Intracellular calcium cycling plays an important role in cardiac short-term memory during dynamic pacing, as demonstrated by the significant abbreviation of APD accommodation after ryanodine administration in canine ventricular myocardium.
Hypothesis-generating for Ca²⁺ in cardiac short-term memory; human studies required before clinical translation.
Cardiac short-term memory is an intrinsic property of paced myocardium that reflects the influence of pacing history. Using an optical mapping method to record membrane voltage and intracellular calcium (Ca(2 +)(i)), this study investigated the properties and mechanisms of short-term memory in isolated and perfused canine wedge preparations. In addition to the dynamic and S1S2 pacing protocols, a perturbed downsweep pacing protocol was used to get a complete overview of the restitution portrait. Abrupt changes in basic cycle length (BCL) were applied to investigate the accommodation process of action potential duration (APD). The results showed unobvious differences of memory among the epi-, mid- and endo-myocytes, implying an insignificant memory-induced transient heterogeneity in APD across the transmural canine hearts. With the decrease of pacing rate S1, memory gradually elevated and achieved a maximum around 400 ms, and then reduced as S1 decreased further, indicating a non-monotonic relationship between memory and the pacing rate. After suppressing the Ca(2 +)(i) transient with ryanodine (3 µmol l(-1)), the accommodation process of APD to a new BCL significantly abbreviated (τ = 37.41 ± 4.42 stimuli before ryanodine, τ = 15.84 ± 4.74 stimuli after ryanodine, p < 0.01). Therefore, Ca(2 +)(i) cycling was suggested to play an important role in memory during dynamic pacing.
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Zhang et al. (2010) studied Cardiac short-term memory and electrical restitution. Ryanodine vs. Before ryanodine was evaluated on Accommodation process of action potential duration (APD) to a new basic cycle length (BCL) (p=<0.01).
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