Circulating levels of plasminogen and oxidized phospholipids bound to plasminogen distinguish between atherothrombotic and non-atherothrombotic myocardial infarction.
Oxidized phospholipids (OxPL) are abundant in atherosclerotic plaques. They are also bound to circulating plasminogen after myocardial infarction (MI), and their binding to plasminogen may accentuate fibrinolysis. We sought to assess whether circulating levels of plasminogen and OxPL bound to plasminogen (OxPL-PLG) increase following acute MI and whether this increase differs between atherothrombotic (Type 1) and non-atherothrombotic (Type 2) MI. We measured circulating levels of plasminogen and OxPL-PLG at 0, 6, 24, 48 h, and >3 months (stable state) following acute MI and following an angiogram for stable coronary artery disease (CAD). Forty-nine subjects met the criteria for acute MI, of whom 34 had clearly defined atherothrombotic (n = 22) or non-atherothrombotic (n = 12) MI; 15 patients met the criteria for stable CAD. Mean baseline levels of plasminogen and OxPL-PLG were lower in the acute MI group than in the stable CAD group (9.75 vs 20.2, p < 0.0001 for plasminogen and 165.5 vs 275.1, p = 0.0002 for OxPL-PLG) and did not change over time or between time points, including the 3-month follow-up. Mean baseline levels of plasminogen and OxPL-PLG were also lower in atherothrombotic (Type 1) than in non-atherothrombotic (Type 2) MI subjects (8.65 vs 12.1, p < 0.03 for plasminogen and 164.5 vs 245.7, p = 0.02 for OxPL-PLG), and this relationship did not change over time or between time points. Plasminogen and OxPL-PLG were lower in patients presenting with an acute MI than in those with stable CAD and also in those with atherothrombotic MI (Type 1) vs. those with non-atherothrombotic MI (Type 2). These findings persisted at a median follow-up of 3 months post-MI. The association of plasminogen and OxPL-PLG with acute MI, particularly atherothrombotic MI (Type 1), could reflect a reduced fibrinolytic capacity, associated with an increased risk of atherothrombotic events differentiating stable CAD from unstable CAD and atherothrombotic MI (Type 1) from non-atherothrombotic MI (Type 2). Additional study with a larger sample size is warranted.
Division of Cardiovascular Medicine, Department of Medicine, KentuckyOne/Jewish Hospital, University of Louisville, 550 South Jackson Street, Louisville, KY, 40202, USA. APDeFi01@louisville.edu.|Johns Hopkins University, Baltimore, MD, USA. APDeFi01@louisville.edu.
Andrew P
AP
DeFilippis
Department of Physiology, University of Louisville, Louisville, KY, USA.
Ilya
I
Chernyavskiy
Division of Cardiovascular Medicine, Department of Medicine, KentuckyOne/Jewish Hospital, University of Louisville, 550 South Jackson Street, Louisville, KY, 40202, USA.
Alok R
AR
Amraotkar
Division of Cardiovascular Medicine, and Bioinformatics, Department of Medicine, University of Louisville, Louisville, KY, USA.
Patrick J
PJ
Trainor
Department of Medicine, SUNY Upstate Medical University, Syracuse, NY, USA.
Shalin
S
Kothari
Department of Medicine, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.
Imtiaz
I
Ismail
School of Medicine, University of Louisville, Louisville, KY, USA.
Charles W
CW
Hargis
Department of Emergency Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Frederick K
FK
Korley
Division of Cardiology, University of Basel, Basel, Switzerland.
Gregor
G
Leibundgut
Division of Cardiovascular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA, USA.
Sotirios
S
Tsimikas
Department of Bioinformatics and Biostatistics, University of Louisville, Louisville, KY, USA.
Shesh N
SN
Rai
Division of Cardiovascular Medicine, Department of Medicine, KentuckyOne/Jewish Hospital, University of Louisville, 550 South Jackson Street, Louisville, KY, 40202, USA.
Aruni
A
Bhatnagar
D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis; D005342:Fibrinolysis; D005500:Follow-Up Studies; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood / Q000145:classification / Q000175:diagnosis* / Q000209:etiology; D010084:Oxidation-Reduction; D010743:Phospholipids / Q000097:blood / Q000378:metabolism*; D010958:Plasminogen / Q000378:metabolism*; D011485:Protein Binding; D012306:Risk; D013997:Time Factors
D010743:Phospholipids; D010958:Plasminogen
Acute myocardial infarction; Atherothrombosis; Biomarkers; Oxidized phospholipids; Plasminogen