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. 1998 May;79(5):474–480. doi: 10.1136/hrt.79.5.474

Enhanced dispersion of epicardial activation-recovery intervals at sites of histological inhomogeneity during regional cardiac ischaemia and reperfusion

E Gottwald 1, M Gottwald 1, S Dhein 1
PMCID: PMC1728703  PMID: 9659194

Abstract

Objective—To examine how epicardial activation and repolarisation patterns change in the course of ischaemia, and how these changes are related to the underlying histological structures.
Methods—Langendorff perfused isolated rabbit hearts were submitted to 30 minutes of left anterior descending coronary artery occlusion followed by 30 minutes of reperfusion. A 256 channel epicardial map was plotted during the various experimental phases. Activation time points were determined as t(dU/dtmin) and repolarisation time points as t(dU/dtmax). From these data the local activation-recovery interval (ARI), its dispersion (SD of ARI), and the geometry of the activation spread could be analysed. After the experiments the hearts were processed histologically and the mapping data were projected onto histological slides.
Results—There was elevation of the ST segment within the occluded area, which recovered during reperfusion. Within this area, ARI was significantly shortened and its dispersion was maximally enhanced. The enhancement of dispersion was pronounced at sites of histological inhomogeneity like fat, connective tissue, or vessels. There was also a change in the preferential direction of activation spread within the occluded zone with a marked transverse propagation of the activation wavefront, whereas under normal conditions the activation followed the longitudinal fibre axis. In addition, the total activation time in the occluded area was significantly prolonged.
Conclusions—Ischaemia alters the local activation pattern with enhanced dispersion, especially at sites of histological irregularity, transverse shift of the activation waves, and a general slowing of conduction, which may explain the increased susceptibility to arrhythmia in hearts with enhanced histological irregularities—for example, an infarct or in multi-infarcted hearts, or after myocarditis. 

 Keywords: dispersion;  epicardial activation-recovery interval;  ischaemia

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Figure 1  .

Figure 1  

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(A) Schematic representation of the experimental setup and analysis. Left upper panel: mapping system with 256 unipolar electrodes. Right upper and lower panels: the principle of vector construction: from the activation time and position of the central electrode and those electrodes, which were activated after the central electrodes, vectors were calculated and added to produce a resulting vector giving the direction and apparent velocity of the local activation. Left lower panel: projection of the resulting vector field on the composed histological image, with the construction of the angle between the fibre axis and the local activation vector. (B) Left panel: position of the concave electrode plate in relation to the ischaemic zone and the occlusion of the left anterior coronary artery branch. Right panel: typical unipolar potentials, with indication of the activation time point (determined as time point of dU/dtmin) and the repolarisation time point (determined as the time point of dU/dtmax). For details see Methods.

Figure 2  .

Figure 2  

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(A) Graphically reproduced images of the left ventricular wall during control (upper panel) and after 10 minutes of regional ischaemia (lower panel) in a typical experiment. The square represents the shape of the electrode grid, while black areas represent vessel sections. Numbers indicate the activation-recovery interval (ARI) in ms  at that particular electrode. Vectors show local velocity and orientation of the propagating wave front at that point. Around the grid, original recordings of the unipolar ECGs of the respective electrode are displayed. The ischaemic border zone is represented as a black line in the lower part of the figure. The formerly homogeneously distributed ARI, which resemble each other closely in morphology, change to heterogeneous ARI with different morphology; the most pronounced shortening is in the direction of the propagating wavefront behind the vessel reflected by a shifted T wave in the ECG to the left and a less pronounced shortening directly in front of the vessel in the direction of the wavefront. Total activation time under control conditions was 5 ms , and after 10 minutes of ischaemia, 11 ms . (B) Left panel: ARI of the left ventricular wall under equilibrium conditions. Right panel: ARI of the left ventricular wall after 10 minutes of regional ischemia. The location of the vessels as seen in the histological image are displayed.

Figure 3  .

Figure 3  

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(A) QTc, calculated as ARI (activation-recovery interval)/BCL (basic cycle length), of the left ventricular wall; (B) Local dispersion of the left ventricular wall. Values are given as the means of six experiments in the course of ischaemia and reperfusion. Error bars = SEM. *p < 0.05 v values after 60 minutes of equilibration (Con).

Figure 4  .

Figure 4  

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Activation-recovery interval (ARI) isochrones of a typical experiment. The isochrones indicate areas of ARI within the same range as given by the numbers. The graph shows the situation for the equilibration period, at two and 10 minutes of regional ischaemia, and after 30 minutes of reperfusion.

Figure 5  .

Figure 5  

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Absolute number of vectors that deviate from the fibre axis between 65° and 90° during the course of the experiment. All values are given as means of six experiments. Error bars = SEM. *p < 0.05 v control (that is, 60 minutes at equilibrium).

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