Macro re-entry around the SAN.

<p>A: Modified 3D model with atrial fibrosis between the SAN and epicardial surface. B: Simulation of macro re-entry. Bi shows data where insulating border was omitted, where the initiated macro re-entry induced atrial fibrillation. Bii shows data when insulating border-SEPs configuration was included where atrial flutter was observed. In each, Bi and Bi, top row shows time frames from the simulation and bottom row illustrates the mechanism. The periods for SAN and atrial pacing in each simulation is also given.</p

External re-entry.

<p><b>Effects of atrial tachycardia on SAN excitation.</b> A: Transmural and epicardial views of the initiated scroll wave (green isosurfaces) and the transmural filament (black line) of the scroll wave. Whereas the full model is shown, 5 anatomical cases were simulated. B: Data for 5 anatomical cases in five columns. The atrial anatomy is omitted for clarity. First row shows representative number and shape of filaments. Second and third rows show dominant frequency (DF) maps of 5 s of data. Slices through the SAN (second row) and through the paranodal area (third row) are shown. C: Time course of filament numbers. The data were smoothed by moving window averaging for clarity.</p

3D electro-anatomical human SAN model.

<p>A: Action potential profiles of atrial (cyan), SAN (red), and paranodal area (blue) cells. Gray box: Epicardial (Bi and Bii) and endocardial (Ci and Cii) views of the 3D anatomy consisting of atrial tissue (cyan), SAN (red), paranodal area (blue), insulating border (yellow tissue encasing of the SAN in Bii and Cii), and SEPs. Left panels (Bi, Ci) show the anatomy without border-SEPs. Right column (Bii, Cii) shows the anatomy with the insulating border-SEPs. D: Cell-cell coupling centre to periphery diffusion gradient inside the SAN. The diffusion increases from the SAN’s centroid towards the atrium. The paranodal area (blue) is shown for anatomical reference. E: An instance of uniform distribution of SAN action potential cycle lengths in a range of 800 ms to 1000 ms with a mean of 850 ms. An instance of SAN cell cycle lengths is illustrated in <b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0183727#pone.0183727.s001" target="_blank">S1 Fig</a>.</b> The paranodal area’s cycle length was kept at 1400 ms throughout.</p

SAN activation times and leading pacemaker sites under basal conditions.

<p>I, A-D: Colour coded SAN activation times are shown in four cases. Leading pacemaker site’s (white sphere within the SAN) coordinates and period of atrial pacing, P, for each case are shown. Paranodal area (blue in panels C and D) when present is shown. Atrial tissue (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0183727#pone.0183727.g001" target="_blank">Fig 1</a>) and atrial activation are omitted from the panels for clarity. II. Locations of LPS in anatomical variants. The location of minimum diffusion with the SAN is coincident with the SAN only LPS. III. Cycle lengths of individual SAN cells.</p

Fibrosis within the old human SAN.

<p>The dashed red lines delineate SAN pacemakers. The left panel shows a representative slice from a young heart while the right panel shows a slice from an old heart. The Masson’s trichrome staining shows cell cytoplasm (pink) and connective tissue or fibrosis (blue, blue-green). Whereas the left panel’s SAN region is dominated by pink staining, the right panel has diffuse fibrosis.</p

SAN micro re-entry without SEPs.

<p>A: Epicardial as well as transmural views of SAN (red), paranodal area (blue), and non-conducting intra-SAN fibrosis (gray). The morphology of the fibrosis is further illustrated by the transmural left and right views. Locations of the omitted SEPs are shown by circular symbols to provide further anatomical landmarks. B: Evolution of micro re-entry. Top row (Bi) shows data from simulation without insulating border. Bottom row (Bii) shows data from simulation with insulating border without SEPs. Bi data show dissipation of re-entry due to absence of insulating border. Sixth panel illustrates the mechanism. Bii shows data with the insulating border configuration where the re-entry persisted unhindered. Sixth panel illustrates the mechanism.</p

Media 2: 3D absolute shape measurement of live rabbit hearts with a superfast two-frequency phase-shifting technique

Originally published in Optics Express on 11 March 2013 (oe-21-5-5822

Media 1: 3D absolute shape measurement of live rabbit hearts with a superfast two-frequency phase-shifting technique

Originally published in Optics Express on 11 March 2013 (oe-21-5-5822

Media 3: 3D absolute shape measurement of live rabbit hearts with a superfast two-frequency phase-shifting technique

Originally published in Optics Express on 11 March 2013 (oe-21-5-5822

Ventricular remodeling in heart failure.

<p>(A) Ventricular remodeling of major ion channel subunits and accessory proteins in heart failure. (B) Regional specificity of targets in failing and nonfailing hearts of both genders.</p