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Usefulness of real-time myocardial perfusion imaging to evaluate alterations of myocardial blood flow in patients with stable angina pectoris undergoing elective percutaneous coronary interventions.

Korosoglou G, Geiger B, Hansen A, Hardt SA, Giannitsis E, Selter C, Katus HA, Kuecherer H

Department of Cardiology, University of Heidelberg, Heidelberg, Germany. Grigorios_Korosoglou@med.uni-heidelberg.de

Release of cardiac enzymes has been reported in patients with stable angina who undergo elective percutaneous coronary intervention (PCI) and has been associated with adverse clinical outcomes. The aim of the present study was to investigate whether impaired microvascular integrity can be detected using myocardial contrast echocardiography in patients undergoing elective PCI, and whether it is related to the extent of postprocedural troponin T elevation. We investigated consecutive patients with stable angina (n = 19) who were scheduled for elective angioplasty with stent placement. Myocardial contrast echocardiography was performed before and 2 to 4 hours and 24 hours after coronary intervention. Contrast images were analyzed visually and quantitatively measuring the peak signal intensity (A) and the slope of the signal intensity rise (beta) in 16 myocardial segments. The product of A x beta was calculated in each segment to estimate the regional myocardial blood flow. Troponin T was collected serially before and 2 to 4 hours and 24 hours after PCI. Five patients (26%) had elevated troponin T 24 hours after PCI (range 0.03 to 0.46 microg/L). Eight patients (42%), including all 5 patients with elevated troponin T levels, demonstrated impaired microvascular integrity 2 to 4 hours after PCI in >or=2 myocardial segments (range 2 to 4) within the perfusion territory of the target vessel. Of the 11 patients without evidence of impaired myocardial perfusion by myocardial contrast echocardiography, none had elevated troponin T levels at follow-up. Quantitative analysis of myocardial blood flow showed that impaired perfusion after PCI was partially reversible. Thus, A x beta had decreased significantly at 2 to 4 hours after PCI (3.4 +/- 1.6 vs 8.8 +/- 3.4 dB/s baseline, p <0.01), reincreased after 24 hours (6.4 +/- 2.3 dB/s at 24 hours vs 3.4 +/- 1.6 dB/s at 2 to 4 hours, p <0.01), but did not return to baseline (8.8 +/- 3.4 dB/s at baseline vs 6.4 +/- 2.3 dB/s at 24 hours, p <0.01). The perfusion defect size 2 to 4 hours after PCI was closely related to the troponin T levels after 24 hours (r(2) = 0.80, p <0.0001). In conclusion, impaired microvascular integrity is partially present in patients with stable angina who undergo elective PCI, is partially reversible, and is closely related to the release of troponin T. Because judgment of interventional success has shifted downstream to tissue level perfusion, myocardial contrast echocardiography may be useful to monitor such alterations in myocardial tissue perfusion.

Published 28 September 2005 in Am J Cardiol, 96(7): 885-91.
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