BACKGROUND: Lp(a) lipoprotein has structural homology with plasminogen and has been shown to inhibit plasminogen activation in vitro. OBJECTIVE: To determine whether the serum concentration of Lp(a) lipoprotein present when streptokinase was given in acute myocardial infarction influenced the outcome as judged by electrocardiographic methods. PATIENTS AND DESIGN: Serum Lp(a) lipoprotein concentration was measured in 135 consecutive patients admitted with a diagnosis of acute myocardial infarction who received streptokinase treatment. Recovery from myocardial injury was assessed by the reduction in the sum of ST segment elevation measured from the J point (STJ) in the electrocardiogram immediately before streptokinase was given compared with that three hours later. RESULTS: The serum Lp(a) lipoprotein concentrations were measured within 12 hours of the onset of symptoms of myocardial infarction and were higher than in healthy reference populations. Recovery from myocardial infarction could be assessed from the STJ in 116 patients (86% of the series). Those in whom it could not had bundle branch block, left ventricular hypertrophy, did not survive three hours, or had started intravenous nitrate treatment or some other clinical procedure before or at the time the second electrocardiogram was to be recorded. Patients with reductions in STJ after streptokinase that were > 4 mm (the median decrease) had mean (range) serum Lp(a) lipoprotein concentrations of 41.0 (0.8-220) mg/dl and those with a smaller reduction in STJ had concentrations of 29.1 (1.7-151) mg/dl. The difference was not statistically significant. CONCLUSION: In this study Lp(a) lipoprotein concentration did not significantly influence the outcome of thrombolytic treatment with streptokinase.
BACKGROUND:Lp(a) lipoprotein has structural homology with plasminogen and has been shown to inhibit plasminogen activation in vitro. OBJECTIVE: To determine whether the serum concentration of Lp(a) lipoprotein present when streptokinase was given in acute myocardial infarction influenced the outcome as judged by electrocardiographic methods. PATIENTS AND DESIGN: Serum Lp(a) lipoprotein concentration was measured in 135 consecutive patients admitted with a diagnosis of acute myocardial infarction who received streptokinase treatment. Recovery from myocardial injury was assessed by the reduction in the sum of ST segment elevation measured from the J point (STJ) in the electrocardiogram immediately before streptokinase was given compared with that three hours later. RESULTS: The serum Lp(a) lipoprotein concentrations were measured within 12 hours of the onset of symptoms of myocardial infarction and were higher than in healthy reference populations. Recovery from myocardial infarction could be assessed from the STJ in 116 patients (86% of the series). Those in whom it could not had bundle branch block, left ventricular hypertrophy, did not survive three hours, or had started intravenous nitrate treatment or some other clinical procedure before or at the time the second electrocardiogram was to be recorded. Patients with reductions in STJ after streptokinase that were > 4 mm (the median decrease) had mean (range) serum Lp(a) lipoprotein concentrations of 41.0 (0.8-220) mg/dl and those with a smaller reduction in STJ had concentrations of 29.1 (1.7-151) mg/dl. The difference was not statistically significant. CONCLUSION: In this study Lp(a) lipoprotein concentration did not significantly influence the outcome of thrombolytic treatment with streptokinase.
Authors: A S Iskandrian; R Lichtenberg; B L Segal; G S Mintz; E D Mundth; A H Hakki; D Kimbiris; C E Bemis; M N Croll; S A Kane Journal: Circulation Date: 1982-02 Impact factor: 29.690
Authors: J H Chesebro; G Knatterud; R Roberts; J Borer; L S Cohen; J Dalen; H T Dodge; C K Francis; D Hillis; P Ludbrook Journal: Circulation Date: 1987-07 Impact factor: 29.690
Authors: H D White; R M Norris; M A Brown; M Takayama; A Maslowski; N M Bass; J A Ormiston; T Whitlock Journal: N Engl J Med Date: 1987-10-01 Impact factor: 91.245
Authors: V W Armstrong; P Cremer; E Eberle; A Manke; F Schulze; H Wieland; H Kreuzer; D Seidel Journal: Atherosclerosis Date: 1986-12 Impact factor: 5.162