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Effects of lipoprotein(a) on thrombolysis

Lipoprotein(a) (Lp(a)) and plasminogen share a high degree of structural homology. Therefore it has been suggested that elevated levels of Lp(a) may inhibit the profibrinolytic activity at the cell surface and increase the risk of thrombosis by competitive inhibition of plasminogen. In the present s...

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Bibliographic Details
Main Authors: Hodenberg, Eberhard von (Author) , Pestel, Eva (Author) , Kreuzer, Jörg (Author) , Freitag, Mathias (Author) , Bode, Christoph (Author)
Format: Article (Journal)
Language:English
Published: January 1994
In: Chemistry and physics of lipids
Year: 1994, Volume: 67/68, Pages: 381-385
ISSN:1873-2941
DOI:10.1016/0009-3084(94)90160-0
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/0009-3084(94)90160-0
Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/0009308494901600
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Author Notes:Eberhard von Hodenberg, Eva Pestel, Jörg Kreuzer, Mathias Freitag, Christoph Bode

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520 |a Lipoprotein(a) (Lp(a)) and plasminogen share a high degree of structural homology. Therefore it has been suggested that elevated levels of Lp(a) may inhibit the profibrinolytic activity at the cell surface and increase the risk of thrombosis by competitive inhibition of plasminogen. In the present study we evaluated whether high levels of Lp(a) affect thrombolytic therapy in patients with acute myocardial infarction. Forty-one patients with acute myocardial infarction were treated with a combination of recombinant tissue-type plasminogen activator and human single-chain urokinase-type plasminogen activator. Coronary patency was assessed angiographically 90 min after initiation of treatment. Thrombolysis was successful in 30 and unsuccessful in 11 patients. Patients with high Lp(a) levels (> 25 mg/dl) (n = 9) responded equally well to thrombolytic therapy (8 of 9, patency 89%) as did patients with normal or low levels of Lp(a) (22 of 32, patency 70%, difference P > 0.1). The results demonstrate that high levels of Lp(a) do not influence thrombolysis in patients with acute myocardial infarction when low-dose pharmacologic concentrations of recombinant tissue-type plasminogen activator and human single chain urokinase-type plasminogen activator are applied in combination. 
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