Streptokinase Therapy For Myocardial Infarction Research Articles

Serum sickness and acute renal failure after streptokinase therapy for myocardial infarction

A patient developed serum sickness and acute renal failure following therapy with streptokinase for myocardial ischaemia. There was a previous history of a cellulitic infection of the leg, and antibodies to streptokinase were measurable in a serum sample taken from the patient before therapy. A cryoglobulin was detected at the time of presentation with serum sickness. This contained polyclonal IgG (with anti-streptokinase activity), streptokinase, and C3. Circulating immune complexes were demonstrated by C1q-binding assay. Deposition of C3 was observed in skin and renal biopsies, and bound to erythrocytes. Renal histology, however, showed acute tubular necrosis, with no vasculitis or inflammatory cell infiltrate. This case provides an unusual example of the characterization of an immune complex comprising a specific antibody and an exogenous antigen, and has clinical implications for the use of streptokinase.

Evaluation of in vivo immune complex formation and complement activation in patients receiving intravenous streptokinase.

The usefulness of several different methods for detecting immune complex formation and complement activation in the circulation were applied to samples from patients receiving intravenous Streptokinase therapy for myocardial infarction. Streptokinase is a foreign antigen and can cause immune reactions. We collected samples from 13 patients, before Streptokinase administration (baseline), at the end of infusion (1 h), 12 h later and on day 7. We measured IgG containing immune complexes (IgG-IC), free C3d and antibodies to Streptokinase by ELISA, and CR1, C3d and C4d on erythrocytes by flow cytometric assay. Antibodies to Streptokinase are common, as all but two of the patients had measurable antibody levels. During Streptokinase treatment there was a drop in antibody levels, most prominent in those patients who had high baseline levels. At the same time increased levels of free C3d and erythrocyte-bound C3d were observed. After 12 h free C3d was usually back to baseline level, but C3d on erythrocytes was still raised. These data indicate the formation of Streptokinase immune complexes in patients with high Streptokinase antibody levels, and show that these complexes are cleared rapidly from the circulation, leaving more persistent signs of complement activation. We conclude that free C3d is a good indicator of ongoing complement activation, whereas C3d on erythrocytes indicates that complement activation has recently taken place.

Platelet Reactivity and Streptokinase Resistance following Antecedent Streptokinase Therapy for Myocardial Infarction

Aims: To assess the efficacy of second-time administration of streptokinase (SK). First-time thrombolysis with SK in myocardial infarction (MI) is established but the efficacy of subsequent SK is unknown. Methods and Results: Platelet reactivity to shear stress, spontaneous and SK-induced thrombolysis were measured in vitro in 28 patients who had received SK for MI and compared to 15 controls. SK antibody (Ab) titres were inversely related to time from MI. Platelet reactivity was greatly enhanced in patients (p < 0.0001). Spontaneous thrombolysis in patients was poor and in 17 failed to occur. In contrast, thrombolysis occurred in all but 1 control. In patients platelet reactivity was strongly related to thrombolytic activity (r = –0.516; p = 0.0029). SK in vitro was at least 4 times more effective in controls than in patients. Conclusion: The chances of achieving patency with second administration of SK are poor. Ab titre is not a reliable predictor of resistance.

Tissue Plasminogen Activator and Cholesterol Crystal Embolization

Letters and Corrections15 October 1989Tissue Plasminogen Activator and Cholesterol Crystal EmbolizationManick Bhardwaj, MD, Richard Goldweit, MD, Jay Erlebacher, MD, Massoud Kashani, MD, David Levin, MD, George Leber, MDManick Bhardwaj, MDSearch for more papers by this author, Richard Goldweit, MDSearch for more papers by this author, Jay Erlebacher, MDSearch for more papers by this author, Massoud Kashani, MDSearch for more papers by this author, David Levin, MDSearch for more papers by this author, George Leber, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-111-8-687 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor:Cholesterol crystal embolization has been seen frequently in patients who undergo angiographic procedures after thrombolytic therapy (1). We describe a patient whose cholesterol crystal embolization occurred spontaneously after recombinant tissue-type plasminogen activator thrombolysis without an antecedent invasive vascular procedure. A 62-year-old woman with a history of hypertension and hypercholesterolemia presented with 2 hours of chest pain and electrocardiographic changes indicating acute inferior myocardial infarction. She had no history of angiography or recent surgical procedures. At initial examination there was no skin rash. Peripheral pulses were normal, but a systolic bruit was heard just below the umbilicus. She...Reference1. SchwartzMcDonald MG. Cholesterol embolization syndrome: occurrence after intravenous streptokinase therapy for myocardial infarction. JAMA. 1987;258:1934-5. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Manick Bhardwaj, MD; Richard Goldweit, MD; Jay Erlebacher, MD; Massoud Kashani, MD; David Levin, MD; George Leber, MDAffiliations: Englewood Hospital Englewood, NJ 07631 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAcute Kidney Injury in Acute Ischemic Stroke Patients in Clinical TrialsThrombolyticsCholesterol Embolization Syndrome Induced by Thrombolytic TherapyAtheroembolic disease following administration of tissue plasminogen activator (TPA)Isolated splenic infarction following left cardiac catheterization: Case report and a review of the literatureSevere Adverse Cutaneous Reactions to DrugsProspective Assessment of Cholesterol Embolization in Patients With Acute Myocardial Infarction Treated With Thrombolytic vs Conservative TherapyPain Relief and Clinical Improvement Temporally Related to the Use of Pentoxifylline in a Patient with Documented Cholesterol Emboli—A Case ReportCase 38-1993Cholesterol embolization syndrome after intravenous tissue plasminogen activator for acute myocardial infarctionCholesterol Embolism in Intensive Care PatientsDrugs affecting blood coagulation and hemostasis 15 October 1989Volume 111, Issue 8Page: 687-688KeywordsAngiographyCholesterolElectrocardiographyHypertensionIschemiaMyocardial infarctionRashesTissue plasminogen activator ePublished: 1 December 2008 Issue Published: 15 October 1989 PDF downloadLoading ...

Cholesterol Emboli and Streptokinase Therapy

To the Editor. —Drs Schwartz and McDonald1recently described two cases of cholesterol embolization syndrome occurring after receiving intravenous streptokinase therapy for myocardial infarction. I disagree with them about their conclusion. Cholesterol embolization syndrome occurs spontaneously but has been described after vascular surgery, arteriographic procedures2,3including coronary angiography,2and oral anticoagulant therapy including warfarin sodium.4Extensive atherosclerosis, systemic hypertension, and diabetes mellitus represent other risk factors. Furthermore, some of these conditions are frequently associated.3 In the first case reported by Drs Schwartz and McDonald, coronary arteriography preceded streptokinase treatment before the occurrence of the cholesterol embolization syndrome. In the second case, after the streptokinase had been given, coronary arteriography and two weeks of warfarin therapy followed before the cholesterol embolization syndrome developed. There is therefore no reason to blame the intravenous streptokinase therapy, and so the title of this article is inappropriate and misleading. Cholesterol