitive thrombi.

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Fibrinolytic parameters, lipid status and lipoprotein(a) in ischemic stroke patients

Srpski arhiv za celokupno lekarstvo ◽

10.2298/sarh10s1012v ◽

2010 ◽

Vol 138 (suppl. 1) ◽

pp. 12-17 ◽

Cited By ~ 8

Author(s):

Biljana Vuckovic ◽

Mirjana Djeric ◽

Tatjana Ilic ◽

Visnja Canak ◽

Suncica Kojic-Damjanov ◽

...

Keyword(s):

Ischemic Stroke ◽

Plasminogen Activator ◽

Clot Lysis ◽

Stroke Patients ◽

Lipid Status ◽

Lysis Time ◽

Euglobulin Clot Lysis Time ◽

Fibrinolytic Parameters ◽

Pai 1 ◽

Clot Lysis Time

Introduction. Ischemic stroke is the third leading cause of mortality and morbidity in most countries in the world. Impaired fibrinolysis, as well as disordered lipid metabolism have been recognized as risk factors for this disease. Objective. To study some of fibrinolytic parameters, lipid status and lipoprotein(a) - Lp(a) in ischemic stroke patients in Serbia and to examine associations between Lp(a) and fibrinolytic parameters. Methods. Sixty ischemic stroke patients (case group, mean age 63.48?9.62 years) and 30 age and sex matched healthy controls (control group, mean age 60.2?7.96 years) were studied. Results. A significantly longer euglobulin clot lysis time (219.7?78,8 min. vs 183.5?58,22 min; p=0.005) and higher levels of plasminogen activator inhibitor-1 (PAI-1) (48.5?17.1 ng/ml vs 27.1?10.1 ng/ml; p=6.2?10-11), tissue-type plasminogen activator antigen (t-PA) (11.1?7.14 ng/ml vs 6,.0?3.66 ng/ml; p=5.2?10-5) and D-dimer (382.27?504.22ng/ml vs 116.12?88.81 ng/ml; p=0.0002) were found in cases compared to controls. There were no significant differences in fibrinogen levels (4.30?0.84 g/l vs 4.09?0.64 g/l; p=0.23) or plasminogen activity (92.67?11.37 % vs 96.87?9.48%; p=0.085). There was no significant difference in Lp(a) concentration between cases and controls (0.15?0.11 g/l vs 0.12?0.11 g/l; p=0.261). However, in the cases, but not in the controls, multivariate analysis of associations between fibrinolytic parameters and Lp(a) showed the highest correlation between t-PA and PAI-1, and the latent effect of Lp(a) on t-PA and PAI-1. Conclusions. Our results show that there are important differences in the characteristics of the fibrinolytic mechanism in ischemic stroke patients compared to healthy population. The major differences are prolonged euglobulin clot lysis time and elevated PAI-1 and t-PA antigen in ischemic stroke patients. In addition, Lp(a) appears to be involved in the inhibition of fibrinolysis in ischemic disease through a mechanism unrelated to its serum concentrations.

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Abstract 47: Proteomic Profiling of Acute Stroke Patients Highlights the Importance of vWF and vWF-Cleaving Protease (ADAMTS13) in Thrombolysis

Stroke ◽

10.1161/str.45.suppl_1.47 ◽

2014 ◽

Vol 45 (suppl_1) ◽

Author(s):

MingMing Ning ◽

Elizabeth Van Cott ◽

Mary Lopez ◽

Dave Sarracino ◽

Thomas Wickham ◽

...

Keyword(s):

Ischemic Stroke ◽

Clinical Outcome ◽

Acute Ischemic Stroke ◽

Clinical Utility ◽

Animal Studies ◽

Initial Step ◽

Clot Lysis ◽

Proteomic Profiling ◽

Stroke Patients ◽

Clot Burden

Introduction: Recent animal studies show rADAMTS13 (vWF cleaving protease) to block tPA-induced BBB opening, reducing tPA-related hemorrhage and augmenting tPA’s thrombolytic effect. From proteomic screening, we found ADAMTS13/vWF to be an important pathway in tPA responders. Thus, the vWF/ADAMTS13 (vWF cleaving protease) axis may be an important modifier of tPA response in the clinical setting. But the effect of tPA on the ADAMTS13/vWF balance has not been studied directly in stroke patients post-tPA. Here we measured vWF and ADAMTS13 in acute ischemic stroke patients post IV tPA to investigate their clinical utility to follow tPA response. Methods: Quantitative Mass Spectrometry (MS), latex immuno-turbidimetric assay, and ELISA were performed in acute ischemic stroke plasma over time, with clinical outcome measured at 3 months. Response was defined per NINDS trial as mRankins<=2 and >= 4 points improvement on NIHSS. Results: Post tPA (up to 72 hours), ADAMTS13 is persistently and significantly higher in tPA responders than in non-responders (Figure 1A). Conversely, within 72 hrs post tPA, the ratio of vWF/ADAMTS13 (a measure of clot burden vs clot lysis) is significantly higher in tPA patients who did not improve compared to those who did. tPA patients also had lower vWF/ADAMTS13 ratios than non-tPA strokes (Figure 1B). Conclusion: Through dynamic changes detected in the vWF/ADAMTS13 pathway, our data suggest the balance of clot burden vs lysis is crucial in tPA response as measured in patient plasma in real time. More vWF degradation in tPA patients via ADAMTS13 is correlated to better clinical outcome within the first 72 hours, and conversely, increased clot burden was found in tPA non-responders. Studying endogenous ADAMTS13 activity in tPA response is an initial step to obtain evidence for its potential clinical utility. And vWF/ADAMTS13 ratio may be a biologically relevant and potentially clinically useful marker of clotting/lytic status in early thrombolysis.

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Activated Protein C Increases Fibrin Clot Lysis by Neutralization of Plasminogen Activator Inhibitor No Evidence for a Cofactor Role of Protein S

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647055 ◽

1988 ◽

Vol 60 (02) ◽

pp. 328-333 ◽

Cited By ~ 44

Author(s):

N J de Fouw ◽

Y F de Jong ◽

F Haverkate ◽

R M Bertina

Keyword(s):

Plasminogen Activator ◽

Protein C ◽

Blood Platelets ◽

Plasminogen Activator Inhibitor ◽

Protein S ◽

Tissue Type ◽

Clot Lysis ◽

Activator Inhibitor ◽

Pai 1

summaryThe effect of purified human activated protein G (APC) on fibrinolysis was studied using a clot iysis system consisting of purified glu-plasminogen, tissue-type plasminogen activator, plasminogen activator inhibitor (released from endothelial cells or blood platelets), fibrinogen, 125T-fibrinogen and thrombin. All proteins were of human origin.In this system APC could increase fibrinolysis in a dose dependent way, without affecting fibrin formation or fibrin crosslinking. However, this profibrinolytic effect of APC could only be observed when plasminogen activator inhibitor (PAI-l) was present. The effect of APC was completely quenched by pretreatment of APC with anti-protein C IgG or di-isopropylfluorophosphate. Addition of the cofactors of APC:protein S, Ca2+-ions and phospholipid-alone or in combination did not enhance the profibrinolytic effect of APC. These observations indicate that human APC can accelerate in vitro clot lysis by the inactivation of PAI-1 activity. However, the neutralization of PAI-1 by APC is independent of the presence or absence of protein S, phospholipid and Ca2+-ions.

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Anti-thrombotic Effect of a PAI-1 Inhibitor in Rats Given Endotoxin

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650231 ◽

1996 ◽

Vol 75 (01) ◽

pp. 118-126 ◽

Cited By ~ 27

Author(s):

T Abrahamsson ◽

V Nerme ◽

M Strömqvist ◽

B Åkerblom ◽

A Legnehed ◽

...

Keyword(s):

Plasminogen Activator Inhibitor ◽

Rat Plasma ◽

Clot Lysis ◽

Fibrin Deposition ◽

Plasminogen Activator Inhibitor 1 ◽

Fab Fragment ◽

Dose Dependent Decrease ◽

Pai 1

SummaryThe aim of this study was to investigate the anti-thrombotic effects of an inhibitor of the plasminogen activator inhibitor-1 (PAI-1) in rats given endotoxin. In studies in vitro, PRAP-1, a Fab-fragment of a polyclonal antibody against human PAI-1, was shown to inhibit PAI-1 activity in rat plasma as well as to stimulate clot-lysis of the euglobulin fraction derived from rat plasma. Endotoxin administered to anaesthetised rats produced a marked increase in plasma PAI-1 activity. To study fibrin formation and lysis in vivo after intravenous (i. v.) injection of the coagulant enzyme batroxobin, 125I-fibrinogen was administered to the animals. The thrombi formed by batroxobin were rapidly lysed in control animals, while the rate of lysis was markedly attenuated in rats given endotoxin. PRAP-1 was administered i.v. (bolus + infusion) to rats given endotoxin and batroxobin and the PAI-1 inhibitor caused a dose-dependent decrease in the 125I-fibrin deposition in the lungs. An immunohistochemical technique was used to confirm this decrease in density of fibrin clots in the tissue. Furthermore, PRAP-1 decreased plasma PAI-1 activity in the rats and this reduction was correlated to the decrease in lung 125I-fibrin deposition at the corresponding time point. It is concluded that in this experimental model the PAI-1 antibody PRAP-1 may indeed inhibit thrombosis in animals exposed to endotoxin.

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The Roles of α2-Antiplasmin and Plasminogen Activator Inhibitor 1 (PAI-1) in the Inhibition of Clot Lysis

Thrombosis and Haemostasis ◽

10.1055/s-0038-1649570 ◽

1993 ◽

Vol 70 (02) ◽

pp. 301-306 ◽

Cited By ~ 51

Author(s):

Linda A Robbie ◽

Nuala A Booth ◽

Alison M Croll ◽

Bruce Bennett

Keyword(s):

Plasminogen Activator ◽

Plasminogen Activator Inhibitor ◽

Fibrin Clot ◽

Clot Lysis ◽

Plasminogen Activator Inhibitor 1 ◽

Dependent Inhibition ◽

Activator Inhibitor ◽

Pai 1

SummaryThe relative importance of the two major inhibitors of fibrinolysis, α2-antiplasmin (α2-AP) and plasminogen activator inhibitor (PAI-1), were investigated using a simple microtitre plate system to study fibrin clot lysis in vitro. Cross-linked fibrin clots contained plasminogen and tissue plasminogen activator (t-PA) at concentrations close to physiological. Purified α2-AP and PAI-1 caused dose-dependent inhibition. All the inhibition due to normal plasma, either platelet-rich or poor, was neutralised only by antibodies to α2-AP. Isolated platelets, at a final concentration similar to that in blood, 2.5 × 108/ml, markedly inhibited clot lysis. This inhibition was neutralised only by antibodies to PAI-1. At the normal circulating ratio of plasma to platelets, α2-AP was the dominant inhibitor. When the platelet:plasma ratio was raised some 20-fold, platelet PAI-1 provided a significant contribution. High local concentrations of PAI-1 do occur in thrombi in vivo, indicating a role for PAI-1, complementary to that of α2-AP, in such situations.

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In Vitro Clot Lysis as a Potential Indicator of Thrombus Resistance to Fibrinolysis – Study in Healthy Subjects and Correlation with Blood Fibrinolytic Parameters

Thrombosis and Haemostasis ◽

10.1055/s-0038-1656041 ◽

1997 ◽

Vol 77 (04) ◽

pp. 725-729 ◽

Cited By ~ 11

Author(s):

Mario Colucci ◽

Silvia Scopece ◽

Antonio V Gelato ◽

Donato Dimonte ◽

Nicola Semeraro

Keyword(s):

Plasminogen Activator ◽

Clot Lysis ◽

Individual Response ◽

Plasminogen Activator Inhibitor 1 ◽

Autologous Plasma ◽

Wide Range ◽

Blood Clots ◽

Physiological Variations ◽

Pai 1

SummaryUsing an in vitro model of clot lysis, the individual response to a pharmacological concentration of recombinant tissue plasminogen activator (rt-PA) and the influence on this response of the physiological variations of blood parameters known to interfere with the fibrinolytic/thrombolytic process were investigated in 103 healthy donors. 125I-fibrin labelled blood clots were submersed in autologous plasma, supplemented with 500 ng/ml of rt-PA or solvent, and the degree of lysis was determined after 3 h of incubation at 37° C. Baseline plasma levels of t-PA, plasminogen activator inhibitor 1 (PAI-1), plasminogen, α2-anti-plasmin, fibrinogen, lipoprotein (a), thrombomodulin and von Willebrand factor as well as platelet and leukocyte count and clot retraction were also determined in each donor. rt-PA-induced clot lysis varied over a wide range (28-75%) and was significantly related to endogenous t-PA, PAI-1, plasminogen (p <0.001) and age (p <0.01). Multivariate analysis indicated that both PAI-1 antigen and plasminogen independently predicted low response to rt-PA. Surprisingly, however, not only PAI-1 but also plasminogen was negatively correlated with rt-PA-ginduced clot lysis. The observation that neutralization of PAI-1 by specific antibodies, both in plasma and within the clot, did not potentiate clot lysis indicates that the inhibitor, including the platelet-derived form, is insufficient to attenuate the thrombolytic activity of a pharmacological concentration of rt-PA and that its elevation, similarly to the elevation of plasminogen, is not the cause of clot resistance but rather a coincident finding. It is concluded that the in vitro response of blood clots to rt-PA is poorly influenced by the physiological variations of the examined parameters and that factors other than those evaluated in this study interfere with clot dissolution by rt-PA. In vitro clot lysis test might help to identify patients who may be resistant to thrombolytic therapy.

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Abstract 74: Early Arterial Recanalization After Intra-venous Tissue-Plasminogen-Activator Treatment in the Interventional Management of Stroke-3 Study

Stroke ◽

10.1161/str.45.suppl_1.74 ◽

2014 ◽

Vol 45 (suppl_1) ◽

Author(s):

Ruediger Von Kummer ◽

Andrew M Demchuk ◽

Lydia D Foster ◽

Bernard Yan ◽

Wouter J Schonewille ◽

...

Keyword(s):

Ischemic Stroke ◽

Clinical Outcome ◽

Acute Ischemic Stroke ◽

Internal Carotid ◽

Arterial Occlusion ◽

Posterior Circulation ◽

Stroke Patients ◽

Vessel Occlusion ◽

Tissue Plasminogen ◽

Arterial Recanalization

Background: Data on arterial recanalization after IV t-PA treatment are rare. IMS-3 allows the study of variables affecting arterial recanalization after IV t-PA in acute ischemic stroke patients with CTA-proved major artery occlusions. Methods: Of 656 acute ischemic stroke patients in IMS-3, 306 were examined with baseline CTA and randomized either to IV t-PA (N=95) or to IV t-PA followed by digital subtraction angiography (DSA) and endovascular therapy (EVT) (N=211). Comparison of baseline CTA to DSA within 5 hours of stroke onset assessed early arterial recanalization after IV t-PA. A central core lab categorized DSA vessel occlusion as “no, partial, or complete”. We studied the association between arterial occlusion sites on baseline CTA with early recanalization for the endovascular group and analyzed its impact on clinical outcome at 90 days. Results: In the EVT group, 22 patients (10.4%) had no CTA intracranial occlusions, but 1 extracranial occlusion; 42 patients (19.9%) had occlusions of intracranial internal carotid artery (ic-ICA); 10 patients (4.7%) had tandem occlusions of the cervical ICA and middle cerebral artery (MCA); 95 patients (45.0%) had MCA-trunk (M1) occlusions, 33 patients (15.6%) had M2 occlusions, 3 patients (1.4%) had M3/4 occlusions, and 6 patients (2.8%) occlusions within posterior circulation. Partial or complete recanalization occurred in 28.6% of patients before DSA and was marginally associated with occlusion site (p=0.0525) (8 patients (19.0%) with ic-ICA occlusion, 0 patients with tandem ICA/MCA occlusions, 34 patients (35.8%) with M1 occlusions, 11 patients (33.3%) with M2 occlusions, 0 patients with M3/4 occlusions, and 1 patient (16.7%) with occlusion within posterior circulation). Three CTA negative patients had intracranial occlusions on DSA. Thirty-two patients (59.3%) with early recanalization achieved mRS of 0-2 at 90 days compared to 51 patients (38.4%) without early recanalization (p=0.0099). There was no relationship between early recanalization and time to IV t-PA or mean t-PA dose. Conclusion: Before EVT, IV rt-PA may facilitate arterial recanalization and better clinical outcome in about one third of patients.

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