Europace Advance Access originally published online on May 14, 2008
Europace 2008 10(8):988-997; doi:10.1093/europace/eun123
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Electrophysiology/ablation
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
Manuscript submitted 14 December 2007. Accepted after revision 16 April 2008.
* Corresponding author. Tel: +1 919 286 6860; fax: +1 919 286 6861.E-mail address: kruco001{at}mc.duke.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionConclusionsFundingAcknowledgementsReferences |
|---|
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
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsFundingAcknowledgementsReferences |
|---|
Reperfusion-induced ventricular arrhythmias (VAs) have interested researchers since their first description in 1935.1
Preclinical models of reperfusion arrhythmias explored patho- and electrophysiological mechanisms and assessed anti-arrhythmic drug efficacy,2 generating concern about possible initiation of malignant arrhythmias with intracoronary thrombolytic therapy in patients with ST-elevation myocardial infarction (STEMI).3 Clinical experience, however, proved reassuring.3,4 Widespread use of intravenous thrombolytics saw reperfusion VAs [particularly accelerated idioventricular rhythms (AIVRs)] regarded optimistically as a non-invasive electric biomarker of successful epicardial reperfusion.5 More recently, it has been suggested that the presence of reperfusion-induced VAs following primary percutaneous coronary intervention (PCI) reflects an adverse cellular response to epicardial recanalization,6 although this is controversial.7,8
The mechanistic and prognostic implications of reperfusion VAs hinge upon precisely defining the timing and quality of epicardial reperfusion, and on capturing arrhythmias and differentiating those specifically correlated with reperfusion. Previous studies lack angiographic documentation of reperfusion; many used sporadic sampling or otherwise highly selected sustained VAs,9–12 while only a few smaller reports correlated angiographic recanalization and continuous rhythm capture.5,6,13,14 Further, VAs can result from ischaemia and infarction as well as from reperfusion, but such distinctions have never been reported in human subjects.
We sought to develop a more precise definition for reperfusion-induced VAs in human subjects by using simultaneously acquired angiographic and 24 h continuous high-fidelity electrocardiography (ECG) recordings to characterize the timing and quality of reperfusion, correlated with quantitative analysis of all VAs observed in a cohort of subjects with anterior STEMI treated with primary PCI.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsFundingAcknowledgementsReferences |
|---|
Study population
The data used for this retrospective analysis were obtained from subjects participating in the CAldaret ST-Elevation Myocardial Infarction (CASTEMI) study, which has been previously reported.15
Briefly, CASTEMI was a multicentre, randomized, double-blind trial that evaluated adjunctive MCC-135 (caldaret) in subjects undergoing primary PCI for acute STEMI, defined as >20 min of chest pain with onset <6 h from presentation, with >10 mm ST-segment elevation summed over the presenting 12-lead ECG. No drug effect was detected; thus, for this analysis, data for all CASTEMI patients with anterior MI and final TIMI grade 3 flow after primary PCI were pooled. Data were collected by an independent clinical research organization and subjected to quality control and validation procedures.
Angiographic analysis for TIMI flow
TIMI flow grades, as determined by coronary angiography in the setting of primary PCI, were assessed by an independent angiographic core laboratory blinded to all data apart from coronary angiograms (Bio-Imaging Technologies, Leiden, The Netherlands). TIMI flow grade was determined according to classifications used in the Thrombolysis In Myocardial Infarction (TIMI) trial.16
Electrocardiographic data acquisition
All subjects received continuous 24 h digital 12-lead ECG monitoring (NEMON 180+, NorthEast Monitoring, Inc., Maynard, MA, USA) initiated prior to PCI.17 The NEMON system acquires and stores a standard digital 12-lead ECG every 60 s in high-fidelity 720 Hz mode. The system simultaneously records continuous 3-lead beat-to-beat Holter rhythm on a digital clock that supports precise temporal correlations (Figure 1). Each research site's NEMON clock was synchronized to the catheterization laboratory clock so that ECG changes, rhythm changes, and changes in infarct-related artery (IRA) flow could be precisely correlated. Continuous digital ECG and Holter data were encrypted and blinded to the clinical team. Encrypted data were sent to the eECG core laboratory (eECG Core Laboratory, Duke Clinical Research Institute, Durham, NC, USA) for independent, blinded, continuous ST-segment recovery and quantitative arrhythmia analyses.
|
Continuous ST-segment recovery analysis
Continuously updated 12-lead ST-segment recovery analysis criteria and their correlations with infarct artery patency and myocardial reperfusion have been described in detail.18
,19 Briefly, determination of peak ST-segment deviation is based on the lead with greatest deviation, taken from the most abnormal ECG recorded during the monitoring period. Transitions between periods of 50% recovery from the immediately preceding peak or ST-segment re-elevation of >150 µV over preceding recovered ST-segment levels are continuously updated until stable 50% recovery, with stable defined as sustained for at least 4 h (Figure 1).
Quantitative rhythm analysis
Quantitative beat-to-beat rhythm analysis was performed on all digital 3-lead Holter recordings using Holter 5 software (NorthEast Monitoring, Inc.) with full disclosure visualization, waveform superimposition, and digitally sorted ECG morphology ‘bins’. All automatically assigned waveform labels were manually verified for every cardiac cycle from each subject, and VAs were discriminated from other sinus, supraventricular, aberrant, or pacemaker rhythms. Ventricular premature complexes (VPCs) were defined as premature beats with QRS-complex morphology that differed from baseline and had a width of at least 120 ms without an associated preceding P wave.20 A fusion beat (normal beat morphology fused with VPC morphology) was also considered a VPC. VAs were further categorized as isolated, couplets, or runs of three or more consecutive VPCs [including non-sustained and sustained AIVRs and ventricular tachycardias (VTs)], and total VPCs (sum of all isolated VPCs plus VPCs in couplets or runs). To generate quantitative VA rates over 24 h, total VPC counts were bundled into 5 min blocks for temporal correlation with stable ST-segment recovery and angiographic observations. Episodes of ventricular fibrillation in these recordings were also verified and documented. Ventricular fibrillation was defined as irregular undulations of varying shape and amplitude on ECG without discrete QRS or T waves, followed by visible direct-current cardioversion on Holter monitoring.21
Terminology and definitions
Ventricular arrhythmia bursts
Quantitative VA rates over the course of Holter recordings were used to characterize subject-specific background VA density. Ventricular arrhythmia bursts above this background were detected using an automated statistical outlier method, described in detail below. Once quantitative beat-to-beat Holter analysis for VAs was completed, subjects could be dichotomously classified as having or not having VA bursts. In all patients with VA bursts, timing (by onset) after reperfusion, duration, quantity, and density (per 5 min block) of VPCs, and ventricular rhythmic content (isolated VPCs, VPCs in couplets, or runs of three or more consecutive VPCs) of the bursts could be defined.
Reperfusion
Anatomic reperfusion was defined angiographically as the time of first documented re-establishment of TIMI 3 flow in the IRA, based on data recorded by the site. Physiological reperfusion was evaluated with continuous ST-segment recovery analysis as a non-invasive method not only for confirming angiographic IRA patency but also as a reflection of the reversal of ischaemia in the infarct zone. Physiological reperfusion was defined by stable ST-segment recovery, with timing defined as the transition from the peak ST-segment level immediately preceding 50% stable ST-segment recovery. We considered first documentation of TIMI 3 flow restoration in the IRA (anatomic reperfusion) associated with stable ST-segment recovery (physiological reperfusion) as the measure of timing (‘zero time’) and quality of reperfusion for temporal correlations with quantitative analysis of VAs (VA bursts).
Statistical methods
Outlier detection methodology
This method uses all VA counts obtained over the course of the Holter recording for a patient and automatically separates outliers (VA burst counts), if any, from background VA counts. Background counts are considered to arise from a Poisson distribution with mean µ. A VA count is considered an outlier when it is statistically significantly large enough that it likely does not arise from background VA activity. To establish which VA counts are significantly large, we considered type I error 
= 0.01 with a conservative Bonferroni adjustment for multiplicity of comparisons by dividing by 288 [the number of 5 min intervals in a 24 h Holter recording (288 = 24*60/5)]. Thus, a VA count above cutoff C(µ) equal to the (1 – /288) quantile of the background count distribution with mean µ is considered an outlier. This method is based on the forward search and is an iterative process, because it is unknown a priori which VA counts form the background VA activity.22 To form the initial background collection of VA counts, we chose a low mean µ = 1 corresponding to a cutoff equal to seven VAs/5 min interval. Ventricular arrhythmia counts below this initial cutoff level were considered as initial ‘background,’ which was required to contain at least 10% of the recorded VA counts; rarely, few next-smallest VA counts >7 were added to the initial ‘background’ collection to satisfy this requirement. Based on the current set of background counts, a new background average µ was computed and the next (higher) cutoff point C(µ) was determined as before, based on this new higher mean µ. If any VA count currently outside the background collection was below the new cutoff level, the smallest such count was added to the existing background collection and the next average µ with the next cutoff C(µ) was computed. The iteration was repeated until the background could not be enlarged, either because all recorded VA counts were already in the background (i.e. no outliers, and thus, no bursts detected), or VA counts not currently in the background were all above the current cutoff C(µ) and thus were identified as outliers forming the initial VA bursts. For patients with initial bursts, a statistical smoothing of counts over the duration of Holter recording was performed, and single-burst counts or groups of time-contiguous burst counts with maximum smoothed value below the last cutoff C(µ) were eliminated. The resulting collection of burst counts, if any remained, formed the subject's final VA bursts.
Other statistical analyses
Univariable comparisons of patient characteristics between subjects with reperfusion bursts vs. those without were performed with the 2-sample Wilcoxon rank sum test for continuous variables and the Fisher exact test for dichotomous variables. A P value <0.05 was considered statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsFundingAcknowledgementsReferences |
|---|
Continuous ECG data
More than 17 000 000 cardiac cycles from more than 3600 h of continuous Holter monitoring were analysed from all 157 anterior STEMI subjects with angiographically documented TIMI 3 flow after primary PCI. Average starting time of continuous ECG monitoring was 156 min following onset of chest pain and 42 min prior to primary PCI, with an average recording duration of 23.3 h per subject.
Ventricular arrhythmia bursts and reperfusion
Ventricular arrhythmias were present on Holter in 156/157 (99.3%) subjects; VA bursts concomitant with or subsequent to reperfusion occurred in 97/157 (62%) of the subjects. A study subject with VA bursts concomitant with angiographic TIMI 3 flow restoration (anatomic reperfusion) associated with stable ST recovery (physiological reperfusion) is visually presented in Figure 2. The distribution of time intervals between onset of reperfusion (defined as first angiographic TIMI 3 flow with 50% stable ST-segment recovery) and VA bursts is summarized in Figure 3. Of all VA bursts, 72% occurred within 20 min of onset of reperfusion (95% CI: 26.7, 72).
|
|
Characteristics of reperfusion ventricular arrhythmia bursts
The characteristics of VA bursts during or subsequent to reperfusion (reperfusion VA bursts) are summarized in Table 1. The median time from onset of reperfusion to first VA burst was 4 min (IQR: 0–43.3). VA bursts comprised a median total of 1290 VPCs (with a median of 97 VPCs per 5 min interval) and persisted for a total median duration of 105 min. Runs of three or more VPCs appeared to be more common in VA bursts than were isolated VPCs or couplets; in background VAs, however, isolated VPCs were more common (Figure 4).
|
|
Correlation with key subject characteristics
Demographic and clinical descriptors for subjects with or without VA bursts during or subsequent to reperfusion are listed in Table 2. Characteristics were generally well-matched between the groups. Subjects with bursts had significantly higher absolute peak ST-segment levels (P < 0.001) and showed possible trends towards earlier clinical presentations, with shorter time from onset of chest pain to first angiographic evidence of blood flow in the IRA (P = 0.05).
|
Timing of anatomic and physiological reperfusion
Temporal association between concomitantly acquired anatomic evidence of reperfusion with angiography and physiological evidence of reperfusion with continuous ST recovery monitoring is summarized for all subjects in Figure 5A. As can be seen in Figure 5B, the curve for subjects with reperfusion bursts is right-shifted relative to those without, indicating that subjects with bursts more frequently had further ST-segment deviation after angiographic reperfusion than those without bursts (P = 0.064).
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsFundingAcknowledgementsReferences |
|---|
Our analysis shows that with simultaneous angiographic TIMI flow grading, continuous high-fidelity 12-lead ST-segment recovery, and beat-to-beat Holter rhythm analysis, reperfusion-induced VAs can be defined more precisely in subjects with anterior STEMI. Our data suggest that VA bursts in excess of subject-specific background VA rates are temporally associated with angiographic TIMI 3 flow restoration (anatomic reperfusion) and stable ST-segment recovery (physiological reperfusion). We therefore consider reperfusion-induced VAs in human subjects to be defined by the presence of these reperfusion VA bursts. This definition provides a uniquely quantitative characterization of VAs specifically related to both epicardial recanalization and myocardial reperfusion. Unlike previous definitions, reperfusion VA bursts are statistically defined as outliers relative to a quantified, patient-specific background VA density and can thus include any of the many ventricular rhythms, from isolated VPCs to sustained fast VTs, that may comprise reperfusion arrhythmias. This definition may also be especially relevant to modern primary PCI therapy for STEMI, as both angiographic and ECG monitoring signals are technologies already routinely used in managing these patients.
From the earliest days of thrombolytics to the modern era of primary PCI for STEMI, reperfusion arrhythmias have sustained a wide range of mechanistic and prognostic interests.3,5,6,8–14,23–29 A major barrier to advancing understanding in this area, or even to achieving a meaningful synthesis of available reports, is the present heterogeneity of definitions used for reperfusion as well as for reporting and timing of VAs, or the correlation of the two. Observational reports of arrhythmias in large cohorts receiving thrombolytics almost certainly include arrhythmias from patients who never reperfuse, as recanalization rates with thrombolytics exceeding 75% of the patients treated have never been reported.30–35 In addition, sporadic capture of arrhythmias in some reports is likely subject to observational bias,35,36 whereas other reports, which include only sustained arrhythmias requiring cardioversion/defibrillation, will by definition exclude other potentially important, albeit less life-threatening, electrophysiological signals directly related to reperfusion.7,37
Our Holter data show that virtually all subjects experienced VAs in the course of infarction; however, this was not necessarily related to reperfusion per se. This is consistent with the report of Miller et al.,13 who analysed Holter data in patients with simultaneous angiographic observations associated with delivery of intracoronary thrombolytics, and it was found that quantification of VAs, both overall and by specific category, could not distinguish patients who reperfused from those who did not. Ventricular arrhythmia bursts may provide a conceptual framework for identifying unique events useful for specifically characterizing reperfusion-related electrophysiological signals above the background activity level.
The temporal proximity of such bursts to reperfusion events, whether defined anatomically or physiologically, supports the hypothesis that such sudden outlier rates of ventricular ectopic activity, identified through simultaneously acquired continuous ECG and angiographic data (obtained by protocol from all CASTEMI subjects) can be used to better define reperfusion VAs.
We should emphasize that our goal in defining reperfusion VA bursts is not to discriminate between successful and failed reperfusion; rather, in an era in which primary PCI produces TIMI 3 flow in more than 80% of the patients treated, our objective is to extend understanding of the electromechanical events that constitute the cellular response to TIMI 3 reperfusion. Thus, as in the primary analysis of the CASTEMI study, we have examined only subjects in whom final TIMI 3 flow was achieved.
It is generally understood that cohorts characterized by epicardial recanalization and TIMI 3 flow are not actually homogeneous.38 Populations with TIMI 3 flow can be meaningfully stratified by both microvascular ‘blush’ and ST-segment recovery, reflecting microvascular distribution of contrast and physiological cellular response to reperfusion, respectively.39–41 Well-defined reperfusion VA bursts may provide an additional ‘electric biomarker’ reflecting cellular signals that can be used to characterize quality of reperfusion. Engelen et al.6 studied acute-phase Holter data in anterior STEMI patients with successful TIMI 3 reperfusion and ST-segment recovery who were followed up for 6 months with serial echocardiographic measurement of infarct zone contractility and found that quantitative Holter characterization of VA density was highly predictive of failure to recover LV function.
Although our objective in performing this analysis of subjects with anterior STEMI from the CASTEMI cohort was not to establish mechanistic or clinical outcome correlations to reperfusion VA bursts, nonetheless, the observed correlation of such bursts with higher ST peak deviation and with the ‘right-shift’ of the time delay from anatomic to physiological reperfusion peak is noteworthy. Worsening of ST-segment elevation following angiographic reperfusion has been previously reported as a marker of adverse cellular response to reperfusion.24,25,42 The greater tendency for patients with reperfusion VA bursts to show delayed peaking of ST injury current following angiographic reperfusion compared with patients without such bursts suggests a mechanistic effect consonant with the findings of Engelen et al.; i.e. that reperfusion followed by additional ST-segment elevation and reperfusion VA bursts may indicate patients with cytotoxic reperfusion responses who are less likely to recover mechanical function of the infarct zone.
Limitations
Our study has a number of limitations, chief among which is the fact that our analysis is intended to provide observational details and a novel definition for reperfusion VA bursts. As such, our findings, although suggestive, cannot fully elucidate the mechanistic or prognostic significance of the observed phenomenon. Further, our study is retrospective, albeit prospectively planned across blinded core laboratory and data coordinating centre angiographic, ST-segment recovery, Holter arrhythmia, and clinical descriptor datasets. Finally, our findings are drawn from a modest cohort of subjects with anterior STEMI undergoing primary PCI. Important subgroup analyses are limited by cohort size, logistical consideration, and by the limitations inherent in the data collected for the study that formed the basis of our retrospective analysis; thus, the generalizability of our observations to non-anterior MIs or to patients treated with thrombolytic therapy and other medication must be regarded with caution.
Mechanistic questions remain as well. Although heart rate variability data were not available from the eECG Core laboratory in these studies, the relationship between heart rate behaviour and reperfusion VA bursts is interesting for future research. Even with continuous ECG monitoring and early angiography associated with primary PCI in the CASTEMI study, it is conceivable that some patients had transient or ‘cyclic’ changes in IRA patency prior to enrollment and monitoring. Whether or not such events might be protective, or might ‘precondition’ the infarct zone substrate, cannot be determined from our data.
|
Conclusions |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsFundingAcknowledgementsReferences |
|---|
In the current era of primary PCI for STEMI characterized by final TIMI 3 flow success rates of >80%, short- and long-term implications of reperfusion VAs cannot be imputed from existing literature, primarily due to limitations in existing definitions. By combining concomitant ECG monitoring and angiographic evidence of epicardial recanalization in conjunction with a patient-specific statistical definition of VA bursts outside of background ventricular ectopy rates, we have developed a novel definition of reperfusion arrhythmias that is more quantitative, comprehensive, and specific than any hitherto described. Further testing in larger patient cohorts is necessary in order to assess the degree to which this definition enables further insight into the mechanistic and prognostic implications of VAs in the modern era of STEMI therapy.
|
Funding |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsFundingAcknowledgementsReferences |
|---|
Support for this study was provided by the Hein Wellens Foundation, Maastricht, The Netherlands, and by the Duke Clinical Research Institute ECG Core Laboratory, Durham, North Carolina, U.S.A.
|
Acknowledgements |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsFundingAcknowledgementsReferences |
|---|
The authors thank the Hein Wellens Foundation, which supported this work. The authors also thank Phil d'Almada, MS, MApSt, Cindy L. Green, PhD, and Karen S. Pieper, MS, for assistance with data programming and management, and Penny Hodgson, MS, and Jonathan McCall for editorial assistance with this manuscript.
Conflict of interest: none declared.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsFundingAcknowledgementsReferences |
|---|
[1] Tennant R, Wiggers CJ. The effect of coronary occlusion on myocardial contraction. Am J Physiol (1935) 112:351–61.
[2] Manning AS, Hearse DJ. Reperfusion-induced arrhythmias: mechanisms and prevention. J Mol Cell Cardiol (1984) 16:497–518.[Web of Science][Medline]
[3] Krumholz HM, Goldberger AL. Reperfusion arrhythmias after thrombolysis. Electrophysiologic tempest, or much ado about nothing. Chest (1991) 99:135–40S.[CrossRef]
[4] Solomon SD, Ridker PM, Antman EM. Ventricular arrhythmias in trials of thrombolytic therapy for acute myocardial infarction. A meta-analysis. Circulation (1993) 88:2575–81.
[5] Gorgels AP, Vos MA, Letsch IS, Verschuuren EA, Bär FW, Janssen JH, et al. Usefulness of the accelerated idioventricular rhythm as a marker for myocardial necrosis and reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol (1988) 61:231–5.[CrossRef][Web of Science][Medline]
[6] Engelen DJ, Gressin V, Krucoff MW, Theuns DA, Green C, Cheriex EC, et al. Usefulness of frequent arrhythmias after epicardial recanalization in anterior wall acute myocardial infarction as a marker of cellular injury leading to poor recovery of left ventricular function. Am J Cardiol (2003) 92:1143–9.[CrossRef][Web of Science][Medline]
[7] Mehta RH, Harjai KJ, Grines L, Stone GW, Boura J, Cox D, et al. Sustained ventricular tachycardia or fibrillation in the cardiac catheterization laboratory among patients receiving primary percutaneous coronary intervention: incidence, predictors, and outcomes. J Am Coll Cardiol (2004) 43:1765–72.
[8] Ilia R, Zahger D, Cafri C, Abu-Ful A, Weinstein JM, Yaroslavtsev S, et al. Predicting survival with reperfusion arrhythmias during primary percutaneous coronary intervention for acute myocardial infarction. Isr Med Assoc J (2007) 9:21–3.[Web of Science][Medline]
[9] Cercek B, Lew AS, Laramee P, Shah PK, Peter TC, Ganz W. Time course and characteristics of ventricular arrhythmias after reperfusion in acute myocardial infarction. Am J Cardiol (1987) 60:214–8.[CrossRef][Web of Science][Medline]
[10] Ilia R, Amit G, Cafri C, Gilutz H, Abu-Ful A, Weinstein JM, et al. Reperfusion arrhythmias during coronary angioplasty for acute myocardial infarction predict ST-segment resolution. Coron Artery Dis (2003) 14:439–41.[CrossRef][Web of Science][Medline]
[11] Goldberg S, Greenspon AJ, Urban PL, Muza B, Berger B, Walinsky P, et al. Reperfusion arrhythmia: a marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarction. Am Heart J (1983) 105:26–32.[CrossRef][Web of Science][Medline]
[12] Chiladakis JA, Vlachos N, Patsouras N, Mazarakis A, Manolis AS. Usefulness of reperfusion ventricular arrhythmias in non-invasive prediction of early reperfusion and sustained coronary artery patency in acute myocardial infarction. J Thromb Thrombolysis (2001) 12:231–6.[CrossRef][Medline]
[13] Miller FC, Krucoff MW, Satler LF, Green CE, Fletcher RD, Del Negro AA, et al. Ventricular arrhythmias during reperfusion. Am Heart J (1986) 112:928–32.[CrossRef][Web of Science][Medline]
[14] Gressin V, Louvard Y, Pezzano M, Lardoux H. Holter recording of ventricular arrhythmias during intravenous thrombolysis for acute myocardial infarction. Am J Cardiol (1992) 69:152–9.[CrossRef][Web of Science][Medline]
[15] Bär FW, Tzivoni D, Dirksen MT, Fernandez-Ortiz A, Heyndrickx GR, Brachmann J, et al. Results of the first clinical study of adjunctive CAldaret (MCC-135) in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction: the randomized multicentre CASTEMI study. Eur Heart J (2006) 27:2516–23.
[16] The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group. N Engl J Med (1985) 312:932–6.[Medline]
[17] Stone GW, Webb J, Cox DA, Brodie BR, Qureshi M, Kalynych A, et al. Distal microcirculatory protection during percutaneous coronary intervention in acute ST-segment elevation myocardial infarction: a randomized controlled trial. J Am Med Assoc (2005) 293:1063–72.
[18] Krucoff MW, Croll MA, Pope JE, Pieper KS, Kanani PM, Granger CB, et al. Continuously updated 12-lead ST-segment recovery analysis for myocardial infarct artery patency assessment and its correlation with multiple simultaneous early angiographic observations. Am J Cardiol (1993) 71:145–51.[CrossRef][Web of Science][Medline]
[19] Shah A, Wagner GS, Granger CB, O'Connor CM, Green CL, Trollinger KM, et al. Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis. Reexamining the ‘gold standard’ for myocardial reperfusion assessment. J Am Coll Cardiol (2000) 35:666–72.
[20] Wellens HJ. Electrophysiology: ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart (2001) 86:579–85.
[21] Al-Khatib SM, Granger CB, Huang Y, Lee KL, Califf RM, Simoons ML, et al. Sustained ventricular arrhythmias among patients with acute coronary syndromes with no ST-segment elevation: incidence, predictors, and outcomes. Circulation (2002) 106:309–12.
[22] Atkinson AC. Fast very robust methods for the detection of multiple outliers. J Am Stat Assoc (1994) 89:1329–39.[CrossRef][Web of Science]
[23] Gressin V, Gorgels AP, Louvard Y, Lardoux H, Bigelow RH. Is arrhythmogenicity related to the speed of reperfusion during thrombolysis for myocardial infarction? Eur Heart J (1993) 14:516–20.
[24] Doevendans PA, Gorgels AP, van der Zee R, Partouns J, Bär FW, Wellens HJ. Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol (1995) 75:1206–10.[CrossRef][Web of Science][Medline]
[25] Wehrens XH, Doevendans PA, Ophuis TJ, Wellens HJ. A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty. Am Heart J (2000) 139:430–6.[CrossRef][Web of Science][Medline]
[26] Wu ZK, Iivainen T, Pehkonen E, Laurikka J, Tarkka MR. Ischemic preconditioning suppresses ventricular tachyarrhythmias after myocardial revascularization. Circulation (2002) 106:3091–6.
[27] Hohnloser SH, Zabel M, Olschewski M, Kasper W, Just H. Arrhythmias during the acute phase of reperfusion therapy for acute myocardial infarction: effects of beta-adrenergic blockade. Am Heart J (1992) 123:1530–5.[CrossRef][Web of Science][Medline]
[28] Bonnemeier H, Ortak J, Wiegand UK, Eberhardt F, Bode F, Schunkert H, et al. Accelerated idioventricular rhythm in the post-thrombolytic era: incidence, prognostic implications, and modulating mechanisms after direct percutaneous coronary intervention. Ann Noninvasive Electrocardiol (2005) 10:179–87.[CrossRef][Web of Science][Medline]
[29] Zhao JL, Yang YJ, Pei WD, Sun YH, Chen JL, Gao RL. Effect of statin therapy on reperfusion arrhythmia in patients who underwent successful primary angioplasty. Clin Res Cardiol (2008) 97:147–51.[CrossRef][Web of Science][Medline]
[30] A prospective trial of intravenous streptokinase in acute myocardial infarction (I.S.A.M.). Mortality, morbidity, and infarct size at 21 days. The I.S.A.M. Study Group. N Engl J Med (1986) 314:1465–71.[Abstract]
[31] Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI). Lancet (1986) 1:397–402.[CrossRef][Medline]
[32] Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet (1988) 2:349–60.[Medline]
[33] Simoons ML, Serruys PW, vd Brand M, Bär F, de Zwaan C, Res J, et al. Improved survival after early thrombolysis in acute myocardial infarction. A randomised trial by the Interuniversity Cardiology Institute in The Netherlands. Lancet (1985) 2:578–82.[Web of Science][Medline]
[34] Wilcox RG, von der Lippe G, Olsson CG, Jensen G, Skene AM, Hampton JR. Trial of tissue plasminogen activator for mortality reduction in acute myocardial infarction. Anglo-Scandinavian Study of Early Thrombolysis (ASSET). Lancet (1988) 2:525–30.[CrossRef][Web of Science][Medline]
[35] Shah PK, Cercek B, Lew AS, Ganz W. Angiographic validation of bedside markers of reperfusion. J Am Coll Cardiol (1993) 21:55–61.[Abstract]
[36] Kircher BJ, Topol EJ, O'Neill WW, Pitt B. Prediction of infarct coronary artery recanalization after intravenous thrombolytic therapy. Am J Cardiol (1987) 59:513–5.[CrossRef][Web of Science][Medline]
[37] Newby KH, Thompson T, Stebbins A, Topol EJ, Califf RM, Natale A. Sustained ventricular arrhythmias in patients receiving thrombolytic therapy: incidence and outcomes. The GUSTO Investigators. Circulation (1998) 98:2567–73.
[38] Roe MT, Ohman EM, Maas AC, Christenson RH, Mahaffey KW, Granger CB, et al. Shifting the open-artery hypothesis downstream: the quest for optimal reperfusion. J Am Coll Cardiol (2001) 37:9–18.
[39] van't Hof AW, Liem A, de Boer MJ, Zijlstra F. Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction. Zwolle Myocardial infarction Study Group. Lancet (1997) 350:615–9.[CrossRef][Web of Science][Medline]
[40] Andrews J, Straznicky IT, French JK, Green CL, Maas AC, Lund M, et al. ST-segment recovery adds to the assessment of TIMI 2 and 3 flow in predicting infarct wall motion after thrombolytic therapy. Circulation (2000) 101:2138–43.
[41] Stone GW, Peterson MA, Lansky AJ, Dangas G, Mehran R, Leon MB. Impact of normalized myocardial perfusion after successful angioplasty in acute myocardial infarction. J Am Coll Cardiol (2002) 39:591–7.
[42] Miida T, Oda H, Toeda T, Higuma N. Additional ST-segment elevation immediately after reperfusion and its effect on myocardial salvage in anterior wall acute myocardial infarction. Am J Cardiol (1994) 73:851–5.[CrossRef][Web of Science][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  R. H. Mehta, A. Z. Starr, R. D. Lopes, J. S. Hochman, P. Widimsky, K. S. Pieper, P. W. Armstrong, C. B. Granger, and for the APEX AMI Investigators Incidence of and Outcomes Associated With Ventricular Tachycardia or Fibrillation in Patients Undergoing Primary Percutaneous Coronary Intervention JAMA, May 6, 2009; 301(17): 1779 - 1789. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Majidi, A. S. Kosinski, S. M. Al-Khatib, M. E. Lemmert, L. Smolders, A. van Weert, J. H.C. Reiber, D. Tzivoni, F. W.H.M. Bar, H. J.J. Wellens, et al. Reperfusion ventricular arrhythmia 'bursts' predict larger infarct size despite TIMI 3 flow restoration with primary angioplasty for anterior ST-elevation myocardial infarction Eur. Heart J., April 1, 2009; 30(7): 757 - 764. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||