(Circulation. 2000;102:636.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
PTX3, A Prototypical Long Pentraxin, Is an Early Indicator of Acute Myocardial Infarction in Humans
From the Istituto di Ricerche Farmacologiche Mario Negri, Milan (G.P., M.I., A.P.M., P.G., A.M., R.L.); Department of Biotechnology, Section of General Pathology, University of Brescia (A.M.); Divisions of Cardiology of Desio (G.I., S.S.), Seriate (F.A.), Casale Monferrato (F.P.), Brescia (M.M., L.D.C.), and Lugano (T.M.); Department of Pathology, University of Parma (D.C., G.O.); and Clinical Chemistry Laboratory, Legnano Hospital (G.R.), Italy; and the Department of Biochemistry, Boston University, Boston, Mass (J.D.S.).
Correspondence to Roberto Latini, MD, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milano, Italy. E-mail latini{at}irfmn.mnegri.it
Background—Inflammation is an important component of ischemic heart disease. PTX3 is a long pentraxin whose expression is induced by cytokines in endothelial cells, mononuclear phagocytes, and myocardium. The possibility that PTX3 is altered in patients with acute myocardial infarction (AMI) has not yet been tested.
Methods and Results—Blood samples were collected from 37 patients admitted to the coronary care unit (CCU) with symptoms of AMI. PTX3 plasma concentrations, as measured by ELISA, higher than the mean+2 SD of age-matched controls (2.01 ng/mL) were found in 27 patients within the first 24 hours of CCU admission. PTX3 peaked at 7.5 hours after CCU admission, and mean peak concentration was 6.94±11.26 ng/mL. Plasma concentrations of PTX3 returned to normal in all but 3 patients at hospital discharge and were unrelated to AMI site or extent, Killip class at entry, hours from symptom onset, and thrombolysis. C-reactive protein peaked in plasma at 24 hours after CCU admission, much later than PTX3 (P<0.001). Patients >64 years old and women had significantly higher PTX3 concentrations at 24 hours (P<0.05). PTX3 was detected by immunohistochemistry in normal but not in necrotic myocytes.
Conclusions—PTX3 is present in the intact myocardium, increases in the blood of patients with AMI, and disappears from damaged myocytes. We suggest that PTX3 is an early indicator of myocyte irreversible injury in ischemic cardiomyopathy.
Key Words: myocardial infarction • pentraxins • myocytes • proteins
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