The architecture of interstitial fibrosis and wave front direction are key determinants of activation delay during premature stimulation in chronically diseased human myocardium.
Hypothesis-generating in animal fibrosis models; leaves open translation to human conduction and arrhythmia risk.
The study demonstrates that in chronically diseased human myocardium, nonuniform anisotropic characteristics imposed by long fibrotic strands cause a progressive increase of activation delay, starting at long coupling intervals of premature stimuli. The increase strongly depends on the direction of the wave front with respect to fiber direction and the architecture of fibrosis.
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Kawara et al. (2001) studied this question.
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