Occlusive Coronary Thrombosis Research Articles

Thrombolysis for acute myocardial infarction in Moroccan patients: Data from FES-AMI registry

Acute myocardial infarction (AMI) is the most serious form of acute coronary syndrome. It is essentially due to occlusive coronary thrombosis complicating rupture of atherosclerosis plaque. The aim of the management of this extreme emergency is to restore the coronary flow as soon as possible either by thrombolysis or by primary angioplasty depending on local conditions. To assess clinical, angiographic, therapeutic and prognostic features of Moroccan patients thrombolysed by tenecteplase in AMI. FES-AMI is a monocentric prospective registry that included all patients hospitalized for management of AMI within 5 days of onset of symptoms. We analyzed from this registry all patients who had undergone thrombolysis with tenecteplase between June 2006 and August 2018. We enrolled 900 patients. 79% of patients were males and mean age was 60 years old. 57% of patients were smokers, 35% were diabetics and 26% were hypertensives. A total of 71% of patients had more than 2 risk factors. In 80% of cases, patients are thrombolysed beyond the 3rd hour. Our patients received thrombolytic therapy within an average of 5 hours and 14 min after the onset of chest pain. All patients received Aspirin, Clopidogrel and Heparin. TIMI flow grade 2 or 3 has been found in 95% of successful thrombolysis. 60% of patients had multi-vessel disease. The heart failure complicated the myocardial infarction in 35% of cases. 8% of patients presented an atrial fibrillation, 5% a ventricular tachycardia, 3% a ventricular fibrillation and 4% a third-degree atrioventricular block. The rate of intracranial hemorrhage was 1%. The in-hospital mortality was 7.1%. Fibrinolysis remains an important option for reperfusion in acute myocardial infarction in Morocco. Higher rates of patency were observed in successful thrombolysis in our registry. Intracranial hemorrhage was the most serious complication of fibrinolytic therapy and its frequency did not exceed 1%.

Hypereosinophilic syndrome associated with occlusive coronary thrombosis and right ventricular thrombus

A 44-year-old man with HES who developed a large thrombus in the right ventricle as well as multiple occlusive coronary thrombi died of cardiac failure. Autopsy showed that a large thrombus in the right ventricle was associated with eosinophilic endocarditis. In addition, an occlusive thrombus formed in the circumflex and right coronary arteries with eosinophilic infiltrate in the walls. The findings suggest a causal relationship between coronary thrombosis and eosinophilia. To the authors' knowledge this is the first report to document the clinical and histological findings of coronary thrombosis in a patient with HES.

Cardiological management

Mrs Patel's case shows the challenge of assessing young patients with possible cardiac chest pain.1 The location of her chest discomfort may be considered atypical, but Marin Marinovic correctly notes...

Pathophysiology of Gender Difference in Prognosis of Asymptomatic Carotid Stenosis: Research and Future Implications

Pathophysiology of Gender Difference in Prognosis of Asymptomatic Carotid Stenosis: Research and Future Implications

Plaque Instability Frequently Occurs Days or Weeks Before Occlusive Coronary Thrombosis: A Pathological Thrombectomy Study in Primary Percutaneous Coronary Intervention

Plaque Instability Frequently Occurs Days or Weeks Before Occlusive Coronary Thrombosis: A Pathological Thrombectomy Study in Primary Percutaneous Coronary Intervention

Plaque Instability Frequently Occurs Days or Weeks Before Occlusive Coronary Thrombosis: A Pathological Thrombectomy Study in Primary Percutaneous Coronary Intervention

Plaque Instability Frequently Occurs Days or Weeks Before Occlusive Coronary Thrombosis: A Pathological Thrombectomy Study in Primary Percutaneous Coronary Intervention

Overview of contemporary reperfusion strategies in acute ST-elevation myocardial infarction

The rupture of an atherosclerotic plaque in an epicardial coronary artery with subsequent occlusive coronary thrombosis has been established as the decisive event in the pathogenesis of an acute coronary syndrome, which encompasses the clinical entities of unstable angina, non-ST- and ST-elevation myocardial infarction. This article focuses on contemporary treatment strategies for patients with acute ST-elevation myocardial infarction and reviews the role of pharmacologic thrombolysis and mechanical reperfusion by percutaneous transluminal approaches. Statements of the latest guidelines for the treatment of ST-elevation myocardial infarction are included, as well as some recently distributed information not covered by the guideline publications. Finally, some future perspectives for the treatment of acute ST-elevation myocardial infarction are outlined.

Issue Highlights

HomeCirculationVol. 111, No. 9Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published8 Mar 2005https://doi.org/10.1161/circ.111.9.1093Circulation. 2005;111:1093WORLDWIDE SURVEY ON THE METHODS, EFFICACY, AND SAFETY OF CATHETER ABLATION FOR HUMAN ATRIAL FIBRILLATION, by Cappato et al.Catheter ablation of atrial fibrillation is evolving rapidly. This survey from 181 responding centers provides an indication of the dramatic growth of the procedure between the mid-1990s, when fewer than 100 patients were treated, and 2002, when >5000 patients received ablation annually at these centers alone. Methods, criteria for patient selection, and outcomes varied among centers. A beneficial effect on symptoms was reported for more than half of patients without antiarrhythmic drug therapy, and more received benefit with continued drug therapy. Approximately one quarter of patients required two procedures. Major complications, including cardiac tamponade and stroke, occurred in 6%. Although these data are subject to the reporting bias inherent in a survey, they provide a useful look at the outcomes and problems with this procedure during the initial period of its rapid growth. See p 1100.COST-EFFECTIVENESS OF EPLERENONE COMPARED WITH PLACEBO IN PATIENTS WITH MYOCARDIAL INFARCTION COMPLICATED BY LEFT VENTRICULAR DYSFUNCTION AND HEART FAILURE, by Weintraub et al.As costs of health care increase and expensive new therapies are shown to have benefit, it is important to question whether the intervention is economically attractive from a societal perspective. The Eplerenone Post–Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) demonstrated that selective aldosterone blockade with eplerenone reduced mortality and morbidity in patients with left ventricular systolic dysfunction and heart failure after an acute myocardial infarction. Over 16 months, eplerenone reduced the risk of death by 17% and the risk of death from cardiovascular causes or hospitalization for cardiovascular events by 13%. The risk of serious hyperkalemia increased. Weintraub and colleagues have used the EPHESUS trial results in an economic analysis to determine the how well the benefits associated with the therapy balance the costs. They compare the cost-effectiveness of eplerenone therapy with many other commonly used interventions in cardiology. See p 1106.PLAQUE INSTABILITY FREQUENTLY OCCURS DAYS OR WEEKS BEFORE OCCLUSIVE CORONARY THROMBOSIS: A PATHOLOGICAL THROMBECTOMY STUDY IN PRIMARY PERCUTANEOUS CORONARY INTERVENTION, by Rittersma et al.Unstable coronary syndromes are caused primarily by plaque disruption leading to platelet activation, stimulation of coagulation, and occlusion of the vessel. When patients have a myocardial infarction, however, the amount of time between initiation of this process and clinical presentation is unknown. In this issue of Circulation, Rittersma and colleagues examine this question by studying aspirated material from intracoronary thrombectomy samples obtained during angioplasty. They found that at least half of the patients had coronary thrombi that were days to weeks old. The observation that patients presenting with acute myocardial infarction have a high likelihood of having established clot could have therapeutic implications and might explain the lack of efficacy of antithrombotics in certain patients. See p 1160.Visit www.circ.ahajournals.org:Images in Cardiovascular MedicineUnexpected Profound Transient Anterior ST Elevation After Occlusion of the Conus Branch of the Right Coronary Artery During Angioplasty. See p e113.Download figureDownload PowerPointVisualization of Endomyocardial Fibrosis by Delayed-Enhancement Magnetic Resonance Imaging. See p e115.CorrespondenceLetter Regarding Article by Martinelli et al, “Risk Factors and Recurrence Rate of Primary Deep Vein Thrombosis of the Upper Extremities. ” See p e118.Letter Regarding Article by Korshunov and Berk, “Strain-Dependent Vascular Remodeling: The ‘Glagov Phenomenon’ Is Genetically Determined. ” See p e119. Previous Back to top Next FiguresReferencesRelatedDetailsCited By CAO L, DENG T, LIANG S, TAN X and MENG J (2014) Determination of Herbicides and Its Metabolite in Soil and Water Samples by Capillary Electrophoresis-laser Induced Fluorescence Detection Using Microwave-assisted Derivatization, Analytical Sciences, 10.2116/analsci.30.759, 30:7, (759-766), . March 8, 2005Vol 111, Issue 9 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.111.9.1093 Originally publishedMarch 8, 2005 PDF download Advertisement

Plaque Instability Frequently Occurs Days or Weeks Before Occlusive Coronary Thrombosis

Acute ST-elevation myocardial infarction (STEMI) is caused by sudden occlusive coronary thrombosis, after plaque disruption; however, a considerable time interval between plaque disturbance and the onset of symptoms has been suggested. We therefore studied the age of intracoronary thrombi, aspirated during angioplasty in patients with acute STEMI. Percutaneous intracoronary thrombectomy during angioplasty was performed in 211 consecutive STEMI patients within 6 hours after onset of anginal symptoms. The aspirated material was histologically screened on thrombus and plaque components, and thrombus age was classified as fresh (<1 day), lytic thrombus (1 to 5 days), and organized thrombus (>5 days). In all patients, intracoronary-derived material was retrieved in the filter of the collection bottle. Thrombus was identified in 199 (95%) of 211 patients. In 12 patients (5%), only plaque components were identified, and in 85 patients (41%), both thrombus and plaque material were aspirated. In 18 (9%) of 199 patients, the thrombus was organized, and in 70 patients (35%), the thrombus showed lytic changes, whereas in 98 (49%), a completely fresh thrombus was found. In 14 (7%) of 199 patients, the thrombus showed combined features of both fresh thrombus and organized thrombus. In at least 50% of patients with acute STEMI, coronary thrombi were days or weeks old. This indicates that sudden coronary occlusion is often preceded by a variable period of plaque instability and thrombus formation, initiated days or weeks before onset of symptoms.

Inhibition of platelet activity in vivo by amlodipine alone and combined with aspirin

Platelets are known to contribute to the initiation and progression of coronary artery narrowing by atherosclerotic plaques. Platelets also initiate periodic occlusive coronary arterial thrombosis that leads to unstable angina and myocardial infarction. Aspirin is the most widely used platelet inhibitor. However, if blood levels of epinephrine are elevated, some of the platelet inhibition produced by aspirin is diminished. Amlodipine, a second generation dihydropyridine calcium channel blocker, was studied in a widely used dog model of experimental coronary artery thrombosis. Amlodipine 1 mg/kg alone or amlodipine 0.4 mg/kg with 5 mg/kg of aspirin IV completely abolished the experimental coronary thrombosis and prevented the exacerbation of coronary thrombosis by epinephrine 0.2 μg/kg/min. This protective effect did not appear until 60 minutes after the amlodipine was given, suggesting a delayed onset of action. Long-acting dihydropyridine calcium channel blockers are used in patients with hypertension, angina, and coronary artery disease. They also may offer the patient some protection against fatal or nonfatal myocardial infarction via their platelet-inhibiting effects.

Role of activation-dependent platelet membrane glycoproteins in development of subacute occlusive coronary stent thrombosis

Platelets have an important role in coronary thrombosis. We studied 151 consecutive patients undergoing implantation of Palmaz-Schatz stents because of suboptimal results after coronary balloon angioplasty treated by intense anticoagulation. Surface exposure of the constitutively expressed glycoprotein complex IIb-IIIa (CD41), P-selectin (CD62P) and of the GPIIb-IIIa complex activated exposure (of ligand-induced binding site-1) were determined, in addition to platelet count and plasma fibrinogen, before and daily for 12 days after stenting in peripheral venous blood samples. Six of 151 patients (3.9%) developed subacute stent thrombosis within the first week after stenting. The relative risk of stent thrombosis was 18.5-fold for patients with enhanced GPIIb-IIIa surface expression (P < 0.003; 95% confidence interval 2.1 to 163.1) before stent placement. In the period after stenting, platelet activation occurred, with an increase in fibrinogen receptor activity and P-selectin degranulation above pre-stent values (P < 0.01). In logistic regression analysis, GPIIb-IIIa before stenting emerged as a risk factor for stent thrombosis, independent of the activational status of platelets, platelet count or fibrinogen levels (P < 0.02). However, after stenting, P-selectin surface expression acquired prognostic importance for stent thrombosis (P < 0.05). We conclude that changes in platelet membrane glycoproteins are of prognostic value in predicting subacute stent thrombosis.

The pathophysiology of the onset of morning cardiovascular events

Evidence obtained over the past decade indicates that myocardial infarction (MI) and sudden death are not random events but rather, in many cases, may be triggered by the daily activities of the subject. The importance of physical or mental stresses as triggers is suggested by the parallel morning increased onsets of MI, sudden cardiac death, and stroke. Unstable angina and MI are usually precipitated by thrombus formation over a disrupted plaque that causes partial or complete obstruction of coronary artery blood flow. This process may be caused by physiologic factors that lead to rupture of a vulnerable plaque and subsequent thrombosis. Beta-blockers and aspirin, which can diminish these physiologic processes, have been shown to blunt or abolish the morning peak of onset of acute MI. It is hypothesized that occlusive coronary thrombosis occurs when an atherosclerotic plaque becomes vulnerable to rupture, and mental or physical stress causes the plaque to rupture. Increases in coagulability or vasoconstriction triggered by daily activities may also contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation of the onset of acute cardiovascular disease suggests the need for pharmacologic protection of patients during the vulnerable periods and provides clues to the mechanism of disease onset, the investigation of which may lead to improved methods of prevention.

Activation of coagulation and fibrinolysis in acute or chronic coronary artery disease

Thrombin- and plasmin-related indices were measured in peripheral blood of 50 patients at the onset of acute myocardial infarction (AMI) and 35 chronic stable angina (CSA) patients to establish which are most indicative of acute occlusive coronary thrombosis. AMI compared with CSA had significantly higher plasma prothrombin fragment F1.2, thrombin-antithrombin III (TAT) and plasmin-antiplasmin (PAP) complexes (direct indices), but similar soluble fibrin and D-dimer levels (indirect indices). F1.2, TAT and PAP were > the 90th percentile of CSA levels in 15, 10 and 29 AMI patients, respectively. Thus, direct indices of thrombin and plasmin formation appear more indicative of acute coronary thrombosis than indirect ones. In AMI, raised F1.2, TAT and PAP in only some patients is consistent with wide variability in the activity of the underlying thrombotic process.

Triggering and hourly variation of onset of arterial thrombosis.

Information obtained during the past decade suggests that the onset of myocardial infarction and sudden cardiac death is frequently triggered by daily activities. The importance of physical or mental stress in triggering coronary thrombosis is supported by finding that (1) the frequencies of the onset of myocardial infarction, sudden cardiac death, and stroke show marked circadian variations, with similar increases in the period from 6 AM to noon; (2) the frequency of transient myocardial ischemia shows a similar increase in the morning, and episodes are often preceded by mental or physical triggers; (3) a ruptured atherosclerotic plaque, often nonobstructive by itself, lies at the base of most coronary thrombi; (4) a number of physiologic processes that could lead to plaque rupture, a hypercoagulable state, or coronary vasoconstriction, are accentuated in the morning; and (5) aspirin and beta-adrenergic blocking agents that affect certain of these processes have been shown to prevent disease onset. The hypothesis presented is that occlusive coronary thrombosis occurs when (1) an atherosclerotic plaque becomes vulnerable to rupture; (2) mental or physical stress causes the plaque to rupture; and (3) increases in coagulability or vasoconstriction, triggered by daily activities, contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation--and the possibility of frequent triggering--of the onset of acute disease suggests the need for pharmacologic protection of patients during the vulnerable periods and provides clues to the mechanism of disease onset, the investigation of which may lead to improved methods of prevention.

Thrombolytic effects of a novel modified tissue plasminogen activator, E6010, on coronary thrombosis in the pig.

This study was conducted to compare the thrombolytic effect of a novel modified tissue plasminogen activator, E6010, with that of recombinant human tissue plasminogen activator (t-PA), administered by single intravenous bolus injection in pigs with occlusive coronary thrombosis. Thrombosis was induced by electrical stimulation of the intimal surface of the left circumflex coronary artery. Coronary blood flow velocity and hemodynamic parameters were observed for 1 hr after complete cessation of coronary flow. Ten minutes after heparin injection (300 U/kg), E6010, t-PA or placebo was intravenously administered as a bolus. E6010 at 0.2 and 0.4 mg/kg caused recanalization of the occluded coronary artery in 1 of 6 and 5 of 5 pigs, respectively. The time to recanalization after 0.4 mg/kg of E6010 was 22 +/- 11 min (mean +/- S.E.M.). t-PA (0.4 mg/kg) caused recanalization in only 1 of 5 pigs. Recanalization did not occur in any of the 6 animals administered placebo. Plasma clearance of E6010 was smaller than that of t-PA (4.9 +/- 0.3 vs. 9.4 +/- 3.8 ml/min/kg). There were no significant differences in plasma levels of fibrinogen, alpha 2-plasmin inhibitor and plasminogen among the placebo, E6010 and t-PA groups. These results suggest that the slower clearance of E6010 from plasma contributes to the effective thrombolytic action of E6010 following single intravenous bolus injection.

Thrombolytic Effects of a Novel Modified Tissue Plasminogen Activator, E6010, on Coronary Thrombosis in the Pig

This study Was conducted to compare the thrombolytic effect of a novel modified tissue plasminogen activator, E6010, with that of recombinant human tissue plasminogen activator (t-PA), administered by single intravenous bolus injection in pigs with occlusive coronary thrombosis. Thrombosis was induced by electrical stimulation of the intimal Surface of the left circumflex coronary artery. Coronary blood flow velocity and hemodynamic parameters were observed for 1 hr after complete cessation of coronary flow. Ten minutes after heparin injection (300 U/kg), E6010, t-PA or placebo was intravenously administered as a bolus. E6010 at 0.2 and 0.4 mg/kg caused recanalization of the occluded coronary artery in 1 of 6 and 5 of 5 pigs, respectively. The time to recanalization after 0.4 mg/kg of E6010 was 22 ± 11 min (mean ± S.E.M.). t-PA (0.4 mg/kg) caused recanalization in only 1 of 5 Pigs. Recanalization did not occur in any of the 6 animals administered plasma clearance of E6010 was smaller than that of t-PA (4.9 ± 0.3 vs. 9.4 ± 3.8 ml/min/kg). There were no significant differences in plasma levels of fibrinogen, α2-plasmin inhibitor and plasminogen among the placebo, E6010 and t-PA groups. These results suggest that the slower clearance of E6010 from plasma contributes to the effective thrombolytic action of E6010 following single intravenous bolus injection.

Gemfibrozil Reduces Plasma Prothrombin Fragment F1+2 Concentration, a Marker of Coagulability, in Patients with Coronary Heart Disease

The effects of gemfibrozil on several indices of haemostatic activity were explored in male patients with coronary heart disease (CHD). Sixty-three of 71 patients completed a crossover study in which gemfibrozil 1,200 mg/day and matching placebo were each taken in randomised order for 2 months in a double-blind manner, separated by a 2-month washout period. Serum cholesterol decreased by an average (95% confidence interval) of 12 (9 to 15)% and non-fasting triglyceride concentration by 43 (34 to 51)% during active treatment. Plasma prothrombin fragment F1 + 2 concentration, a marker of the in vivo rate of generation of thrombin, was 25 (12 to 37)% lower on average while on gemfibrozil than during the placebo phase. Factor VII coagulant activity (VIIc) and antigen concentration, and fibrinopeptide A concentration were not influenced by gemfibrozil in the group overall. However, the VIIc response appeared to be dependent upon the untreated cholesterol level. Hypercholesterolaemic men (cholesterol greater than 6.5 mmol/l) experienced a significant reduction in VIIc averaging 6% of standard during active therapy. Other effects of gemfibrozil were a 5 (2 to 9)% increase in plasma fibrinogen by a gravimetric method, an 11 (8 to 13)% increase in platelet count, and a 6 (2 to 10)% reduction in white cell count. The reduced incidence of CHD following gemfibrozil therapy in hyperlipidaemic patients may arise in part through a reduction in procoagulant activity and thus the risk of an occlusive coronary thrombosis.

Von Willebrand Factor and Animal Models: Contributions to Gene Therapy, Thrombotic Thrombocytopenic Purpura, and Coronary Artery Thrombosis

Use of animal models of von Willebrand factor (vWF) deficiency, both inherited and induced, continues to advance the knowledge of vWF-related diseases. Three examples are reviewed in this article--von Willebrand's disease (vWD), thrombotic thrombocytopenic purpura, and coronary artery thrombosis. The success of gene transfer by liver and bone marrow transplantation in porcine vWD and canine hemophilia A, with a change in phenotype that establishes improved hemostasis, portends imminent testing of gene therapy in these models. With use of recombinant technology, the phenotype of hemophilia B fibroblasts has been transformed to normal, as evidenced by secretion of the normal hemostatically active protein. This result is a prelude to implantation in hemophilic animals. Thrombotic thrombocytopenic purpura is characterized by qualitative and quantitative alterations in vWF. A new animal model induced by the venom factor botrocetin, a cofactor of vWF, closely mimics the human syndrome. A proposed pathophysiologic mechanism for thrombotic thrombocytopenic purpura is outlined. The third contribution is recognition that occlusive coronary thrombosis is a vWF-dependent condition. Without vWF, as in porcine vWD or normal pigs treated with a monoclonal anti-vWF antibody, occlusive thrombi do not develop, even with luminal stenosis. The thrombogenicity of coronary atheromas, including those with fissures of the fibrous cap, is also vWF-dependent.

Effect of aspirin on local prostaglandin production and serotonin accumulation in a canine model with coronary cyclic flow variations or thrombosis

We have reported that thromboxane A 2 and serotonin are two important mediators of coronary cyclic flow variations (CFVs) caused by recurrent platelet aggregation and dislodgement on a stenosed coronary arterial wall with endothelial injury. To test the hypothesis that blocking the synthesis of thromboxane A 2 would not prevent serotonin release, 1.1, 4.6, and 9.2 mg/kg of aspirin were administered through the left atrium to 27 dogs with CFVs. The CFV elimination rate was 70% in the aspirin-treated dogs. Thromboxane B 2 and serotonin concentrations were measured in different coronary arterial segments. There were significantly lower thromboxane B 2 and 6-keto-PFG 1a levels in the stenosed left arterior descending (LAD) segments with increasing dosage of aspirin-208 ± 36, 24 ± 31, 50 ± 6 ng/g ( P<0.0001) and 125 ± 27, 58 ± 38, 25 ± 5 ng/g ( P<0.0001), respectively. Serotonin levels were significantly higher in stenosd LAD (265.7 ± 131.2 ng/g) than in LAD segments proximal or distal to the stenosis and in corresponding circumflex coronary artery segments, 17.1 ± 3.7, 18.6 ± 3.7, and 19.2 ± 5.1 ng/g, respectively ( P<0.05) following the highest dose of aspirin. In 41 additional dogs, electrical injury was used to initiate thrombosis in the circumflex artery and in those receiving aspirin (15mg/kg) ( n=5), occlusive thrombus formation was inhibited. However, the local accumulation of serotonin was not significantly different between the control (194 ± 27 ng/g) ( n=36) and the aspirin-treated group (167 ± 19 ng/g) ( n=5). In vitro platelet aggregation induced by arachidonic acid was inhibited by the in vivo adminstration of 1.1 mg/kg of aspirin and abolished by 4.6 + 1.1 and 9.2 + 4.6 + 1.1 mg/kg of aspirin. However, serotonin-induced platelet aggregation was not affected following all doses of aspirin. Thus, aspirin eliminates CFVs in 70% of dogs, and markedly diminishes thromboxane A 2 and prostacyclin concentrations in stenosed canine coronary arteries, but it does not prevent local serotonin accumulation. Similarly, aspirin prevents occlusive coronary thrombosis in dogs with electrically-induced endothelial injury, but it did not prevent local assumulation of serotonin. These experimental findings suggest that cyclo-oxygenese inhibition does not prevent serotonin accumulation at sites of coronary artery endothelial injury, and they thereby help provide a potential explanation of the lack of complete protection provided by aspirin in eliminating CFVs in this experimental model.

Thrombolytic effect of a novel modified tissue plasminogen activator, E-6010, on occlusive coronary thrombosis in pigs: H. Adachi, N. Nagaoka, T. Yuzuriha, T. Shoji. Department of Pharmacology, Eisai Tsukuba Research Laboratories, Tsukuba, Japan

Thrombolytic effect of a novel modified tissue plasminogen activator, E-6010, on occlusive coronary thrombosis in pigs: H. Adachi, N. Nagaoka, T. Yuzuriha, T. Shoji. Department of Pharmacology, Eisai Tsukuba Research Laboratories, Tsukuba, Japan