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. (J Cardiovasc Electrophysiol, Vol. 14, pp. 269‐278, March 2003)

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.

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.

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.

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In the event of MBG 3, VA bursts were associated with significantly larger infarct size even if optimal epicardial and microvascular reperfusion was present.

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