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Background In the setting of non ST segment elevation (NSTE) acute coronar y syndromes(ACS), the pathophysiological mechanisms underlying post percutaneou s coronary intervention (PCI) cardiac troponin I (cTnI) elevation remain unclear . Methods and Results We evaluated the relationship between troponin elevation and tissue level perfusion using the TIMI flow grade, corrected TIMI frame coun t, TIMI myocardial perfusion grade(TMPG), andmyocardial contrast enhancement by intracoronary myocardial contrast echocardiography (MCE) before and immediately after PCI performed within 24 to 48 hours of hospital admission in 42 high ris k(angina at rest, unequivocal ST segment depression, and cTnI elevation) patien ts with NSTE ACS. All patients were treated with glycoprotein IIb/IIIa inhibito rs (27 with tirofiban and 15 with abciximab) and had successful PCI. Fourteen p atients had a postprocedural cTnI elevation, whereas 28 did not. TMPG 0/1 after PCI was observed more frequently in patients with postprocedural cTnI elevation (43%versus 7%; P< 0.02). cTnI levels were higher among patients with TMPG 0/1 versus patients with TMPG 2/3 (5.3±2.7 versus 1.5±1.3 ng/mL; P< 0.0001). Patie nts with postprocedural cTnI elevation also presented a significantly lower numb er of perfused segments at MCE (59%versus 81%; P=0.02) as well as a lower MCE score index (0.65±0.38 versus 0.89±0.21; P < 0.02). Conclusions Postp rocedu ral cTnI elevation in high risk patients with NSTE ACS is associated with an a bnormal tissue level perfusion.
Background In the setting of non ST segment elevation (NSTE) acute coronar y syndromes (ACS), the pathophysiological mechanisms underlying post percutaneou coronary intervention (PCI) cardiac troponin I (cTnI) elevation remain unclear. Methods and Results We evaluated the relationship between troponin elevation and tissue level perfusion using the TIMI flow grade, corrected TIMI frame coun t, TIMI myocardial perfusion grade (TMPG), andmyocardial contrast contrast enhancement by intracoronary myocardial contrast echocardiography (MCE) before and immediately after PCI performed within 24 to 48 hours of hospital admission in 42 high ris k (angina at rest, unequivocal ST segment depression, and cTnI elevation) patien ts with NSTE ACS. All patients were treated with glycoprotein IIb / IIIa inhibito rs (27 with tirofiban and 15 with abciximab) and had successful PCI Fourteen p atients had a postprocedural cTnI elevation, but 28 did not. TMPG 0/1 after PCI was observed more frequently in patients w cTnI levels were higher among patients with TMPG 0/1 versus patients with TMPG 2/3 (5.3 ± 2.7 versus 1.5 ± 1.3 ng / mL; P <0.0001) . Patients with postprocedural cTnI elevation also presented a significantly lower numb er of perfused segments at MCE (59% versus 81%; P = 0.02) as well as a lower MCE score index (0.65 ± 0.38 versus 0.89 ± 0.21; P <0.02 Conclusions Postp rocedu ral cTnI elevation in high risk patients with NSTE ACS is associated with an a normal tissue level perfusion.