Image-based motion correction for optical mapping of cardiac electrical activity.

Optical mapping, with membrane-bound, voltage-sensitive dyes, is widely used for in vitro recording of cardiac electrical activity. The spatial registration of such maps is lost when the heart moves with respect to a fixed photodetector array and contraction can generate substantial artifact if background fluorescence is not uniformly distributed. While motion artifact is commonly suppressed with electromechanical uncoupling agents, there are circumstances where these are undesirable. This study outlines a novel image-based approach for retrospective motion artifact correction. Isolated Langendorff-supported rat hearts (n = 8), stained with di-4-ANEPPS, were illuminated at 516 ± 14 nm and fluorescent emission (>565 ± 10 nm) was acquired with a charge multiplying CCD camera. Background fluorescence was segmented in successive frames and stabilized using a non-rigid image registration algorithm. The resultant image deformation was used to estimate material point movement on the heart surface, so that total fluorescence could be mapped frame-by-frame to appropriate reference pixels. Finally, residual motion artifact was identified and removed. The effectiveness of this correction method was evaluated over 18 experimental datasets. Signal-to-noise ratio was increased more than fourfold, and activation time and action potential duration (APD) could be estimated at 24% more pixels than in the raw data. The variability of all APD measures was substantially reduced (i.e. APD50 estimated as 83.8 ± 45.8 ms before correction was 52.1 ± 4.7 ms afterward). This approach provides a robust means of recovering optical action potentials in the presence of substantial motion artifact.

High-resolution 3-dimensional reconstruction of the infarct border zone: impact of structural remodeling on electrical activation.

RATIONALE: Slow nonuniform electric propagation in the border zone (BZ) of a healed myocardial infarct (MI) can give rise to reentrant arrhythmia. The extent to which this is influenced by structural rather than cellular electric remodeling is unclear. OBJECTIVE: To determine whether structural remodeling alone in the infarct BZ could provide a substrate for re-entry by (i) characterizing the 3-dimensional (3D) structure of the myocardium surrounding a healed MI at high spatial resolution and (ii) modeling electric activation on this structure. METHODS AND RESULTS: Anterior left ventricular (LV) infarcts were induced in 2 rats by coronary artery ligation. Three-dimensional BZ volume (4.1 mm(3) and 5.6 mm(3)) were imaged at 14 days using confocal microscopy. Viable myocytes were identified, and their connectivity and orientation were quantified. Preserved cell networks were observed in the subendocardium and subepicardium of the infarct. Myocyte tracts traversed the BZ, and there was heavy infiltration of collagen into the adjacent myocardium. Myocyte connectivity decreased by ≈65% over 250 µm across the BZ. This structure was incorporated into 3D network models on which activation was simulated using Luo-Rudy membrane dynamics assuming normal cellular electric properties. Repetitive stimulation was imposed at selected BZ sites. Stimulus site-specific unidirectional propagation occurred in the BZ with rate-dependent slowing and conduction block, and reentry was demonstrated in one substrate. Activation times were prolonged because of tract path length and local slowing. CONCLUSIONS: We have used a detailed image-based model of the infarct BZ to demonstrate that structural heterogeneity provides a dynamic substrate for electric reentry.