Ventricular arrhythmia burst is an independent indicator of larger infarct size even in optimal reperfusion in STEMI.

OBJECTIVE: We hypothesized that ventricular arrhythmia (VA) bursts during reperfusion phase are a marker of larger infarct size despite optimal epicardial and microvascular perfusion. METHODS: 126 STEMI patients were studied with 24h continuous, 12-lead Holter monitoring. Myocardial blush grade (MBG) was determined and VA bursts were identified against subject-specific background VA rates in core laboratories. Delayed-enhancement cardiovascular magnetic resonance imaging was used to determine infarct size. RESULTS: In the group with MBG 3 no significant differences were found for baseline characteristics between burst versus no burst (102 vs. 24). In those with optimal epicardial and microvascular reperfusion (TIMI 3, stable ST-recovery, and MBG 3), VA burst was associated with larger infarct size (N=102/126; median 11.0 vs. 5.1%; p=0.004). CONCLUSION: In the event of MBG 3, VA bursts were associated with significantly larger infarct size even if optimal epicardial and microvascular reperfusion was present.

Implications of ventricular arrhythmia "bursts" with normal epicardial flow, myocardial blush, and ST-segment recovery in anterior ST-elevation myocardial infarction reperfusion: a biosignature of direct myocellular injury "downstream of downstream".

AIMS: Establishing epicardial flow with percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) is necessary but not sufficient to ensure nutritive myocardial reperfusion. We evaluated whether adding myocardial blush grade (MBG) and quantitative reperfusion ventricular arrhythmia "bursts" (VABs) surrogates provide a more informative biosignature of optimal reperfusion in patients with Thrombolysis in Myocardial Infarction (TIMI) 3 flow and ST-segment recovery (STR). METHODS AND RESULTS: Anterior STEMI patients with final TIMI 3 flow had protocol-blinded analyses of simultaneous MBG, continuous 12-lead electrocardiogram (ECG) STR, Holter VABs, and day 5-14 SPECT imaging infarct size (IS) assessments. Over 20 million cardiac cycles from >4500 h of continuous ECG monitoring in subjects with STR were obtained. IS and clinical outcomes were examined in patients stratified by MBG and VABs. VABs occurred in 51% (79/154) of subjects. Microcirculation (MBG 2/3) was restored in 75% (115/154) of subjects, of whom 53% (61/115) had VABs. No VABs were observed in subjects without microvascular flow (MBG of 0). Of 115 patients with TIMI 3 flow, STR, and MBG 2/3, those with VABs had significantly larger IS (median: 23.0% vs 6.0%, p=0.001). Multivariable analysis identified reperfusion VABs as a factor significantly associated with larger IS (p=0.015). CONCLUSIONS: Despite restoration of normal epicardial flow, open microcirculation, and STR, concomitant VABs are associated with larger myocardial IS, possibly reflecting myocellular injury in reperfusion settings. Combining angiographic and ECG parameters of epicardial, microvascular, and cellular response to STEMI intervention provides a more predictive "biosignature" of optimal reperfusion than do single surrogate markers.

Impact of early, late, and no ST-segment resolution measured by continuous ST Holter monitoring on left ventricular ejection fraction and infarct size as determined by cardiovascular magnetic resonance imaging.

BACKGROUND: The goal of this study is to determine the predictive value of ST-segment resolution (STR) early after percutaneous coronary intervention (PCI), late STR, and no STR for left ventricular ejection fraction (LVEF) and infarct size (IS) by cardiovascular magnetic resonance (CMR) at follow-up in patients with ST-segment elevation myocardial infarction. METHODS: The analysis included 199 patients who were enrolled in the PRoximal Embolic Protection in Acute myocardial infarction and Resolution of ST-Elevation trial and in whom both continuous ST Holter and CMR at follow-up were available. Patients were stratified into 3 groups: (1) early complete (≥70%) STR measured immediately after last contrast injection (n = 113); (2) late complete STR (n = 52), defined as complete STR from 30 to 240 minutes after PCI; and (3) no complete STR after 240 minutes (n = 34). RESULTS: Patients with early STR had more preserved LVEF and smaller IS compared to patients with late STR or no STR (LVEF: early STR, 54% ± 8%; late STR, 46% ± 13%; no STR, 43% ± 11%; and IS: 3.9 ± 3.3 g/m(2); 8.0 ± 6.9 g/m(2); 12.0 ± 6.0 g/m(2); respectively; all P < .0001). Early STR was independently predictive for LVEF (ß = 8.5; P = .0005) and IS (ß = -7.0; P < .0001). Late STR was not predictive for LVEF (ß = 1.6; P = .51) but predictive for IS (ß = -3.5; P = .003). CONCLUSIONS: Patients with early complete STR after primary PCI have better preserved LVEF and smaller IS. Patients with late complete STR do not have better preserved LVEF but do have smaller IS. ST-segment resolution is a strong, independent predictor of LVEF and IS as assessed by CMR.

RR-interval irregularity precedes ventricular fibrillation in ST elevation acute myocardial infarction.

BACKGROUND: Sudden cardiac arrest is a leading cause of death in industrialized countries, and ischemic ventricular fibrillation (VF) is a frequent cause. OBJECTIVE: The purpose of this study was to determine whether patients with ST elevation myocardial infarction (STEMI) who develop ischemic VF show more overall RR-interval irregularity (RRI) than do STEMI patients without ischemic VF. METHODS: Ischemic VF was identified in 41 patients from 1,473 digital 12-lead Holter recordings from three separate STEMI studies. Continuous 3-lead and 12-lead electrocardiogram (ECG) snapshots recorded every minute were compared between all ischemic VF patients and 123 random patients without ischemic VF. Time intervals from start of Holter to ischemic VF and equivalent intervals in the controls were used for calculations. ECG variables related to conduction intervals and severity of ischemia were measured using the most ischemic 12-lead ECG. RRI was calculated as the square root of the mean squared differences of successive RR intervals. For RRI, all QRS complexes, including ventricular ectopic beats, were used. RESULTS: No baseline differences were observed between the study and control groups, except for male preponderance among ischemic VF patients (90% vs 72%, P = .019). QRS interval, ECG ischemia severity, RRI, and number of ventricular ectopic beats were significantly associated with ischemic VF. Multivariate analysis revealed RRI (odds ratio 1.006, 95% confidence interval 1.001-1.010, P = .016) and ST deviation score (odds ratio 1.073, 95% confidence interval 1.041-1.106, P <.001) as the only statistically significant predictors of ischemic VF. CONCLUSION: In the period before ischemic VF, RRI and ST deviation score are associated with ischemic VF in STEMI patients. These findings could have important pathophysiologic and clinical implications.

Reperfusion ventricular arrhythmia 'bursts' predict larger infarct size despite TIMI 3 flow restoration with primary angioplasty for anterior ST-elevation myocardial infarction.

Aims Successful epicardial reperfusion with primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) can paradoxically evoke myocardial reperfusion injury, which may be signalled by temporally associated ventricular arrhythmias (VAs). We correlated reperfusion VA 'bursts' with final infarct size (IS) in patients with restored TIMI 3 flow following PCI for anterior STEMI. Methods and results All 128 anterior STEMI patients with final TIMI 3 flow had continuous 24 h digital 12-lead ECG with simultaneous Holter recording initiated prior to PCI, and Day 7/discharge SPECT imaging IS assessment. Angiography, SPECT imaging, continuous ST recovery, and quantitative rhythm analyses were performed. Reperfusion VA bursts were defined against patient-specific background VA rates and timed as concomitant with or following first angiographic TIMI 3 flow restoration associated with > or =50% stable ST recovery; they were then correlated with IS and global left ventricular ejection fraction (LVEF) at Day 7/discharge. Bursts occurred in 81/128 (63%) patients and were significantly correlated with larger IS and worse LVEF (median: 21.0 vs. 10.0%, P < 0.001; 35.5 vs. 46.5%, P < 0.001, respectively). In multivariable analyses that adjusted for known predictors of IS, the association of bursts with larger IS remained significant; similar results were seen for worse LVEF. Conclusion Reperfusion VA bursts predict larger IS despite TIMI 3 flow restoration with > or =50% stable ST recovery following PCI for anterior STEMI. Well-characterized reperfusion VAs may provide a novel biomarker of reperfusion injury.

Preexcitation and myocardial infarction: conditions with confusing electrocardiographic manifestations.

The electrocardiogram allows easy recognition of myocardial infarction and preexcitation syndromes but may cause confusion when both conditions are present simultaneously. Two cases where myocardial infarction is masked and/or mimicked by a preexcitation syndrome are presented.

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.

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 >or=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.

Effects of acute atrial dilation on heterogeneity in conduction in the isolated rabbit heart.

INTRODUCTION: Atrial dilation plays an important role in the development and persistence of atrial fibrillation (AF). The mechanisms by which atrial dilation increases the vulnerability to AF are not fully understood. METHODS AND RESULTS: In 11 isolated rabbit hearts, the right atrium was acutely dilated by increasing the intra-atrial pressure from 2 to 9 and 14 cm H2O. A rectangular mapping array of 240 electrodes (spatial resolution 0.5 mm) was positioned on the free wall of the right atrium. The atrium was paced from four different sites at intervals of 240 and 125 msec. At normal atrial pressure (2 cm H2O), conduction was uniform in all directions with an anisotropy ratio between 1.5 and 1.7. Increasing the pressure to 9 cm H2O decreased the normalized conduction velocity during rapid pacing by 18%. The incidence of areas of slow conduction and conduction block increased from 6.6% and 1.6% to 10.2% and 3.3%. At 14 cm H2O, conduction velocity decreased by 31% and the percentage of slow conduction and block further increased to 11.5% and 6.6% (P < 0.001). The appearance of lines of intra-atrial block was largely dependent on the pacing site. Whereas during pacing at the cranial part of the crista terminalis no increase in conduction delays occurred, pacing from the low right atrium unmasked several lines of block oriented parallel to the major trabeculae and the crista terminalis. In an additional series of six hearts the left atrium also was mapped. The effect of dilation of the left atrium was comparable to that of the right atrium. Increasing the atrial pressure to 14 cm H2O increased the amount of intra-atrial conduction block threefold to fourfold. CONCLUSION: Acute atrial dilation results in slowing of conduction and an increase of the amount of intra-atrial conduction block. The increase in spatial heterogeneity in conduction was related to the anisotropic properties of the atrial wall.