Intracoronary Thrombolysis in Evolving Myocardial Infarction

Ganz, William; Buchbinder, Neil A.; Marcus, Harold S.; Mondkar, Avinash; O'Connor, Lawrence; Maddahi, Jamshid; Berman, David A.; Charuzi, Yzhar; Beeder, Clain; Peter, Thomas; Shah, Prashant; Shell, William E.

doi:10.1007/978-3-642-68085-4_55

Cited by 9 publications

(14 citation statements)

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“…Our results are consistent with findings in animal studies that early revascularization can reduce the predicted extent of MI (3,12). The results from several studies (5,7,9,(13)(14)(15) are in good agreement with our findings, demonstrating that early intervention is essential for myocardial salvage.…”

Section: Discussionsupporting

confidence: 92%

Effect of Very Early Intravenous Streptokinase Infusion in Patients with Evolving Myocardial Infarction

Wik

Dale

1988

Journal of Internal Medicine

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The effect of very early infusion of 1.5 × 106 U of streptokinase intravenously was studied in 29 patients with nitroglycerin‐resistant chest pain and ST‐segment elevation. Infarct size was estimated from maximal LD1 isoenzyme levels, and the diagnosis confirmed by CK‐MB determination. Thrombolytic therapy was started within 1 hour of pain onset in 11 patients (group A), between 1 and 2 hours in 10 (group B), and later than 2 hours in eight patients (group C). Marked differences appeared between the groups. Thus, three patients in group A and one patient in group B did not develop infarction, all had critical LAD stenoses. Three patients in group C died in shock without bleeding. Further, the average maximal LD1 values in the 22 patients who survived their infarction differed significantly between the groups, and were 12.6, 19.1 and 36.2 μkat/l in groups A, B and C, respectively. In conclusion, very early intravenous streptokinase infusion probably reduces myocardial necrosis, and possibly prevents infarction in some patients.

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Section: Discussionsupporting

confidence: 92%

Effect of Very Early Intravenous Streptokinase Infusion in Patients with Evolving Myocardial Infarction

Wik

Dale

1988

Journal of Internal Medicine

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“…These enzymes then rise quickly and peak early. Three investigators have reported early CK peaking at 9-14 hours after the onset of cardiac symptoms in 68 patients treated successfully with STK, compared to 25 hours on average among 19 patients in whom treatment failed (Ganz et al, 1981;Mathey et al, 1981;Schwarz et al, 1982). CK peaking has occurred late among 384 patients with untreated myocardial infarcts at 26.4 h on the average after the onset of chest pain (Udall, 1983).…”

Section: Noninvasive Markers Of Coronary Reperfusionmentioning

confidence: 99%

“…Early reperfusion of acute infarcts and rapid evolution of EKG ST-segment abnormalities are now wellestablished correlates in both animal (Ganz et al, 1981) and humans (Ganz et af., 1981;Mathey et al, 1981;Rentrop et al, 1981). It has been shown by angiography that ST segment changes appear within minutes after coronary reperfusion has occurred in most patients.…”

Section: Noninvasive Markers Of Coronary Reperfusionmentioning

confidence: 99%

“…These may be identified in otherwise healthy adults who experience sudden precordial pains lasting at least 30 minutes and who exhibit EKG ST-segment elevations in selected leads reflecting a given area of ischemic myocardium. Approximately 80% of these infarcts are triggered by acute coronary thrombi (DeWood et al, 1980;Ganz et al, 1981;Mathey et al, 1981;Muller, 1983;Rentrop et al, 1981). On the other hand, most patients having subendocardial infarcts probably should not be treated because the majority of these are not thmmbogenic.…”

Section: Practical Recommendationsmentioning

confidence: 99%

“…therapy. Ganz et al (1981) and others have implied that circulating plasma fails to penetrate blind arterial pouches created by acute coronary thrombi, and therefore catheters are required to fill such pouches directly with STK. Experience with mutine coronary angiography and the fate of contrast material (CM) shed a good deal of light on this question.…”

Section: Streptokinase Sprays and Blind Pouchesmentioning

confidence: 99%

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Recent advances using streptokinase for acute coronary thrombosis

Udall

1984

Clinical Cardiology

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Summary: Most important in comparison to earlierEuropean trials, streptokinase (STK) is administered now at the earliest time possible after acute coronary thrombosis. In this series, STK was started 2.5 (f1.5) h after onset of chest pain, with reperfusion achieved approximately 1 h later in 6 (55%) of 11 patients treated. Posttreatment angiograms will not be required to identify thrombolysis if noninvasive indicators will prvoide this information correctly. Early creatine kinase enzyme peaking 8 to 15 h after chest pain appears to be the most accurate marker available. Among untreated and unsuccessfully treated patients, creatine kinase peaking usually occurs 18-36 h after chest pain. A large intravenous STK loading dose of 1,500,OOO IU produces a plasma concentration of approximately 500 IU/ml, equal to that concentration employed originally by intracoronary infusions. Such large doses have been employed in 60 patients thus far, without an unusual incidence or severity of hemorrhages. High dose, ultmshort-term treatment for only 1 h is being investigated now. Systemic STK penetrates most "blind coronary pouches" and gains access to acute thrombi, as identified by radiocontrast material washout during angiogmphy in patients with severe coronary occlusions. Streptokinase exerts a significant anticoagulant effect, not previous considered, which may be beneficial in the prevention of new clot formation and the rapid dissolution of acute coronary thrombi.

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Quantitative coronary angiography during intracoronary streptokinase in acute myocardial infarction: How long to continue thrombolytic therapy?

et al. 1983

Cathet. Cardiovasc. Diagn.

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An intracoronary infusion of streptokinase is often administered in patients with acute myocardial infarction. To address the question of how long intracoronary streptokinase should be infused, we studied 13 patients with symptoms and electrocardiographic findings suggesting an evolving myocardial infarction. We used subselective catheterization techniques and made quantitative angiographic measurements of the percentage of reduction of coronary artery (CA) diameter before intracoronary streptokinase therapy, immediately after reperfusion was established, and at the completion of streptokinase infusion. Before intracoronary streptokinase and after intracoronary nitroglycerin, nine patients had 100% obstruction of the CA in the "infarct-related vessel." In seven patients reperfusion was established (25 +/- 21 min, mean +/- SD) at which time CA diameter was reduced by 77 +/- 22%. The streptokinase infusion was then continued until repeated films (every 10 to 15 min) suggested no further change at the site of CA obstruction (93 +/- 68 min). The percentage of CA diameter reduction when streptokinase infusion was discontinued was 55 +/- 32%; this value was less (P less than 0.05) than that observed early after reperfusion. These data show that after initial reperfusion was achieved by the use of intracoronary streptokinase, additional streptokinase lessened the reduction of CA diameter. Residual thrombus may be present at the narrowed CA site early after reperfusion, and further "cleanup" can be achieved by prolonging streptokinase infusion.

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Intracoronary Thrombolysis in Evolving Myocardial Infarction

Cited by 9 publications

References 10 publications

Effect of Very Early Intravenous Streptokinase Infusion in Patients with Evolving Myocardial Infarction

Effect of Very Early Intravenous Streptokinase Infusion in Patients with Evolving Myocardial Infarction

Recent advances using streptokinase for acute coronary thrombosis

Quantitative coronary angiography during intracoronary streptokinase in acute myocardial infarction: How long to continue thrombolytic therapy?

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