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PubMed2001

Randomized comparison of a novel anticoagulant, vasoflux, and heparin as adjunctive therapy to streptokinase for acute myocardial infarction: results of the VITAL study (Vasoflux International Trial for Acute Myocardial Infarction Lysis).

BACKGROUND: Vasoflux is a low-molecular-weight heparin derivative that inhibits factor IXa activation of factor X and catalyzes fibrin-bound thrombin inactivation by heparin cofactor II. We studied whether vasoflux improves the results of thrombolysis with streptokinase for acute myocardial infarction. METHODS AND RESULTS: We randomized 277 patients with acute myocardial infarction to standard intravenous unfractionated heparin (UFH) or intravenous vasoflux 1, 4, 8, or 16 mg/kg as a bolus followed by 1, 4, 8, or 16 mg/kg per hour infusion, on top of streptokinase and aspirin, until angiography at 90 minutes. Patency and corrected Thrombolysis in Myocardial Infarction (TIMI) frame count were studied at 60 and 90 minutes. Rates of TIMI grade 3 flow with vasoflux at any dose (35% to 42%) were not different from UFH (41%) at either time point, nor was the corrected TIMI frame count. However, there was an excess of bleeding in the patients randomized to vasoflux 8 or 16 mg/kg: 78% and 71%, compared with 53% for UFH (P =.004 and.043, respectively). Major bleeding was observed in 13% and 28% at these vasoflux doses compared with 8% with UFH (P =.558 and.01, respectively). CONCLUSION: At doses that increase the risk of bleeding, the addition of vasoflux to streptokinase and aspirin did not lead to improved patency rates compared with UFH. Targeting factor IXa and heparin cofactor II may not be a useful adjunct to thrombolysis.

Adult↗

PubMed1986

Should coronary artery bypass be delayed following successful direct coronary artery streptokinase thrombolysis during evolving myocardial infarction?

The effect of deferring immediate coronary artery bypass was evaluated in two groups of similar patients having successful direct coronary artery thrombolysis with streptokinase in the treatment of evolving myocardial infarction. Within 6 hours of onset of myocardial infarction, 140 patients underwent immediate cardiac catheterization and infusion of intracoronary streptokinase up to 500,000 units. Of those patients having restoration of orthograde coronary blood flow coupled with immediate evidence of myocardial salvage, 31 patients (group I) had immediate coronary artery bypass and 34 patients (group II) had coronary artery bypass deferred. Group I had no hemorrhagic, hemodynamic, or new cardiac complications. There were no deaths, reinfarction, recurrence of angina, or loss of salvaged myocardium at restudy. In group II, 11 of 34 patients had early reinfarction (p less than 0.01 vs. group I), 16 of 34 patients had recurrent angina (p less than 0.01 vs. group I) and two deaths occurred from cardiac causes. Subsequent coronary bypass was needed in 16 patients. All restudied reinfarction patients lost restored myocardium. We concluded that immediate coronary artery bypass is safe after acute myocardial infarction and coronary artery thrombolysis with streptokinase, delay of coronary artery bypass leads to an unacceptable incidence of reinfarction and recurrent severe angina, and early coronary artery bypass is needed to ensure success of thrombolysis.

Coronary Artery Bypass↗

PubMed1998

Molecular co-operation between protein PAM and streptokinase for plasmin acquisition by Streptococcus pyogenes.

Bacterial surface-associated plasmin formation is believed to contribute to invasion, although the underlying molecular mechanisms are poorly understood. To define the components necessary for plasmin generation on group A streptococci we used strain AP53 which exposes an M-like protein ("PAM") that contains a plasminogen-binding sequence with two 13-amino acid residues long tandem repeats (a1 and a2). Utilizing an Escherichia coli-streptococcal shuttle vector, we replaced a 29-residue long sequence segment of Arp4, an M-like protein that does not bind plasminogen, with a single (a1) or the combined a1a2 repeats of PAM. When expressed in E. coli, the purified chimeric Arp/PAM proteins both bound plasminogen, as well as plasmin, and when used to transform group A streptococcal strains lacking the plasminogen-binding ability, transformants with the Arp/PAM constructs efficiently bound plasminogen. Moreover, when grown in the presence of plasminogen, both Arp/PAM- and PAM-expressing streptococci acquired surface-bound plasmin. In contrast, plasminogen activation failed to occur on PAM- and Arp/PAM-expressing streptococci carrying an inactivated streptokinase gene: this block was overcome by exogenous streptokinase. Together, these results provide evidence for an unusual co-operation between a surface-bound protein, PAM, and a secreted protein, streptokinase, resulting in bacterial acquisition of a host protease that is likely to spur parasite invasion of host tissues.

Antigens, Bacterial↗

PubMed2004

Platelet scintigraphy results of heparin versus streptokinase treatment in acute deep vein thrombosis.

OBJECTIVE: The aim of the study was to document the therapeutic effects and primary recanalization ratios of either streptokinase or heparin in the therapeutic process of deep vein thrombosis (DVT). The results are obtained with the help of platelet scintigraphy. DESIGN: The investigation was planned as a randomized, controlled and prospective study, including 20 patients within two groups. Group I contained 10 patients undergoing IV infusion therapy of unfractionated heparin while Group II contained 10 patients undergoing thrombolytic therapy using streptokinase. After 8 weeks, scintigraphies using Tc-99m HMPAO-labeled thrombocytes were made, and interpreted by two blinded nuclear medicine physicians. The results are compared using Mann-Whitney U- and chi2-tests. RESULTS: No complication leading to interruption of therapy took place. Significantly smaller pathologic thrombocyte accumulations were detected in the streptokinase group. The difference was statistically significant (p = 0.019). CONCLUSION: Although a general clinical improvement had been observed in all patients, the scintigraphic investigation showed that the thrombolytic therapy maintained a better deep vein luminous patency.

Acute Disease↗

PubMed1967

Generation of chemotactic activity in rabbit serum by plasminogen-streptokinase mixtures.

The addition of plasminogen and streptokinase to rabbit serum results in appearance of chemotactic activity which is relatively heat-labile and dialyzable. Generation of this activity requires heat-labile factors in serum, but not the sixth component of complement. The optimal mole ratio for generation of chemotactic activity is 1:1 to 1:3 for plasminogen to streptokinase. Neither material alone is sufficient to generate the activity in fresh serum. Generation of chemotactic activity can be blocked by the presence of epsilon-aminocaproic acid. This plasmin-generated chemotactic factor sediments slowly in a sucrose density gradient during ultracentrifugation. The addition of plasminogen and streptokinase to rabbit serum containing the preformed chemotactic factor (activated trimolecular complex of C'5, C'6, C'7) causes destruction of the chemotactic factor and loss of hemolytic activity of the sixth component of complement. The same mole ratio of reactants for optimal expression of the phenomenon holds as for plasmin generation of chemotactic activity in untreated serum.

Animals↗

PubMed1981

H-D-val-leu-lys-aminoisophthalic acid, dimethyl ester, is sensitive to streptokinase-activator not to plasmin.

The ability of human plasma and purified human plasmin and plasminogen to hydrolyze a new synthetic substrate, H-D-valine-leucine-lysine-5-aminoisophthalic acid, dimethyl ester, ditrifluoroacetate, was studied. Contrary to published data, we found this substrate was only minimally hydrolyzed by plasmin or urokinase-treated plasminogen or plasma. Plasminogen-free bovine fibrinogen was readily degraded by plasmin and urokinase-activated plasminogen. However, in the presence of streptokinase, the synthetic substrate was highly sensitive to human plasma and purified plasmin and plasminogen. Apparently, the substrate is specific for streptokinase-plasmin and streptokinase-plasminogen activators, not for plasmin.

Enzyme Activation↗

PubMed1990

Coagulation and fibrinolytic changes in evolving acute myocardial infarction treated by high-dose, brief-duration intracoronary or intravenous streptokinase.

Twenty-two patients were infused with 240,000 units streptokinase during a 60-minute period into the ostium of the infarct-related coronary artery (IC), and 23 patients were infused with 1,500,000 units streptokinase intravenously (IV) over 45 minutes; all infusions occurred within 12 hours of the patients' onset of chest pain. Thereafter, heparin was infused for 10 days. Serial coagulation and fibrinolytic parameters were studied over 46 to 72 hours after the streptokinase infusion. A generalized fibrinolytic state was produced in both groups as evidenced by a fall in fibrinogen and plasminogen levels, prolongation of thrombin and reptilase clotting times, a rise in fibrinogen degradation products, and a shortening of the euglobulin lysis time. Recovery to preinfusion levels was similar in both groups of patients. Hemorrhagic complications requiring blood replacement occurred in 7/23 (30%) treated IC, and 4/23 (17%) in the IV group.

Aged↗

PubMed1996

High-dose intravenous magnesium attenuates complement consumption after acute myocardial infarction treated by streptokinase.

OBJECTIVE: This study was designed to detect changes in complement levels following acute myocardial infarction and to test whether magnesium sulphate (MgSO4) administration interferes with the complement response that follows acute myocardial infarction. DESIGN: Twenty-nine patients with acute myocardial infarction treated with streptokinase were included and randomly assigned to three treatment groups. In groups A and B, a bolus of 1 g MgSO4 was infused intravenously followed by 4 g (group A) and 14 g (group B) MgSO4 for 24 h while normal saline was administered in group C (control). Blood samples for C3, C4 and CH-100 were obtained at baseline and repeatedly during the 48 h following the initiation of magnesium infusion. RESULTS: In groups A and C, a remarkable decrease in the levels of C3, C4 and CH-100 was observed when measured 1 h after the end of streptokinase infusion and thereafter for the ensuing 48 h compared to baseline values (P < 0.05). In group B, the decrease in these complement elements was attenuated, and a significant (P < 0.05) delayed decrease of C3 and C4 was observed only at 24 h and later up to 48 h. The mean level of CH-100 in group B was significantly depressed compared to baseline from 3 h and thereafter up to 48 h. Mean C3 values plotted against observation time differed between the three groups (P = 0.021). A similar trend was observed for C4 (P = 0.133) but not for CH-100 (P = 0.46). CONCLUSION: (1) Complement elements are being consumed following acute myocardial infarction treated by streptokinase. (2) High-dose intravenous magnesium attenuates the complement process following acute myocardial infarction. (3) These results might signify that magnesium modulates the inflammatory response that follows infarction.

Adult↗

PubMed1991

Reduced occurrence of atrial fibrillation in acute myocardial infarction treated with streptokinase.

In a historical follow-up study of 152 hospital patients with acute myocardial infarction, the frequency of life-threatening arrhythmias (ventricular fibrillation, sustained ventricular tachycardia, 3rd degree AV-block, 2nd degree AV-block (Mobitz type II), and asystole) and atrial fibrillation in 76 patients treated with streptokinase was compared with their frequency in 76 patients who did not receive a thrombolytic therapy. Among those treated with streptokinase two patients (3%) developed atrial fibrillation, compared with 12 (16%) in the control group (P = 0.009). Life-threatening arrhythmias occurred with equal frequency in the two groups. Further studies should confirm and clarify the mechanism of the reduced frequency of atrial fibrillation in the streptokinase-treated patients.

Aged↗

PubMed1994

Influence of heparin on fibrinogen and D-dimer plasma levels in acute myocardial infarction treated with streptokinase.

The purpose of this study was to investigate whether, to what extent, and through which mechanisms intravenous heparin, administered before and after streptokinase, affects the plasma levels of D-dimer and fibrinogen in myocardial infarction. Data concerning mortality and incidence of coronary recanalization in patients receiving heparin and thrombolytic therapy after acute myocardial infarction are controversial; furthermore, the mechanisms through which heparin acts in combination with thrombolytic therapy are unclear. Thirty-eight patients with acute myocardial infarction treated with streptokinase were considered. Nineteen of them received, immediately before the beginning of thrombolytic treatment, a bolus of heparin (100 U.kg-1 intravenously) and, 2 h later, intravenous heparin in doses raising the partial thromboplastin time to 2-2.5 times the normal value (Group 1); the remaining 19 did not receive anticoagulant treatment (Group 2). Multiple determinations of plasma D-dimer and fibrinogen levels were obtained in all patients before, and in the seven days following thrombolytic treatment. Six hours after streptokinase, fibrinogen decreased from 304 +/- 34 to 61 +/- 34 mg.dl-1 in Group 1 and from 312 +/- 29 to 38 +/- 21 mg.dl-1 in Group 2 (P < 0.02 versus Group 1). The same difference between groups persisted at the 12th and at the 18th hour. D-dimer values, from 0.5 +/- 0.1 microgram.dl-1 in Group 1 and 0.4 +/- 0.1 microgram.dl-1 in Group 2, increased at the 1st hour to 37.2 +/- 36.5 micrograms.dl-1 and 52.2 +/- 39.8 micrograms.dl-1, respectively. A peak value was reached in both groups at the 6th hour, which was followed by a slow decrease.(ABSTRACT TRUNCATED AT 250 WORDS)

Enzyme-Linked Immunosorbent Assay↗

PubMed1994

Effects of streptokinase on infarct size in rabbits in the presence and absence of coronary artery recanalization.

Despite variable efficacy in achieving recanalization, different thrombolytic agents demonstrate similar abilities to reduce mortality following myocardial infarction. We investigated whether factors other than the ability to achieve coronary artery recanalization are important in mediating the beneficial effects associated with thrombolytic therapy during acute myocardial infarction using anaesthetized rabbits. Coronary artery occlusion was produced using either a single ligature (which was released to initiate reperfusion) or by placing two ligatures 5 mm apart to allow the formation of an intraluminal thrombus. In this case, ligature removal followed by thrombolysis was required for recanalization to occur. Experiments were performed in the presence and absence of streptokinase. Streptokinase was most effective in reducing myocardial necrosis when associated with thrombolytic recanalization (total left ventricular infarct size was reduced from 37 +/- 7% to 13 +/- 1%, P < 0.01). However, streptokinase also reduced infarct size in the absence of reperfusion (45 +/- 4% vs 35 +/- 2%, P < 0.05), although further work is needed to clarify the mechanisms.

Animals↗

PubMed1995

Angiographic findings and catheterization laboratory events in patients with primary coronary angioplasty or streptokinase therapy for acute myocardial infarction.

BACKGROUND: The purpose of this study was to evaluate catheterization laboratory events and angiographic findings in patients randomly assigned to undergo primary coronary angioplasty or to receive intravenous streptokinase for acute myocardial infarction. METHODS: We analysed angiographic data in 301 patients with acute myocardial infarction, randomly assigned to undergo primary coronary angioplasty without antecedent thrombolytic therapy or to receive intravenous streptokinase therapy. Follow-up coronary angiography was preferably performed after 3 months. All angiograms were analysed with a quantitative coronary analysis system. RESULTS: Of the 152 patients assigned to angioplasty treatment, 140 underwent this procedure with a success rate of 97%. The residual diameter stenosis of the infarct-related vessel immediately after angioplasty was 27 +/- 15% and there were major events in 14% of the patients in the catheterization laboratory. At follow-up angiography after a mean interval of 92 days in the angioplasty assigned patients, a diameter stenosis of 35 +/- 22% was observed in this group. The restenosis rate was 28% and the reocclusion rate 5%. A Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow immediately after angioplasty was predictive for reocclusion at follow-up (P = 0.001). In the streptokinase assigned patients (149) the infarct-related vessel was patent at follow-up angiography after a mean of 22 days in 66% of the patients with a mean residual diameter stenosis of 77 +/- 20%. CONCLUSION: Primary coronary angioplasty is a highly effective and safe reperfusion modality for patients with acute myocardial infarction. However, TIMI grade 2 flow through the infarct-related vessel immediately after angioplasty is a predictor of reocclusion.

Adult↗

PubMed1984

Serum sickness complicating intravenous streptokinase therapy in acute myocardial infarction.

A case of delayed serum sickness with transient renal impairment is described in a patient who received early high dose intravenous streptokinase following acute myocardial infarction. Review of the literature suggests that serum sickness after streptokinase may occur independently of the dose or route of administration, and could potentially complicate intracoronary streptokinase therapy.

Acute Kidney Injury↗

PubMed1987

Residual coronary stenosis after thrombolysis with rt-PA or streptokinase: acute results and 3 weeks follow-up.

Ninety-one patients with acute myocardial infarction were assigned to intravenous treatment with streptokinase or rt-PA as part of the randomized trial carried out by the European Study Group for Recombinant Tissue-Type Plasminogen Activator (rt-PA). A patent coronary artery was found in 37 of 45 (82%) patients treated with rt-PA and in 27 of 46 (59%) patients treated with streptokinase 75-90 minutes after start of infusion. Patients were subsequently anticoagulated with heparin or dicoumarol up to a repeat angiography 3 weeks after the infarction. Of the 64 patients with successful reperfusion, 3 died and 3 suffered reocclusion of the vessel. Quantitative analysis of the coronary stenosis both immediately after thrombolysis and at 3 weeks follow-up was possible in 33 cases. Residual stenosis (percentage narrowing of diameter) decreased from 74 +/- 14% to 56 +/- 17% (P less than 0.05). No difference was observed between the groups of patients treated with streptokinase (74 +/- 9% to 57 +/- 12%, N = 17) and with rt-PA (74 +/- 17% to 56 +/- 21%, N = 16). Despite the significant regression, a coronary stenosis of more than 50% of the diameter persisted in 82% of the patients three weeks after the infarction.

Cineangiography↗

PubMed1990

Fibrin-dependent activation of plasminogen by a proteolytic digest of streptokinase.

Among four enzymatic digests of streptokinase (SK), the smallest peptide with plasminogenolytic activity was in a tryptic digest; it had a molecular weight of 29,000. A complex of this peptide, SK29, and human plasminogen hydrolysed human fibrin, but a complex of native streptokinase and human plasminogen hydrolysed both human and bovine fibrin. The complex with SK29 caused amidolysis of the synthetic substrate S-2251 in the presence of human fibrin, but was inactive in the presence of human fibrinogen, bovine fibrinogen or bovine fibrin. Analysis of the amino terminal sequence of SK29 indicated that cleavage by trypsin was on the carboxyl side of lysine, the 59th amino acid of streptokinase. These results suggest that the conformational changes caused by human fibrin formation resulted in the generation of an active site of human plasminogen by SK29.

Amino Acid Sequence↗

PubMed1991

Prevention of in vitro fibrinogenolysis during laboratory monitoring of thrombolytic therapy with streptokinase or APSAC.

In the present study, we systematically investigated aprotinin, epsilon-aminocaproic acid (EACA) and tranexamic acid as inhibitors of fibrinogen breakdown and of the generation of fibrinogen degradation products (FgDP). The experimental setting very closely imitated the conditions in practice when collecting blood from patients receiving thrombolytic therapy with streptokinase or APSAC. The minimal concentration of aprotinin required to completely inhibit fibrinogen breakdown and FgDP generation was 200 KIU/ml blood. This was sufficient even at the highest concentrations of streptokinase and APSAC expected to occur in patients (300 U/ml and 46 nM, respectively). However, 200 KIU/ml aprotinin heavily interfered in the determinations of plasminogen and alpha 2-antiplasmin. Relatively low concentrations of EACA (200 mM) and tranexamic acid (35 mM) were sufficient to prevent FgDP generation, but they interfered in the Clauss assay of fibrinogen. A non-interfering concentration of EACA (7 mM) allowed the inhibition of lower concentrations of APSAC (20 nM) and streptokinase. We conclude that at least 200 KIU aprotinin per ml blood is necessary to effectively inhibit in vitro fibrinogenolysis under circumstances likely to be met in clinical practice during thrombolytic therapy.

Aminocaproic Acid↗

PubMed1993

Interplay between platelet-derived 5-hydroxytryptamine and arachidonic acid metabolites limits the thrombolytic efficacy of streptokinase against canine platelet-rich coronary thrombosis.

The comparative contributions of arachidonic acid (AA) metabolites and 5-hydroxytryptamine (5-HT) to the delay of reperfusion and rate of reocclusion after coronary thrombolysis with streptokinase were assessed in dogs using (a) single TXA2 synthase inhibition; (b) single 5-HT2-receptor blockade; (c) dual TXA2 synthase inhibition/PGH2 receptor antagonism; (d) 5-HT2-receptor blockade combined with TXA2 synthase inhibition; and (e) 5-HT2-receptor blockade combined with dual TXA2 synthase/PGH2-receptor antagonism. In open-chest anesthetized dogs, occluding coronary thrombi were induced by severe intimal injury in combination with critical artery stenosis. Fifty minutes after occlusive thrombus formation, the animals received intravenously (i) saline (S); (ii) ketanserin, 0.3 mg/kg (K), a 5-HT2-receptor antagonist; (iii) ridogrel, either at a low dose 0.3 mg/kg (R 0.3), exerting single TXA2 synthase inhibition; or (iv) at 5 mg/kg (R 5), exerting additional TXA2/PGH2-receptor antagonism; or (v) the combination of either dose of ridogrel with ketanserin. Ten minutes later, all dogs received streptokinase (SK; 1,000 IU/kg i.v. + 100 IU/kg/min i.v. infusion for 90 min). High-grade thrombolysis (> or = 50% coronary reperfusion vs. prethrombosis value as assessed by flow measurements) with SK occurred in 3/11 dogs treated with S, in 5/7 with R 0.3 and K, and in 7 of 7 dogs in the other medication groups; this occurred within > or = 55 min with S, R 0.3, and K, within 37 +/- 12 min with R 5 (p < 0.05 vs. solvent and R 0.3), and within 38 +/- 5 and 23 +/- 5 min with R 0.3 + K and R 5 + K, respectively (p < 0.05 vs. S, R 0.3, and K). The occurrence of reocclusion within 120 min after the cessation of SK administration was significantly reduced in all treatment groups, except K. That of cyclic flow reduction was reduced by R 5, R 0.3 + K, and R 5 + K. The peak extent of coronary reperfusion was highest in the K + R groups (S = 33% of preocclusion value; K = 60%; R 0.3 = 68%; R 5 = 76%; K + R 0.3 = 80%, p < 0.05 vs. S; and K + R 5 = 89%, p < 0.05 vs. solvent, R 0.3, and K). This study shows that the interplay between AA metabolites and 5-HT is involved in the platelet-dependent reduction in the thrombolytic efficacy of streptokinase in lysing coronary thrombi.

Animals↗

PubMed1998

Streptokinase-induced activation of the kallikrein-kinin system and of the contact phase in patients with acute myocardial infarction.

Thrombolytic therapy in acute myocardial infarction (AMI) is hampered by a considerable reocclusion rate. Thrombin activity is enhanced, and contact-system activation via plasminemia might be possible. Prospectively we examined the contact phase and the kallikrein-kinin system and additional molecular markers of hemostasis and fibrinolysis in AMI. In 22 patients with AMI, blood sampling was performed at admission and < or =10 days afterward. Eleven patients received 1.5 Mio U streptokinase (group A) and were compared with 11 AMI patients without thrombolytic therapy (group B). All patients had systemic heparinization (5,000 IU bolus, i.v.; 1,000 IU/h, i.v.). In group A (vs. group B), the kallikrein-factor XII system was significantly activated (3 h after start of therapy): kallikrein activity 140 +/- 41 (vs. 43 +/- 8) U/L (p < 0.05); kallikrein inhibition 87 +/- 9 (vs. 113 +/- 7%; p < 0.05), and factor XII 70 +/- 14 (vs. 94 +/- 6%). C1 inhibitor and factor XII inhibition were decreased. High-molecular-weight kininogen consumption indicating bradykinin generation was enhanced (p < 0.01). In group A, thrombin activity (TAT) was increased, and a hypercoagulative state with increased fibrin degradation products (d-dimer) was found. Plasmin activation in group A was reflected by decreased plasminogen and antiplasmin levels (p < 0.01). The findings indicate that streptokinase induces activation of the contact phase-kinin system in vivo associated with a consecutive increase of thrombin and bradykinin generation. Activation of this pathway might substantially contribute to reocclusion after initially successful thrombolytic therapy and to hypotensive reactions observed after streptokinase.

Acute Disease↗