Objectives: Myocardial infarction (MI) may be classified as ST elevation MI (STEMI) or non-ST elevation MI (NSTEMI). Procoagulants such as plasminogen activator inhibitor-1 (PAI-1) as well as markers of inflammation such as C-reactive protein (CRP), serum amyloid A (SAA) and interleukin-6 (IL-6) are elevated in acute coronary syndromes. However, no study has examined whether levels of these markers differ in patients with STEMI as opposed to NSTEMI. We sought to determine whether there are differences in plasma levels of PAI-1, CRP, SAA or IL-6 in patients with STEMI compared to patients with NSTEMI. Methods: Seventy-six consecutive patients presenting with acute MI (37 with STEMI and 39 with NSTEMI) were prospectively enrolled. Blood samples were obtained from patients within 6 h from presentation and plasma PAI-1, CRP, IL-6 and SAA concentrations were measured. Results: Plasma levels of PAI-1 were significantly higher in patients with STEMI compared to NSTEMI: 85.7 ± 5 vs. 61.3 ± 5 ng/ml (p < 0.001), while CRP, SAA and IL-6 levels were not significantly different between STEMI and NSTEMI patients. Conclusions: Higher plasma PAI-1 levels in STEMI patients may contribute to the predilection of these patients to occlusive thrombi and STEMI.

Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC Jr, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK, Ornato JP: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. J Am Coll Cardiol 2004;44:E1–E211.
Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, Chavey WE 2nd, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS, Smith SC Jr, Jacobs AK, Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura R, Ornato JP, Page RL, Riegel B: ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol 2007;50:E1–E157.
Stone GW, Cox D, Garcia E, Brodie BR, Morice MC, Griffin J, Mattos L, Lansky AJ, O’Neill WW, Grines CL: Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction: analysis from the primary angioplasty in myocardial infarction trials. Circulation 2001;104:636–641.
Zhao XQ, Theroux P, Snapinn SM, Sax FL: Intracoronary thrombus and platelet glycoprotein IIb/IIIa receptor blockade with tirofiban in unstable angina or non-Q-wave myocardial infarction: angiographic results from the PRISM-PLUS trial (Platelet receptor inhibition for ischemic syndrome management in patients limited by unstable signs and symptoms). PRISM-PLUS Investigators. Circulation 1999;100:1609–1615.
Ross R: Atherosclerosis – an inflammatory disease. N Engl J Med 1999;340:115–126.
Libby P: Current concepts of the pathogenesis of the acute coronary syndromes. Circulation 2001;104:365–372.
Liuzzo G, Biasucci LM, Gallimore JR, Grillo RL, Rebuzzi AG, Pepys MB, Maseri A: The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina. N Engl J Med 1994;331:417–424.
Ridker PM, Rifai N, Pfeffer MA, Sacks FM, Moye LA, Goldman S, Flaker GC, Braunwald E: Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Circulation 1998;98:839–844.
Morrow DA, Rifai N, Antman EM, Weiner DL, McCabe CH, Cannon CP, Braunwald E: Serum amyloid A predicts early mortality in acute coronary syndromes: a TIMI 11A substudy. J Am Coll Cardiol 2000;35:358–362.
Johnson BD, Kip KE, Marroquin OC, Ridker PM, Kelsey SF, Shaw LJ, Pepine CJ, Sharaf B, Bairey Merz CN, Sopko G, Olson MB, Reis SE: Serum amyloid A as a predictor of coronary artery disease and cardiovascular outcome in women: the National Heart, Lung, and Blood Institute-Sponsored Women’s Ischemia Syndrome Evaluation (WISE). Circulation 2004;109:726–732.
Katayama T, Nakashima H, Takagi C, Honda Y, Suzuki S, Iwasaki Y, Yano K: Prognostic value of serum amyloid A protein in patients with acute myocardial infarction. Circ J 2005;69:1186–1191.
Scarabin PY, Aillaud MF, Amouyel P, Evans A, Luc G, Ferrieres J, Arveiler D, Juhan-Vague I: Associations of fibrinogen, factor VII and PAI-1 with baseline findings among 10,500 male participants in a prospective study of myocardial infarction – the PRIME Study. Prospective Epidemiological Study of Myocardial Infarction. Thromb Haemost 1998;80:749–756.
Rott D, Weiss A, Chajek-Shaul T, Leibowitz D: ST deviation patterns in recurrent myocardial infarctions. Am J Cardiol 2006;98:10–13.
Davies MJ: Stability and instability: the two faces of coronary atherosclerosis: The Paul Dudly White Lecture, 1995. Circulation 1996;94:2013–2020.
Kohler HP, Peter JG: Plasminogen activator inhibitor type 1 and coronary artery disease. N Engl J Med 2000;342:1792–1801.
Eriksson P, Kallin B, van’t Hooft FM, Bavenholm P, Hamsten A: Allele-specific increase in basal transcription of the plasminogen-activator inhibitor 1 gene is associated with myocardial infarction. Proc Natl Acad Sci USA 1995;92:1851–1855.
Onalan O, Balta G, Oto A, Kabakci G, Tokgozoglu L, Aytemir K, Altay C, Gurgey A, Nazli N: Plasminogen activator inhibitor-1 4G4G genotype is associated with myocardial infarction but not with stable coronary artery disease. J Thromb Thrombolysis 2007, E-pub ahead of print.
Sampaio MF, Hirata MH, Hirata RD, Santos FC, Picciotti R, Luchessi AD, de Quateli Doi S, Armaganijan D, Batlouni M: AMI is associated with polymorphisms in the NOS3 and FGB but not in PAI-1 genes in young adults. Clin Chim Acta 2007;377:154–162.
Itakura H, Sobel BE, Boothroyd D, Leung LL, Iribarren C, Go AS, Fortmann SP, Quertermous T, Hlatky MA: Atherosclerotic Disease, Vascular Function and Genetic Epidemiology Advance (ADVANCE) Study. Do plasma biomarkers of coagulation and fibrinolysis differ between patients who have experienced an acute myocardial infarction versus stable exertional angina? Am Heart J 2007;154:1059–1064.
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