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on October 23, 2006

Circulation. 2006
Published online before print October 23, 2006, doi: 10.1161/CIRCULATIONAHA.106.620476
A more recent version of this article appeared on October 31, 2006
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Circulation: October 31, 2006, Volume 114, Number 18
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Right arrow Catheter-based coronary interventions: stents

Submitted on February 12, 2006
Revised on July 14, 2006
Accepted on August 2, 2006

Intracoronary ST-Segment Shift Soon After Elective Percutaneous Coronary Intervention Accurately Predicts Periprocedural Myocardial Injury

Vruyr Balian MD*, Michele Galli MD, Claudio Marcassa MD, Gianni Cecchin MD, Maurice Child MD, Fabio Barlocco MD, Ettore Petrucci MD, Giulia Filippini MD, Riccardo Michi MD, and Marco Onofri MD

From the Cardiologia Interventistica, Azienda Ospedaliera di Busto Arsizio, Varese, Italy (V.B., G.C., M.C., F.B., E.P., G.F., R.M., M.O.); Cardiology Division, Spedali Riuniti ASL6, Livorno, Italy (M.G.); and Cardiology Division, Salvatore Maugeri Foundation IRCCS, Veruno Novara, Italy (C.M).

* To whom correspondence should be addressed. E-mail: vbalian{at}aobusto.it.

Background--Elevation of cardiac biomarkers after coronary angioplasty (percutaneous coronary intervention [PCI]) reflects periprocedural myocardial damage and is associated with adverse cardiac events. We assessed whether periprocedural myocardial damage that occurs despite successful PCI could be rapidly and easily identified by intracoronary ST-segment recording with the use of a catheter guidewire.

Methods and Results--In 108 consecutive stable patients undergoing elective single-vessel PCI, we recorded unipolar ECG from the intracoronary guidewire in the distal coronary before PCI and 2 minutes after the last balloon inflation. After PCI, intracoronary ST-segment shift ≥1 mm from baseline was considered significant. Troponin I levels were measured at baseline and at 8 and 24 hours after intervention, and myocardial damage was defined as troponin I increase above the upper normal value after intervention. All patients had normal cardiac marker values before PCI, and PCI was successful in all (residual stenosis <20%, Thrombolysis in Myocardial Infarction grade 3 flow). After PCI, long-term follow-up data were collected; myocardial damage was detected in 50 patients (46%), although abnormal creatine kinase-MB values were documented in only 11 (10%). Significant intracoronary ST-segment shift after PCI was present in 40 patients (37%; group A) and absent in the remaining 68 (63%; group B). Procedural myocardial damage was documented in 37 group A patients (93%) and in 13 group B patients (19%; P<0.001); significant ECG changes were found on standard ECG after intervention in only 5 patients (13%) and 1 patient (1%) (P<0.05). Sensitivity of intracoronary ST-segment shift for predicting myocardial damage was 74%, and specificity was 95%, with positive and negative predictive values of 93% and 81%, respectively. On multivariate analysis, intracoronary ST-segment shift was the sole independent predictor of myocardial damage (odds ratio, 54.1; 95% confidence interval, 12.1 to 240; P<0.0001). At a median follow-up of 12±5 months, major coronary event-free survival was significantly worse in group A patients (log-rank test {chi}2=4.0; P<0.05).

Conclusions--After successful single-vessel PCI, intracoronary ST-segment shift allows the prompt and inexpensive identification of patients developing myocardial injury, who may require adjunctive therapy and longer in-hospital stay.


Key words: angioplasty • electrocardiography • infarction • revascularization




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D. L. Bhatt
Shifting the Diagnosis of Periprocedural Myocardial Infarction Upstream
Circulation, October 31, 2006; 114(18): 1898 - 1900.
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