Key result
CLS 2210 significantly lowered serum creatine kinase (p=0.01) and myoglobin levels compared to placebo in acute myocardial infarction, whereas streptokinase showed no significant difference.
Why the study?
Does intravenous CLS 2210 or streptokinase reduce biochemical markers of myocardial necrosis in patients with first acute myocardial infarction compared to placebo?
Observational (n=60)
Does intravenous CLS 2210 or streptokinase reduce biochemical markers of myocardial necrosis in patients with first acute myocardial infarction compared to placebo?
Intravenous CLS 2210 (calcium dobesilate) significantly reduces biochemical markers of myocardial necrosis in early acute myocardial infarction compared to placebo, suggesting a potential role in limiting infarct size.
Small early-MI trial of calcium dobesilate versus streptokinase is hypothesis-generating; leaves open comparative efficacy pending larger RCTs.
In a previous double-blind, randomized study, CLS 2210 (a new formula tion of calcium dobesilate) or placebo was administered by intravenous infusion to 41 patients having their first acute myocardial infarction. In the present study 19 comparable patients were treated intravenously with streptokinase under iden tical contidions and the results compared with those from the previous study. In all patients administration was begun within three hours of onset of symptoms and continued over seventy-two hours. Blood samples were taken for the meas urement of serum activity of creatine kinase and its isoenzyme MB, and the se rum and urinary concentrations of myoglobin and glycosaminoglycans were also measured. The purpose of this study was to determine the effects of CLS 2210, place bo, and streptokinase on these biochemical markers of acute myocardial infarc tion, thereby assessing their actions in limiting myocardial necrosis. In the CLS 2210-treated patients, the levels of serum creatine kinase and se rum and urinary myoglobin were significantly lower than in the placebo patients throughout the seventy-two hours (p = 0.01, 0.005, 0.004 respectively). The levels of creatine kinase MB and serum glycosaminoglycan in the CLS 2210 patients were initially higher than in the placebo patients but fell below placebo levels between the fortieth and fifty-fifth hours, respectively (p = 0.89, 0.02). Only the glycosaminoglycan urinary concentrations were higher in the CLS 2210 group than in the placebo group throughout (p = 0.0005). The values for the six variables investigated showed no statistically significant difference between placebo and streptokinase. These findings suggest that CLS 2210 reduces myocardial infarct size in human subjects, probably by the same mechanisms of action (principally, improved cardiac lymphatic drainage) that have been observed in previous animal studies. Combination therapy with thrombolytic agents may, therefore, be advocated, since they exert their protective effect by other mechanisms.
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Szlávy et al. (1992) conducted an observational in Acute myocardial infarction (n=60). CLS 2210 and Streptokinase vs. Placebo was evaluated on Biochemical markers of acute myocardial infarction (serum creatine kinase, myoglobin, creatine kinase MB, glycosaminoglycans) (p=0.01). CLS 2210 significantly lowered serum creatine kinase (p=0.01) and myoglobin levels compared to placebo in acute myocardial infarction, whereas streptokinase showed no significant difference.
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