Europace Advance Access published online on May 14, 2008
Europace, doi:10.1093/europace/eun123
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Reperfusion ventricular arrhythmia bursts in TIMI 3 flow restoration with primary angioplasty for anterior ST-elevation myocardial infarction: a more precise definition of reperfusion arrhythmias
1 Duke Clinical Research Institute, 508 Fulton Street, Room A3012, Durham, NC 27705, USA; 2 Department of Cardiology, University Hospital Maastricht, Maastricht, The Netherlands; 3 Department of Biostatistics and Bioinformatics, Duke University Medical Center, Durham, NC, USA; 4 Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, NC, USA; 5 Bio-Imaging Technologies, Leiden, The Netherlands; 6 Leiden University Medical Center, Leiden, The Netherlands; 7 Shaare Zedek Medical Centre, Jerusalem, Israel; 8 Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands
Aims: We sought to define reperfusion-induced ventricular arrhythmias (VAs) more precisely through simultaneous angiography, continuous ST-segment recovery, and beat-to-beat Holter analyses in subjects with anterior ST-elevation myocardial infarction (STEMI) undergoing primary angioplasty [percutaneous coronary intervention (PCI)].
Methods and results: All 157 subjects with final TIMI 3 flow had continuous 12-lead electrocardiography with simultaneous Holter recording initiated prior to PCI for continuous ST-segment recovery and quantitative VA analyses. Ventricular arrhythmia bursts were detected against subject-specific background VA rates using a statistical outlier method. For temporal correlations, timing and quality of reperfusion were defined as first angiographic TIMI 3 flow with
50% stable ST-segment recovery. Almost all subjects had VAs [156/157 (99%)], whereas VA bursts during or subsequent to reperfusion occurred in 97/157 (62%). The majority of VA bursts (72%) arose within 20 min of reperfusion (95% CI: 26.7, 72), with onset at a median of 4 min post-reperfusion (IQR: 0–43) Bursts comprised a median of 1290 ventricular premature complexes (VPCs) (IQR: 415–4632) and persisted for a median of 105 min (IQR: 35–250). Most background VAs occurred as single VPCs; bursts typically comprised runs of three or more VPCs. Subjects with bursts had higher absolute peak ST segments and more frequent worsening of ST elevation immediately after reperfusion.
Conclusion: Ventricular arrhythmia bursts temporally associated with TIMI 3 flow restoration and stable ST-segment recovery (reperfusion VA bursts) can be precisely defined in subjects with anterior STEMI and may constitute a unique electric biosignal of myocellular response to reperfusion.
Key Words: ST-elevation myocardial infarction, Primary percutaneous coronary intervention, Continuous 12-lead ECG monitoring, Beat-to-beat Holter monitoring, Statistical outlier detection methodology, Reperfusion ventricular arrhythmia bursts
* Corresponding author. Tel: +1 919 286 6860; fax: +1 919 286 6861. E-mail address: kruco001{at}mc.duke.edu
Manuscript submitted 14 December 2007. Accepted after revision 16 April 2008.
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