title: The incidence and mechanism of hypotension following thrombolytic therapy for acute myocardial infarction with streptokinase-containing agents--lack of relationship to pretreatment streptokinase resistance.
abstract: The incidence, amplitude, mechanism and relationship to prior exposure to streptococcal antigen of blood pressure changes to streptokinase-containing thrombolytic agents were investigated in 125 patients treated with either 1.5 x 10(6) IU streptokinase over 60 min or 30 U anistreplase over 5 min, within 6 h of onset of acute myocardial infarction. Twenty-one of 52 patients with anterior and 34 of 73 with inferior myocardial infarction had a hypotensive response. There were no significant differences in the incidence, duration or amplitude of hypotension between the two treatment groups. The maximum mean fall in systolic blood pressure was 16.9 mmHg (95% confidence limits, CL 12.2 to 24.5 mmHg), and the maximum mean fall in diastolic blood pressure was 13.7 mmHg (CL 10.3 to 17.1 mmHg), starting 4 min after start of therapy and resolving within 34 min. Blood pressure changes were well tolerated. Hypotension was not related to pretreatment streptokinase resistance titre, or anti-SK IgG concentration, to changes in plasma fibrinogen, B-beta 15-42 peptide, D-dimer--as indices of thrombin activation and fibrin (-ogen) breakdown--to plasma viscosity. The blood pressure changes following treatment with streptokinase-containing thrombolytic agents in acute myocardial infarction are frequent but well tolerated. The mechanism of hypotension remains unclear, but is not related to prior exposure to streptococcal antigen.
authors.affiliation: Department of Medicine & Therapeutics, University of Glasgow, Western Infirmary/Stobhill General Hospital, U.K.
authors.forename: J D
authors.initials: JD
authors.lastname: Gemmill
authors.forename: K J
authors.initials: KJ
authors.lastname: Hogg
authors.forename: J T
authors.initials: JT
authors.lastname: Douglas
authors.forename: F G
authors.initials: FG
authors.lastname: Dunn
authors.forename: G D
authors.initials: GD
authors.lastname: Lowe
authors.forename: A P
authors.initials: AP
authors.lastname: Rae
authors.forename: W S
authors.initials: WS
authors.lastname: Hillis
mesh_terms: D016255:Anistreplase / Q000009:adverse effects* / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001809:Blood Viscosity / Q000187:drug effects / Q000502:physiology; D004311:Double-Blind Method; D004351:Drug Resistance; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D007022:Hypotension / Q000139:chemically induced* / Q000503:physiopathology; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D013300:Streptokinase / Q000009:adverse effects* / Q000627:therapeutic use; D015912:Thrombolytic Therapy
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D016255:Anistreplase; D005340:Fibrinogen; D013300:Streptokinase