Elevations in troponin I after percutaneous coronary interventions are associated with abnormal tissue-level perfusion in high-risk patients with non-ST-segment-elevation acute coronary syndromes.

BACKGROUND: In the setting of non-ST-segment-elevation (NSTE) acute coronary syndromes (ACS), the pathophysiological mechanisms underlying post-percutaneous 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 count, TIMI myocardial perfusion grade (TMPG), and myocardial 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-risk (angina at rest, unequivocal ST-segment depression, and cTnI elevation) patients with NSTE-ACS. All patients were treated with glycoprotein IIb/IIIa inhibitors (27 with tirofiban and 15 with abciximab) and had successful PCI. Fourteen patients 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). Patients with postprocedural cTnI elevation also presented a significantly lower number 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: Postprocedural cTnI elevation in high-risk patients with NSTE-ACS is associated with an abnormal tissue-level perfusion.